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Subject index volume 51
Advances in Enzyme Regulation 51 (2011) 320–329
Contents lists available at ScienceDirect
Advances in Enzyme Regulation journal homepage: www.elsevier.com/locate/ advenzreg
Subject index volume 51 Achilles’ heel cancer, targeting the cancer initiating cell of, 152–160 effects of cytotoxic effects of docetaxel on CICs by combination with targeted therapies and natural products, 159–160 natural products-dietary supplements and prostate cancer, 155–156 prostate cancer, 153 prostate cancer and radiation therapy, 153 prostate cancer therapy, 153 side effects of radio and chemo-therapies–induction of signaling pathways, 153–154 targeting signal transduction pathways in prostate cancer, 154–155 Akt activated in leukemia cell survival, 38–40, 42–44 regulates de novo lipogenesis though activation of SREBP and its target genes, 196–200, 203–205 role in deciphering the signaling pathways of cancer stem cells of GBM, 164–169 Apoptosis, p53 and ceramide have been shown to regulate, 220–226 AP sites, form when the reaction of hydrogen peroxide with DNA causes bases, 264–265 Arachidonic acid, well known chemoattractant for phagocytes, 59 Archaea, synthesis and use of Ins in, 84–89 Bacteria, inositol in, 84–89 B cell survival regulation by inositol 1,4,5-trisphosphate 3-kinase B, 66–68, 70–71 regulation by inositol 1,4,5-trisphosphate 3-kinase B in Ins(1,4,5)P3 3-kinases, 67–68 mechanisms of Ins(1,3,4,5)P4 action, 68, 70 Biosynthesis, of archaetidylinositol, 84, 87 Bone marrow transplantation, of weeble fetal liver cells into lethally irradiated wild type mice, 103 Cancer, overexpression or over-activity of ChoKa but not ChoKb in, 188–191 Cancer initiating cell, targeting the Achilles' heel of cancer, 152–160 effects of cytotoxic effects of docetaxel on CICs by combination with targeted therapies and natural products, 159–160 natural products-dietary supplements and prostate cancer, 155–156 prostate cancer, 153 prostate cancer and radiation therapy, 153 prostate cancer therapy, 153 side effects of radio and chemo-therapies-induction of signaling pathways, 153–154 targeting signal transduction pathways in prostate cancer, 154–155 Cancer stem cells, promote differentiation into more mature prostate cancer cells, 152, 158 Cell-signaling, functions of the PPIP5Ks, 15 0065-2571/$ – see front matter doi:10.1016/j.advenzreg.2011.03.001
Subject Index / Advances in Enzyme Regulation 51 (2011) 320–329
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Ceramide regulates cell cycle arrest, senescence, and apoptosis, 220–226 role in signal transduction and cellular function., 229–231, 233, 238–239, 241–243 sphingomyelinases mediate the hydrolysis of sphingomyelin in production of, 51, 54, 56 Chemotherapeutic drugs, for treatment of prostate cancer, 156–160 Chimeric mice, role of inositol polyphosphate 4-phosphatase 1 in platelet function using, 103–104 Choline kinase (E.C.2.7.1.32), alpha and beta, in carcinogenesis, different role in lipid metabolism and biological functions, 183–184, 186–191 biochemical characterization of ChoK isoforms, 184, 186–187 ChoK and lipid metabolism, 184, 186 differential role between ChoK isoforms in cell transformation and tumorigenesis, 187–189 genes encoding choline/ethanolamine kinases, 183–184 regulation of ChoK activity, 187 specific inhibition of ChoKa, 189–190 Choline kinase inhibitors, with potential antitumoral activity, 189–191 Chromatin, important regulators of gene expression, 118, 120–121 Chromatin fibers, studies of DNA and, 259, 267–269 Chromatin immunoprecipitation, YBX1 targets identified in colorectal cancer cells by, 133–134 Chromatin organization, pathogenesis of muscular laminopathies associated with, 251 CK2 (EC 2.7.11.1) impact of PTEN regulation on PI3 K-dependent signaling and leukemia cell survival, 37–44 on PI3 K-dependent signaling and leukemia cell survival, impact of PTEN regulation by highly oncogenic non-oncogene, in tumorigenesis and leukemia, 40–41 Class I PI3Ks, signalling via, 27–29, 31–33 Colitis, effects of BLT2-deficiency in, 61 Colorectal cancer, role of YBX1 as a prognostic factor in, 129–130, 132–135 Diphosphoinositol polyphosphates molecular mechanisms of, 13–20, 22 phospholipase C-initiated synthesis of metabolism of, 13–15 protein phosphorylation by, 19–20, 22 receptors for, 17–18 signaling by, 15–17 DNA damage, p53-dependent apoptosis occurs secondary to, 220, 222–225 DNA damage response-associated proteins, role of Fhit proteins in, 210, 212, 215 DNA fibers, analysis of DNA repair on, 259–268 DNA repair, on DNA fibers, 258, 263, 265 DNA replication, temporal and functional analysis in early S phase, 257–270 analysis of, 259–263 analysis of chromatin structure and dynamics of DNA replication, 268–269 analysis of DNA repair on DNA fibers, 263–266 genomic and temporal mapping of DNA replication origins activated early in S phase, 266–268 studies of DNA and chromatin fibers, 259 Drug design, of phosphoinsitide-3-kinase, 273–278 activation by phosphotyrosine peptide (pY-pep) binding, 275 cancer-associated mutations, 276–277 structure of the p110a/niSH2 complex of PI3 Ka, 275 Early S phase, temporal and functional analysis of DNA replicated in, 257–270 analysis of, 259–263 analysis of chromatin structure and dynamics of DNA replication, 268–269 analysis of DNA repair on DNA fibers, 263–266 genomic and temporal mapping of DNA replication origins activated early in S phase, 266–268 studies of DNA and chromatin fibers, 259
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Subject Index / Advances in Enzyme Regulation 51 (2011) 320–329
EDMD see Emery-Dreifuss muscular dystrophy Eicosanoids, 12-HHT was originally identified as a by-product of thromboxane A2 biosynthesis, 61 Emery-Dreifuss muscular dystrophy (EDMD), caused by LMNA mutations, 248, 250, 253 EMT see Epithelial-mesenchymal transition Epigenetics, mechanisms involved in RAS target deregulation, 127, 129, 134 Epithelial to mesenchymal transition (EMT) mechanism of contribution of ILK from a3b1integrin-dependent adhesion on laminin 5 stimulates Akt kinase activity through ILK, 198–199 decreases transcriptional activity of b-catenin and NF-kb, 200–201 knockdown is sufficient to activate GSK-3b, 199–200 regulates cell migration and invasion, 202 regulates level of cytosolic pool of b-catenin, 200 silencing of ILK affects N-cadherin expression, 201–202 siRNA-mediated knockdown of ILK results in decrease of Akt kinase activity, 199 mechanism of contribution of ILK to, 195–203, 205–206 Eukaryotic gene expression, control of gene loops and transcriptional memory, 118–124 characteristics of, 120–121 chromosome conformation capture, 120 dependent upon components of promoter and terminator complexes, 121 genetic suppression and discovery of, 118–119 Ssu72 is an integral component of the CPF 30 -end processing complex, 120 Ssu72 is a Pol II CTD phosphatase, 119–120 TFIIB at the terminator, 121–122 Evolution, and functions of inositol and derivatives, 84–89 all eukaryotes use inositol lipids, 88–89 archaeal synthesis and use of, 85–87 in bacteria, 87–88 Fatty acid, LTB4, derived from arachidonic acid, 59, 61 Fragile histidine triad proteins, are members of the histidine triad gene/gene product family, 208–215 human FHIT locus, 211 Hydrolase activity, 211 interactors, 212–213 role in DNA damage response, 212 role in oxidative and replicative stress, 211–212 Function, regulation and roles of PI3 Kb, major actor in platelet signaling and, 106–114 atypical class IA PI3 K, 108–109 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109 GBM see Glioblastoma multiforme Gene expression profiling, for fibroblasts, epithelial cells and other cell types, 126–127, 133–135 Gene loop, and transcriptional memory, control of eukaryotic gene expression, 118–124 characteristics of, 120–121 chromosome conformation capture, 120 dependent upon components of promoter and terminator complexes, 121 genetic suppression and discovery of, 118–119 Ssu72 is an integral component of the CPF 30 -end processing complex, 120 Ssu72 is a Pol II CTD phosphatase, 119–120 TFIIB at the terminator, 121–122 Gene silencing, difference in tumor size was due to, 131, 135 Glioblastoma multiforme (GBM), deciphering the signaling pathways of cancer stem cells of, 164–169 GPCR see G protein coupled receptor
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G protein coupled receptor (GPCR) is a low-affinity LTB4 receptor, 60, 62 PDZ domain proteins play a pivotal role in, 139–148 Hair cells, of inner ear, highly specialized cells to transduce auditory signals, 172, 175, 177, 180 Histidine triad proteins, Hint and Fhit proteins are members of, 208–215, 210–211 Aprataxin, 210 Hint1, 210 Hint2, 210–211 ILK see Integrin linked kinase Immunology, biological roles of LTB4 and its receptors in, 59–63 12-HHT is an intrinsic ligand for BLT2, 61 molecular identification of BLT1 and BLT2, 59–60 roles of BLT2 in protecting intestinal inflammation, 61 roles of BLT1 in T cells, dendritic cells, and osteoclasts, 62 Inflammation, roles of BLT2 in protection of, 61–62 Inositides, signaling in regulation of cell cycle progression, 2–3, 5, 7, 9 Inositol, for the generation of a multitude of signaling molecules, 74–81 Inositol hexakisphosphate kinase (IP6K), signaling role of, 74–81 inositol pyrophosphate mechanism of action, 78–79 inositol pyrophosphate regulated functions, 79–80 PP-IP5 kinases, 76 regulation of cellular inositol pyrophosphate levels, 76–78 Inositol (Ins), and derivatives, evolution and functions of, 84–89 all eukaryotes use inositol lipids, 88–89 archaeal synthesis and use of, 85–87 in bacteria, 87–88 Inositol phosphate, membrane-anchored inositol lipids and the cytosolic, 66, 68, 71 Inositol polyphosphate 4-phosphatase 1, role in platelet function using a weeble mouse model, 101–104 Inositol pyrophosphates, protein pyrophosphorylation by, 14 Inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), role in B cell survival, development and function, 66 Inositol 1,4,5-trisphosphate 3-kinase B (Itpkb), regulation of B cell survival, development and function by, 66–68, 70–71 Ins(1,4,5)P3 3-kinases, 67–68 mechanisms of Ins(1,3,4,5)P4 action, 68, 70 Ins see Inositol Ins(1,3,4,5)P4 see Inositol 1,3,4,5-tetrakisphosphate Integrin linked kinase (ILK), mechanism of contribution to EMT, 195–203, 205–206 a3b1integrin-dependent adhesion on laminin 5 stimulates Akt kinase activity through ILK, 198–199 decreases transcriptional activity of b-catenin and NF-kb, 200–201 knockdown is sufficient to activate GSK-3b, 199–200 regulates cell migration and invasion, 202 regulates level of cytosolic pool of b-catenin, 200 silencing of ILK affects N-cadherin expression, 201–202 siRNA-mediated knockdown of ILK results in decrease of Akt kinase activity, 199 IP7, able to transfer the b-phosphate to prephosphorylated proteins, 74–80 IP6K see Inositol hexakisphosphate kinase ISC1, serves to function as a binding domain for anionic phospholipids, 51–54 Itpkb see Inositol 1,4,5-trisphosphate 3-kinase B Kinase, over-expressed in yeasts, 13–15, 18–20 Laminopathies, role of prelamin A in, 246–254 altered signalling in muscular laminopathies, 249–250
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mechanisms of skeletal myogenesis and muscle regeneration, 248–249 modulation of expression of nuclear envelope and nuclear lamina proteins during myogenesis, 249 muscular laminopathies, 248 pathogenic mechanism in lipodystrophic laminopathies, 247–248 pathogenic mechanism in progeric laminopathies, 247 pathogenic mechanisms of muscular laminopathies, 250–251 role of, 251–252 Leukemia, involvement of PI3K signaling pathway in, 37–44 Leukotriene B4 receptors, novel roles in immunological regulations, 59–63 12-HHT is an intrinsic ligand for BLT2, 61 molecular identification of BLT1 and BLT2, 59–60 roles of BLT2 in protecting intestinal inflammation, 61 roles of BLT1 in T cells, dendritic cells, and osteoclasts, 62 Lipid kinase frequently mutated in several cancer, 273 signalling in the nucleus, 91–97 Lipid phosphate phosphohydrolase, are lipid phosphatases with broader substrate specificity, 236–237 Lipid signaling subcellular localization, affects downstream metabolism of sphingosine- 1-phosphate and access of sphingosine kinase to its substrates, 243 Mammalian target of rapamycin (mTOR), role in deciphering the signaling pathways of cancer stem cells of GBM, 164–169 MAPK see Mitogen-activated protein kinase MDS see Myelodysplastic syndromes Melanoma, mechanism of ILK signaling in, 195–196, 198–206 Mice, presenting a genetic inactivation of PI3Kb, 106, 108–110, 112–113 Microarray analysis, standard approach for identifying transcriptional targets of the RAS pathway, 126–127, 130, 133–134 Microvilli, interaction of PLCd3 with Myo6 is functional for maintenance of, 172, 174–175, 178–180 Mitogen-activated protein kinase (MAPK), role in deciphering the signaling pathways of cancer stem cells of GBM, 164–169 MTOR see Mammalian target of rapamycin mTORC1, second kinase complex containing mTOR as its catalytic subunit, 282–284, 287–289 Muscle regeneration, involves the activation of muscle satellite cells, 248–250, 254 Mycobacterium, Ins lipids were discovered in, 87–88 Myelodysplastic syndrome (MDS), role of nuclear PLCb1 in, 3, 7–9 Myogenesis, modulation of expression of nuclear envelope and nuclear lamina proteins during, 248–253 Myosin VI, on plasma membrane, phospholipase C novel binding partner of, 171–175, 177–178, 180 expression of Myo6 was decreased in intestine of PLCd3KO mice, 178 identification of Myo6 as a PLCd3 interacting protein, 174, 176 PLCd3 and Myo6 confined to be co-expressed in the hair cells of the inner ear, 175, 176, 177–178 PLCd3 has an essential role for development of microvilli architecture in Caco-2 colonic carcinoma cell line, 178, 179, 180 tail domain of Myo6 is sufficient for binding to the PH domain and C2 domain of PLCd3, 175, 176 Myotubes, cell population undergoes differentiation to form, 248–250, 252–253 N-cadherin, on melanoma cells plays a dual role promoting tumorigenesis, 195–197, 201–203, 205–206 Nestin, in GBM, mTOR and MAPK increased the expression of, 166–169 Neutral sphingomyelinase-2 (nSMase2), phosphoprotein regulated by calcineurin, 51–56 Neutral sphingomyelinase (N-SMases) considered to be key mediators of stress-induced ceramide production cellular compartmentalization, 56 ion dependency, 53 P-loop-like domain, 54
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regulation by anionic phospholipids, 53–54 regulation by interacting proteins, 55–56 regulation by phosphorylation, 54–55 key mediators of stress-induced ceramide production, 51–57 domain structure, 52 Nitrilase family proteins, consist of thiol enzymes involved in natural product biosynthesis, 208–215 NSMase2 see Neutral sphingomyelinase-2 N-SMases see Neutral sphingomyelinase Nuclear, phosphoinositide signalling in, 91–97 PtdIns(4,5)P2, 93–94 PtdIns5P, 95–97 specific regulators of PtdIns(4,5)P2 synthesis, 94–95 Nuclear envelope, roles in myoblast differentiation and/or muscle maintenance, 246–247, 249, 251–253 Nucleus, PLCb1 translocates to, 2–7, 9 Nulcear lamina, modulation of expression of nuclear envelope and, 249, 253 Oncogene, CK2 plays a major role in tumorigenesis by enhancing the transforming potential of, 39–41 Origins of DNA replication, identification of, 259, 267 Ovarian carcinoma, regulation of HMGA2 gene in, 130–131 p53, and regulation of bioactive sphingolipids, 219–226 ceramide, 220–221 glycosphingolipids, 221 sphingolipid metabolizing enzymes, 221–223 sphingolipids in animal models, 224 tumor cell senescence, 224 tumor cell senescence as chemotherapeutic mechanism, 225 tumor suppressor protein, 219–220 p85a, oncogenic mutations occur at the interfaces between, 273–278 p110a, oncogenic mutations occur at the interfaces between, 273–278 p110a/p85a, breaks the interaction of ABD with iSH2 domain of p85, 276–277 PDZ-binding motif, protein interaction motif responsible for subtype-specific regulation of PLC-b, 141– 144, 146, 148 PDZ domain protein subtype-specific role of phospholipase C-b via differential interactions with domain structures and the regulation of PLC-b subtypes by G proteins, 140 NHERF, 142–143 Par-3, 145 PDZ-binding motif, 141 potential PDZ domain proteins that interact with PLC-b subtypes and GPCRs, 146–147 PSD-95, 145–146 role of PDZ domain proteins in subtype-specific role of PLC-b in GPCR-mediated signaling, 141–142 Shank2, 143–145 subtype-specific roles of phospholipase C-b via differential interactions with, 138–148 PHD finger, generally only found in nuclear proteins, 95–96 Phosphatidylcholine (PC), major phospholipid in eukaryotic membranes, 183–184, 186 Phosphatidylethanolamine (PE), ChoK enzymes involved in the synthesis of, 183–184 Phosphatidylinositide-3-kinases (PI3K), design of mutation specific inhibitors of, 273–278 activation by phosphotyrosine peptide (pY-pep) binding, 275 cancer-associated mutations, 276–277 structure of the p110a/niSH2 complex of PI3Ka, 275 Phosphatidylinositol-(3,4,5)-triphosphate (PtdIns(3,4,5)P3), major output signal from the class I PI3Ks, 27, 30–33 Phosphoinosite-3,4,5-triphosphate (PIP3), act as membrane docking sites for pleckstrin homology domain, 273–274
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Subject Index / Advances in Enzyme Regulation 51 (2011) 320–329
Phosphoinositide 3-kinase beta (PI3Kb), major actor in platelet signaling and functions, regulation and roles of, 106–114 atypical class IA PI3K, 108–109 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109 Phosphoinositide 3-kinase (PI3 K) (E.C.2.7.1.153) class IA, signalling via, 27–33 barriers to progress, 33 degradation of PtdIns(3,4,5)P3 signals, 31 issue of the existence of multiple molecular species of phosphoinositides, 30–31 outputs from, 31 past work, 28–29 potential molecular explanations for the phenomenon of class IA PI3K isoform specificity, 32–33 problems faced in explaining isoform specific class IA PI3K signalling on the basis of our current understanding of the pathway, 31–32 regulators of Class IA PI3 K activity, 29–30 translation of PtdIns(3,4,5)P3 signals, 31 signaling and leukemia cell survival, impact of PTEN regulation by CK2 on, 37–44 Phosphoinositide metabolism, phospholipase Cd3 is a key enzyme in, 171, 180 Phosphoinositides genetic disruption of PI3-K unsuitable to distinguish the contributions of, 102 signalling in the nucleus, 91–97 PtdIns(4,5)P2, 93–94 PtdIns5P, 95–97 specific regulators of PtdIns(4,5)P2 synthesis, 94–95 Phospholipase C (PLC) enzyme responsible for hydrolysis, 138–148 nuclear, physiology and pathology of, 2–9 nuclear PLCb1 and cell cycle, 2–5 physiology and pathology of nuclear nuclear PLCb1 and myelodysplastic syndromes, 7–9 nuclear PLCb1 during cell differentiation, 5–7 Phospholipase C (PLC) (E.C.3.1.4.11), novel binding partner of myosin VI on plasma membrane, 171–175, 177–178, 180 expression of Myo6 was decreased in intestine of PLCd3KO mice, 178 identification of Myo6 as a PLCd3 interacting protein, 174, 176 PLCd3 and Myo6 confined to be co-expressed in the hair cells of the inner ear, 175, 176, 177–178 PLCd3 has an essential role for development of microvilli architecture in Caco-2 colonic carcinoma cell line, 178, 179, 180 tail domain of Myo6 is sufficient for binding to the PH domain and C2 domain of PLCd3, 175, 176 Phospholipids, present in and are made by most Archaea and all eukaryotes, 84–87, 89 Phosphorylation, of proteins by diphosphoinositol polyphosphates, 13, 19–20, 22 PI3 K see Phosphatidylinositide-3-kinases PI3 Kb see Phosphoinositide 3-kinase beta PI3Ks see Phosphoinositide 3-kinases PIP3 see Phosphoinosite-3,4,5-triphosphate Platelets, major actor in signaling and functions in, regulation and roles of PI3 Kb, 106–114 atypical class IA PI3 K, 108–109 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109
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PLC see Phospholipase C Posttranslational regulation, of PTEN, importance in leukemia, 40 Prelamin A, role in early steps of muscle differentiation, 246–254 altered signalling in muscular laminopathies, 249–250 mechanisms of skeletal myogenesis and muscle regeneration, 248–249 modulation of expression of nuclear envelope and nuclear lamina proteins during myogenesis, 249 muscular laminopathies, 248 pathogenic mechanism in lipodystrophic laminopathies, 247–248 pathogenic mechanism in progeric laminopathies, 247 pathogenic mechanisms of muscular laminopathies, 250–251 role of, 251–252 Promoter analysis, suggested a role of MAPK pathway and NFY transcription factors in regulating CCNB1 expression and activity, 133 Prostate cancer, second most prevalent cancer affecting men after lung cancer, 153–158, 160 Proteomic, study of protein component of an organism, cell or tissue, 292–302 p70S6 K, TPA induced activation of, 167–169 Pta1, another component of the CPF complex and interacts directly with Ssu72, 121 PtdIns(3,4,5)P3 see Phosphatidylinositol-(3,4,5)-triphosphate PTEN (EC 3.1.3.67), regulation by CK2, impact on PI3K-dependent signaling and leukemia cell survival, 37–44 Pyrophosphate, of IP7 is able to transfer the b-phosphate to prephosphorylated proteins, 74–81 Pyrophosphorylation, in which phosphate group is added onto pre-existing phosphoserine, 79 Radiation therapy, for treatment of prostate cancer, 153–154, 156, 158 RAS targets, mediated deregulation of the transcriptome, 126–127, 129–135 effects of MAPK signaling and epigenetic events on down-regulation of HLA class I and NKG2D ligands, 129–130 heterogeneous and common patterns of transcriptional responses to, 126–127, 128 high mobility AT-hook 2, 130–131 YBX1, 131–134 Reactive oxygen species (ROS), radio- and chemotherapy will result in generation of, 153 Receptor tyrosine kinase, cell surface receptors involved in signal transduction, 292–302 dimerization/activation, 294–297 introduction to proteomic analyses, 293–294 phosphoproteomics, 297–301 role of other PTMs in cell signaling, 301–302 Regulation of the eukaryotic N-SMase family members, 52–56 regulation and roles of PI3 Kb, major actor in platelet signaling and atypical class IA PI3 K, 108–109 and roles of PI3Kb, major actor in platelet signaling and functions, 106–114 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109 ROS see Reactive oxygen species Senescence, p53 and ceramide have been shown to regulate, 219–220, 224–226 Signaling, role of inositol hexakisphosphate kinases, 74–81 inositol pyrophosphate mechanism of action, 78–79 inositol pyrophosphate regulated functions, 79–80 PP-IP5 kinases, 76 regulation of cellular inositol pyrophosphate levels, 76–78 Signaling pathways, are the activation/deactivation of transcriptional regulators, 292–294, 296–298, 300–302
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Signal transduction of phosphoinositide 3 kinase in leukemia, 38 RAS-dependent, role of E2F transcription factors in, 129, 132 Signal transduction inhibitors, effects on prostate cancer initiating cell, 154–156, 158 S6 K see S6-kinase S6-kinase (S6 K), required to facilitate the elongation step of protein translation, 280–285, 287–288 combined silencing of S6K1 and S6K2 does not prevent Akt dependent accumulation of mature SREBP, 284–285 genetic deletion of both S6K1 and S6K2 does not prevent accumulation of mature SREBP, 285, 287–288 Sphingolipid metabolism, sphingosine kinase localization in the control of, 229, 231–239, 241–243 contructs of sphingosine kinase localized to specific intracellular compartments, 233 degradation of S1P preferentially affects the secreted pool of S1P, 236–237 dictates utilization of dihydrosphingosine as a substrate, 238–239, 241–242 non-specific lipid phosphatases preferentially utilize S1P generated at the plasma membrane, 237–238 Sphingolipids bioactive, p53 and regulation of, 219–226 ceramide, 220–221 glycosphingolipids, 221 sphingolipid metabolizing enzymes, 221–223 sphingolipids in animal models, 224 tumor cell senescence, 224 tumor cell senescence as chemotherapeutic mechanism, 225 tumor suppressor protein, 219–220 SMase is important for local regulation of, 55–56 Sphingosine kinase, localization in the control of sphingolipid metabolism, 229, 231–239, 241–243 contructs of sphingosine kinase localized to specific intracellular compartments, 233 degradation of S1P preferentially affects the secreted pool of S1P, 236–237 dictates utilization of dihydrosphingosine as a substrate, 238–239, 241–242 non-specific lipid phosphatases preferentially utilize S1P generated at the plasma membrane, 237–238 Sphingosine kinase (E.C.2.7.1.91), a sphingolipid metabolizing enzyme act as oncogene, 219, 224 Sphingosine-1-phosphate, are critical signaling components in vascular biology, tumorogenesis, inflammation, and immune function, 229–232, 235, 238, 240, 243 Sphingosine-1-phosphate lyase, S1P is the substrate for, 231–232 SREBP see Sterol regulatory element binding proteins Ssu72, plays key role early in the transcription cycle, 119–123 Sterol regulatory element binding proteins (SREBP), are expressed as inactive precursors and reside as integral transmembrane proteins, 280–285, 287–288 combined silencing of S6K1 and S6K2 does not prevent Akt dependent accumulation of mature SREBP, 284–285 genetic deletion of both S6K1 and S6K2 does not prevent accumulation of mature SREBP, 285, 287– 288 Subtype-specific role, of phospholipase C-b via differential interactions with PDZ domain proteins, 138–148 domain structures and the regulation of PLC-b subtypes by G proteins, 140 NHERF, 142–143 Par-3, 145 PDZ-binding motif, 141 potential PDZ domain proteins that interact with PLC-b subtypes and GPCRs, 146–147 PSD-95, 145–146 role of PDZ domain proteins in subtype-specific role of PLC-b in GPCR-mediated signaling, 141–142 Shank2, 143–145
Subject Index / Advances in Enzyme Regulation 51 (2011) 320–329
Temporal order of DNA replication, reside in the epigenetic code specified by chromosomal proteins, 266–269 Thrombosis, weeble chimeric mice have propensity for, 104 Transcription, and gene loops, control of eukaryotic gene expression, 118–124 characteristics of, 120–121 chromosome conformation capture, 120 dependent upon components of promoter and terminator complexes, 121 genetic suppression and discovery of, 118–119 Ssu72 is an integral component of the CPF 30 -end processing complex, 120 Ssu72 is a Pol II CTD phosphatase, 119–120 TFIIB at the terminator, 121–122 Transcriptional regulators, A-type lamins and associated proteins bind to chromatin and, 246, 249 Transcription factor II B (TFIIB), role in gene loops and transcriptional memory, 119–123 Tumor suppressor, PTEN is haploinsufficient for, 37–38, 40, 42, 44 Tumor suppressor proteins, Nit proteins also appear to behave as, 215
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Contents lists available at ScienceDirect
Advances in Enzyme Regulation journal homepage: www.elsevier.com/locate/ advenzreg
Subject index volume 51 Achilles’ heel cancer, targeting the cancer initiating cell of, 152–160 effects of cytotoxic effects of docetaxel on CICs by combination with targeted therapies and natural products, 159–160 natural products-dietary supplements and prostate cancer, 155–156 prostate cancer, 153 prostate cancer and radiation therapy, 153 prostate cancer therapy, 153 side effects of radio and chemo-therapies–induction of signaling pathways, 153–154 targeting signal transduction pathways in prostate cancer, 154–155 Akt activated in leukemia cell survival, 38–40, 42–44 regulates de novo lipogenesis though activation of SREBP and its target genes, 196–200, 203–205 role in deciphering the signaling pathways of cancer stem cells of GBM, 164–169 Apoptosis, p53 and ceramide have been shown to regulate, 220–226 AP sites, form when the reaction of hydrogen peroxide with DNA causes bases, 264–265 Arachidonic acid, well known chemoattractant for phagocytes, 59 Archaea, synthesis and use of Ins in, 84–89 Bacteria, inositol in, 84–89 B cell survival regulation by inositol 1,4,5-trisphosphate 3-kinase B, 66–68, 70–71 regulation by inositol 1,4,5-trisphosphate 3-kinase B in Ins(1,4,5)P3 3-kinases, 67–68 mechanisms of Ins(1,3,4,5)P4 action, 68, 70 Biosynthesis, of archaetidylinositol, 84, 87 Bone marrow transplantation, of weeble fetal liver cells into lethally irradiated wild type mice, 103 Cancer, overexpression or over-activity of ChoKa but not ChoKb in, 188–191 Cancer initiating cell, targeting the Achilles' heel of cancer, 152–160 effects of cytotoxic effects of docetaxel on CICs by combination with targeted therapies and natural products, 159–160 natural products-dietary supplements and prostate cancer, 155–156 prostate cancer, 153 prostate cancer and radiation therapy, 153 prostate cancer therapy, 153 side effects of radio and chemo-therapies-induction of signaling pathways, 153–154 targeting signal transduction pathways in prostate cancer, 154–155 Cancer stem cells, promote differentiation into more mature prostate cancer cells, 152, 158 Cell-signaling, functions of the PPIP5Ks, 15 0065-2571/$ – see front matter doi:10.1016/j.advenzreg.2011.03.001
Subject Index / Advances in Enzyme Regulation 51 (2011) 320–329
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Ceramide regulates cell cycle arrest, senescence, and apoptosis, 220–226 role in signal transduction and cellular function., 229–231, 233, 238–239, 241–243 sphingomyelinases mediate the hydrolysis of sphingomyelin in production of, 51, 54, 56 Chemotherapeutic drugs, for treatment of prostate cancer, 156–160 Chimeric mice, role of inositol polyphosphate 4-phosphatase 1 in platelet function using, 103–104 Choline kinase (E.C.2.7.1.32), alpha and beta, in carcinogenesis, different role in lipid metabolism and biological functions, 183–184, 186–191 biochemical characterization of ChoK isoforms, 184, 186–187 ChoK and lipid metabolism, 184, 186 differential role between ChoK isoforms in cell transformation and tumorigenesis, 187–189 genes encoding choline/ethanolamine kinases, 183–184 regulation of ChoK activity, 187 specific inhibition of ChoKa, 189–190 Choline kinase inhibitors, with potential antitumoral activity, 189–191 Chromatin, important regulators of gene expression, 118, 120–121 Chromatin fibers, studies of DNA and, 259, 267–269 Chromatin immunoprecipitation, YBX1 targets identified in colorectal cancer cells by, 133–134 Chromatin organization, pathogenesis of muscular laminopathies associated with, 251 CK2 (EC 2.7.11.1) impact of PTEN regulation on PI3 K-dependent signaling and leukemia cell survival, 37–44 on PI3 K-dependent signaling and leukemia cell survival, impact of PTEN regulation by highly oncogenic non-oncogene, in tumorigenesis and leukemia, 40–41 Class I PI3Ks, signalling via, 27–29, 31–33 Colitis, effects of BLT2-deficiency in, 61 Colorectal cancer, role of YBX1 as a prognostic factor in, 129–130, 132–135 Diphosphoinositol polyphosphates molecular mechanisms of, 13–20, 22 phospholipase C-initiated synthesis of metabolism of, 13–15 protein phosphorylation by, 19–20, 22 receptors for, 17–18 signaling by, 15–17 DNA damage, p53-dependent apoptosis occurs secondary to, 220, 222–225 DNA damage response-associated proteins, role of Fhit proteins in, 210, 212, 215 DNA fibers, analysis of DNA repair on, 259–268 DNA repair, on DNA fibers, 258, 263, 265 DNA replication, temporal and functional analysis in early S phase, 257–270 analysis of, 259–263 analysis of chromatin structure and dynamics of DNA replication, 268–269 analysis of DNA repair on DNA fibers, 263–266 genomic and temporal mapping of DNA replication origins activated early in S phase, 266–268 studies of DNA and chromatin fibers, 259 Drug design, of phosphoinsitide-3-kinase, 273–278 activation by phosphotyrosine peptide (pY-pep) binding, 275 cancer-associated mutations, 276–277 structure of the p110a/niSH2 complex of PI3 Ka, 275 Early S phase, temporal and functional analysis of DNA replicated in, 257–270 analysis of, 259–263 analysis of chromatin structure and dynamics of DNA replication, 268–269 analysis of DNA repair on DNA fibers, 263–266 genomic and temporal mapping of DNA replication origins activated early in S phase, 266–268 studies of DNA and chromatin fibers, 259
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EDMD see Emery-Dreifuss muscular dystrophy Eicosanoids, 12-HHT was originally identified as a by-product of thromboxane A2 biosynthesis, 61 Emery-Dreifuss muscular dystrophy (EDMD), caused by LMNA mutations, 248, 250, 253 EMT see Epithelial-mesenchymal transition Epigenetics, mechanisms involved in RAS target deregulation, 127, 129, 134 Epithelial to mesenchymal transition (EMT) mechanism of contribution of ILK from a3b1integrin-dependent adhesion on laminin 5 stimulates Akt kinase activity through ILK, 198–199 decreases transcriptional activity of b-catenin and NF-kb, 200–201 knockdown is sufficient to activate GSK-3b, 199–200 regulates cell migration and invasion, 202 regulates level of cytosolic pool of b-catenin, 200 silencing of ILK affects N-cadherin expression, 201–202 siRNA-mediated knockdown of ILK results in decrease of Akt kinase activity, 199 mechanism of contribution of ILK to, 195–203, 205–206 Eukaryotic gene expression, control of gene loops and transcriptional memory, 118–124 characteristics of, 120–121 chromosome conformation capture, 120 dependent upon components of promoter and terminator complexes, 121 genetic suppression and discovery of, 118–119 Ssu72 is an integral component of the CPF 30 -end processing complex, 120 Ssu72 is a Pol II CTD phosphatase, 119–120 TFIIB at the terminator, 121–122 Evolution, and functions of inositol and derivatives, 84–89 all eukaryotes use inositol lipids, 88–89 archaeal synthesis and use of, 85–87 in bacteria, 87–88 Fatty acid, LTB4, derived from arachidonic acid, 59, 61 Fragile histidine triad proteins, are members of the histidine triad gene/gene product family, 208–215 human FHIT locus, 211 Hydrolase activity, 211 interactors, 212–213 role in DNA damage response, 212 role in oxidative and replicative stress, 211–212 Function, regulation and roles of PI3 Kb, major actor in platelet signaling and, 106–114 atypical class IA PI3 K, 108–109 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109 GBM see Glioblastoma multiforme Gene expression profiling, for fibroblasts, epithelial cells and other cell types, 126–127, 133–135 Gene loop, and transcriptional memory, control of eukaryotic gene expression, 118–124 characteristics of, 120–121 chromosome conformation capture, 120 dependent upon components of promoter and terminator complexes, 121 genetic suppression and discovery of, 118–119 Ssu72 is an integral component of the CPF 30 -end processing complex, 120 Ssu72 is a Pol II CTD phosphatase, 119–120 TFIIB at the terminator, 121–122 Gene silencing, difference in tumor size was due to, 131, 135 Glioblastoma multiforme (GBM), deciphering the signaling pathways of cancer stem cells of, 164–169 GPCR see G protein coupled receptor
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G protein coupled receptor (GPCR) is a low-affinity LTB4 receptor, 60, 62 PDZ domain proteins play a pivotal role in, 139–148 Hair cells, of inner ear, highly specialized cells to transduce auditory signals, 172, 175, 177, 180 Histidine triad proteins, Hint and Fhit proteins are members of, 208–215, 210–211 Aprataxin, 210 Hint1, 210 Hint2, 210–211 ILK see Integrin linked kinase Immunology, biological roles of LTB4 and its receptors in, 59–63 12-HHT is an intrinsic ligand for BLT2, 61 molecular identification of BLT1 and BLT2, 59–60 roles of BLT2 in protecting intestinal inflammation, 61 roles of BLT1 in T cells, dendritic cells, and osteoclasts, 62 Inflammation, roles of BLT2 in protection of, 61–62 Inositides, signaling in regulation of cell cycle progression, 2–3, 5, 7, 9 Inositol, for the generation of a multitude of signaling molecules, 74–81 Inositol hexakisphosphate kinase (IP6K), signaling role of, 74–81 inositol pyrophosphate mechanism of action, 78–79 inositol pyrophosphate regulated functions, 79–80 PP-IP5 kinases, 76 regulation of cellular inositol pyrophosphate levels, 76–78 Inositol (Ins), and derivatives, evolution and functions of, 84–89 all eukaryotes use inositol lipids, 88–89 archaeal synthesis and use of, 85–87 in bacteria, 87–88 Inositol phosphate, membrane-anchored inositol lipids and the cytosolic, 66, 68, 71 Inositol polyphosphate 4-phosphatase 1, role in platelet function using a weeble mouse model, 101–104 Inositol pyrophosphates, protein pyrophosphorylation by, 14 Inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), role in B cell survival, development and function, 66 Inositol 1,4,5-trisphosphate 3-kinase B (Itpkb), regulation of B cell survival, development and function by, 66–68, 70–71 Ins(1,4,5)P3 3-kinases, 67–68 mechanisms of Ins(1,3,4,5)P4 action, 68, 70 Ins see Inositol Ins(1,3,4,5)P4 see Inositol 1,3,4,5-tetrakisphosphate Integrin linked kinase (ILK), mechanism of contribution to EMT, 195–203, 205–206 a3b1integrin-dependent adhesion on laminin 5 stimulates Akt kinase activity through ILK, 198–199 decreases transcriptional activity of b-catenin and NF-kb, 200–201 knockdown is sufficient to activate GSK-3b, 199–200 regulates cell migration and invasion, 202 regulates level of cytosolic pool of b-catenin, 200 silencing of ILK affects N-cadherin expression, 201–202 siRNA-mediated knockdown of ILK results in decrease of Akt kinase activity, 199 IP7, able to transfer the b-phosphate to prephosphorylated proteins, 74–80 IP6K see Inositol hexakisphosphate kinase ISC1, serves to function as a binding domain for anionic phospholipids, 51–54 Itpkb see Inositol 1,4,5-trisphosphate 3-kinase B Kinase, over-expressed in yeasts, 13–15, 18–20 Laminopathies, role of prelamin A in, 246–254 altered signalling in muscular laminopathies, 249–250
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mechanisms of skeletal myogenesis and muscle regeneration, 248–249 modulation of expression of nuclear envelope and nuclear lamina proteins during myogenesis, 249 muscular laminopathies, 248 pathogenic mechanism in lipodystrophic laminopathies, 247–248 pathogenic mechanism in progeric laminopathies, 247 pathogenic mechanisms of muscular laminopathies, 250–251 role of, 251–252 Leukemia, involvement of PI3K signaling pathway in, 37–44 Leukotriene B4 receptors, novel roles in immunological regulations, 59–63 12-HHT is an intrinsic ligand for BLT2, 61 molecular identification of BLT1 and BLT2, 59–60 roles of BLT2 in protecting intestinal inflammation, 61 roles of BLT1 in T cells, dendritic cells, and osteoclasts, 62 Lipid kinase frequently mutated in several cancer, 273 signalling in the nucleus, 91–97 Lipid phosphate phosphohydrolase, are lipid phosphatases with broader substrate specificity, 236–237 Lipid signaling subcellular localization, affects downstream metabolism of sphingosine- 1-phosphate and access of sphingosine kinase to its substrates, 243 Mammalian target of rapamycin (mTOR), role in deciphering the signaling pathways of cancer stem cells of GBM, 164–169 MAPK see Mitogen-activated protein kinase MDS see Myelodysplastic syndromes Melanoma, mechanism of ILK signaling in, 195–196, 198–206 Mice, presenting a genetic inactivation of PI3Kb, 106, 108–110, 112–113 Microarray analysis, standard approach for identifying transcriptional targets of the RAS pathway, 126–127, 130, 133–134 Microvilli, interaction of PLCd3 with Myo6 is functional for maintenance of, 172, 174–175, 178–180 Mitogen-activated protein kinase (MAPK), role in deciphering the signaling pathways of cancer stem cells of GBM, 164–169 MTOR see Mammalian target of rapamycin mTORC1, second kinase complex containing mTOR as its catalytic subunit, 282–284, 287–289 Muscle regeneration, involves the activation of muscle satellite cells, 248–250, 254 Mycobacterium, Ins lipids were discovered in, 87–88 Myelodysplastic syndrome (MDS), role of nuclear PLCb1 in, 3, 7–9 Myogenesis, modulation of expression of nuclear envelope and nuclear lamina proteins during, 248–253 Myosin VI, on plasma membrane, phospholipase C novel binding partner of, 171–175, 177–178, 180 expression of Myo6 was decreased in intestine of PLCd3KO mice, 178 identification of Myo6 as a PLCd3 interacting protein, 174, 176 PLCd3 and Myo6 confined to be co-expressed in the hair cells of the inner ear, 175, 176, 177–178 PLCd3 has an essential role for development of microvilli architecture in Caco-2 colonic carcinoma cell line, 178, 179, 180 tail domain of Myo6 is sufficient for binding to the PH domain and C2 domain of PLCd3, 175, 176 Myotubes, cell population undergoes differentiation to form, 248–250, 252–253 N-cadherin, on melanoma cells plays a dual role promoting tumorigenesis, 195–197, 201–203, 205–206 Nestin, in GBM, mTOR and MAPK increased the expression of, 166–169 Neutral sphingomyelinase-2 (nSMase2), phosphoprotein regulated by calcineurin, 51–56 Neutral sphingomyelinase (N-SMases) considered to be key mediators of stress-induced ceramide production cellular compartmentalization, 56 ion dependency, 53 P-loop-like domain, 54
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regulation by anionic phospholipids, 53–54 regulation by interacting proteins, 55–56 regulation by phosphorylation, 54–55 key mediators of stress-induced ceramide production, 51–57 domain structure, 52 Nitrilase family proteins, consist of thiol enzymes involved in natural product biosynthesis, 208–215 NSMase2 see Neutral sphingomyelinase-2 N-SMases see Neutral sphingomyelinase Nuclear, phosphoinositide signalling in, 91–97 PtdIns(4,5)P2, 93–94 PtdIns5P, 95–97 specific regulators of PtdIns(4,5)P2 synthesis, 94–95 Nuclear envelope, roles in myoblast differentiation and/or muscle maintenance, 246–247, 249, 251–253 Nucleus, PLCb1 translocates to, 2–7, 9 Nulcear lamina, modulation of expression of nuclear envelope and, 249, 253 Oncogene, CK2 plays a major role in tumorigenesis by enhancing the transforming potential of, 39–41 Origins of DNA replication, identification of, 259, 267 Ovarian carcinoma, regulation of HMGA2 gene in, 130–131 p53, and regulation of bioactive sphingolipids, 219–226 ceramide, 220–221 glycosphingolipids, 221 sphingolipid metabolizing enzymes, 221–223 sphingolipids in animal models, 224 tumor cell senescence, 224 tumor cell senescence as chemotherapeutic mechanism, 225 tumor suppressor protein, 219–220 p85a, oncogenic mutations occur at the interfaces between, 273–278 p110a, oncogenic mutations occur at the interfaces between, 273–278 p110a/p85a, breaks the interaction of ABD with iSH2 domain of p85, 276–277 PDZ-binding motif, protein interaction motif responsible for subtype-specific regulation of PLC-b, 141– 144, 146, 148 PDZ domain protein subtype-specific role of phospholipase C-b via differential interactions with domain structures and the regulation of PLC-b subtypes by G proteins, 140 NHERF, 142–143 Par-3, 145 PDZ-binding motif, 141 potential PDZ domain proteins that interact with PLC-b subtypes and GPCRs, 146–147 PSD-95, 145–146 role of PDZ domain proteins in subtype-specific role of PLC-b in GPCR-mediated signaling, 141–142 Shank2, 143–145 subtype-specific roles of phospholipase C-b via differential interactions with, 138–148 PHD finger, generally only found in nuclear proteins, 95–96 Phosphatidylcholine (PC), major phospholipid in eukaryotic membranes, 183–184, 186 Phosphatidylethanolamine (PE), ChoK enzymes involved in the synthesis of, 183–184 Phosphatidylinositide-3-kinases (PI3K), design of mutation specific inhibitors of, 273–278 activation by phosphotyrosine peptide (pY-pep) binding, 275 cancer-associated mutations, 276–277 structure of the p110a/niSH2 complex of PI3Ka, 275 Phosphatidylinositol-(3,4,5)-triphosphate (PtdIns(3,4,5)P3), major output signal from the class I PI3Ks, 27, 30–33 Phosphoinosite-3,4,5-triphosphate (PIP3), act as membrane docking sites for pleckstrin homology domain, 273–274
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Phosphoinositide 3-kinase beta (PI3Kb), major actor in platelet signaling and functions, regulation and roles of, 106–114 atypical class IA PI3K, 108–109 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109 Phosphoinositide 3-kinase (PI3 K) (E.C.2.7.1.153) class IA, signalling via, 27–33 barriers to progress, 33 degradation of PtdIns(3,4,5)P3 signals, 31 issue of the existence of multiple molecular species of phosphoinositides, 30–31 outputs from, 31 past work, 28–29 potential molecular explanations for the phenomenon of class IA PI3K isoform specificity, 32–33 problems faced in explaining isoform specific class IA PI3K signalling on the basis of our current understanding of the pathway, 31–32 regulators of Class IA PI3 K activity, 29–30 translation of PtdIns(3,4,5)P3 signals, 31 signaling and leukemia cell survival, impact of PTEN regulation by CK2 on, 37–44 Phosphoinositide metabolism, phospholipase Cd3 is a key enzyme in, 171, 180 Phosphoinositides genetic disruption of PI3-K unsuitable to distinguish the contributions of, 102 signalling in the nucleus, 91–97 PtdIns(4,5)P2, 93–94 PtdIns5P, 95–97 specific regulators of PtdIns(4,5)P2 synthesis, 94–95 Phospholipase C (PLC) enzyme responsible for hydrolysis, 138–148 nuclear, physiology and pathology of, 2–9 nuclear PLCb1 and cell cycle, 2–5 physiology and pathology of nuclear nuclear PLCb1 and myelodysplastic syndromes, 7–9 nuclear PLCb1 during cell differentiation, 5–7 Phospholipase C (PLC) (E.C.3.1.4.11), novel binding partner of myosin VI on plasma membrane, 171–175, 177–178, 180 expression of Myo6 was decreased in intestine of PLCd3KO mice, 178 identification of Myo6 as a PLCd3 interacting protein, 174, 176 PLCd3 and Myo6 confined to be co-expressed in the hair cells of the inner ear, 175, 176, 177–178 PLCd3 has an essential role for development of microvilli architecture in Caco-2 colonic carcinoma cell line, 178, 179, 180 tail domain of Myo6 is sufficient for binding to the PH domain and C2 domain of PLCd3, 175, 176 Phospholipids, present in and are made by most Archaea and all eukaryotes, 84–87, 89 Phosphorylation, of proteins by diphosphoinositol polyphosphates, 13, 19–20, 22 PI3 K see Phosphatidylinositide-3-kinases PI3 Kb see Phosphoinositide 3-kinase beta PI3Ks see Phosphoinositide 3-kinases PIP3 see Phosphoinosite-3,4,5-triphosphate Platelets, major actor in signaling and functions in, regulation and roles of PI3 Kb, 106–114 atypical class IA PI3 K, 108–109 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109
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327
PLC see Phospholipase C Posttranslational regulation, of PTEN, importance in leukemia, 40 Prelamin A, role in early steps of muscle differentiation, 246–254 altered signalling in muscular laminopathies, 249–250 mechanisms of skeletal myogenesis and muscle regeneration, 248–249 modulation of expression of nuclear envelope and nuclear lamina proteins during myogenesis, 249 muscular laminopathies, 248 pathogenic mechanism in lipodystrophic laminopathies, 247–248 pathogenic mechanism in progeric laminopathies, 247 pathogenic mechanisms of muscular laminopathies, 250–251 role of, 251–252 Promoter analysis, suggested a role of MAPK pathway and NFY transcription factors in regulating CCNB1 expression and activity, 133 Prostate cancer, second most prevalent cancer affecting men after lung cancer, 153–158, 160 Proteomic, study of protein component of an organism, cell or tissue, 292–302 p70S6 K, TPA induced activation of, 167–169 Pta1, another component of the CPF complex and interacts directly with Ssu72, 121 PtdIns(3,4,5)P3 see Phosphatidylinositol-(3,4,5)-triphosphate PTEN (EC 3.1.3.67), regulation by CK2, impact on PI3K-dependent signaling and leukemia cell survival, 37–44 Pyrophosphate, of IP7 is able to transfer the b-phosphate to prephosphorylated proteins, 74–81 Pyrophosphorylation, in which phosphate group is added onto pre-existing phosphoserine, 79 Radiation therapy, for treatment of prostate cancer, 153–154, 156, 158 RAS targets, mediated deregulation of the transcriptome, 126–127, 129–135 effects of MAPK signaling and epigenetic events on down-regulation of HLA class I and NKG2D ligands, 129–130 heterogeneous and common patterns of transcriptional responses to, 126–127, 128 high mobility AT-hook 2, 130–131 YBX1, 131–134 Reactive oxygen species (ROS), radio- and chemotherapy will result in generation of, 153 Receptor tyrosine kinase, cell surface receptors involved in signal transduction, 292–302 dimerization/activation, 294–297 introduction to proteomic analyses, 293–294 phosphoproteomics, 297–301 role of other PTMs in cell signaling, 301–302 Regulation of the eukaryotic N-SMase family members, 52–56 regulation and roles of PI3 Kb, major actor in platelet signaling and atypical class IA PI3 K, 108–109 and roles of PI3Kb, major actor in platelet signaling and functions, 106–114 cell types, 113–114 G-protein-coupled receptors, 110–111 integrin aIIbb3, 111–113 stimulated by von Willebrand factor and collagen, 109 ROS see Reactive oxygen species Senescence, p53 and ceramide have been shown to regulate, 219–220, 224–226 Signaling, role of inositol hexakisphosphate kinases, 74–81 inositol pyrophosphate mechanism of action, 78–79 inositol pyrophosphate regulated functions, 79–80 PP-IP5 kinases, 76 regulation of cellular inositol pyrophosphate levels, 76–78 Signaling pathways, are the activation/deactivation of transcriptional regulators, 292–294, 296–298, 300–302
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Signal transduction of phosphoinositide 3 kinase in leukemia, 38 RAS-dependent, role of E2F transcription factors in, 129, 132 Signal transduction inhibitors, effects on prostate cancer initiating cell, 154–156, 158 S6 K see S6-kinase S6-kinase (S6 K), required to facilitate the elongation step of protein translation, 280–285, 287–288 combined silencing of S6K1 and S6K2 does not prevent Akt dependent accumulation of mature SREBP, 284–285 genetic deletion of both S6K1 and S6K2 does not prevent accumulation of mature SREBP, 285, 287–288 Sphingolipid metabolism, sphingosine kinase localization in the control of, 229, 231–239, 241–243 contructs of sphingosine kinase localized to specific intracellular compartments, 233 degradation of S1P preferentially affects the secreted pool of S1P, 236–237 dictates utilization of dihydrosphingosine as a substrate, 238–239, 241–242 non-specific lipid phosphatases preferentially utilize S1P generated at the plasma membrane, 237–238 Sphingolipids bioactive, p53 and regulation of, 219–226 ceramide, 220–221 glycosphingolipids, 221 sphingolipid metabolizing enzymes, 221–223 sphingolipids in animal models, 224 tumor cell senescence, 224 tumor cell senescence as chemotherapeutic mechanism, 225 tumor suppressor protein, 219–220 SMase is important for local regulation of, 55–56 Sphingosine kinase, localization in the control of sphingolipid metabolism, 229, 231–239, 241–243 contructs of sphingosine kinase localized to specific intracellular compartments, 233 degradation of S1P preferentially affects the secreted pool of S1P, 236–237 dictates utilization of dihydrosphingosine as a substrate, 238–239, 241–242 non-specific lipid phosphatases preferentially utilize S1P generated at the plasma membrane, 237–238 Sphingosine kinase (E.C.2.7.1.91), a sphingolipid metabolizing enzyme act as oncogene, 219, 224 Sphingosine-1-phosphate, are critical signaling components in vascular biology, tumorogenesis, inflammation, and immune function, 229–232, 235, 238, 240, 243 Sphingosine-1-phosphate lyase, S1P is the substrate for, 231–232 SREBP see Sterol regulatory element binding proteins Ssu72, plays key role early in the transcription cycle, 119–123 Sterol regulatory element binding proteins (SREBP), are expressed as inactive precursors and reside as integral transmembrane proteins, 280–285, 287–288 combined silencing of S6K1 and S6K2 does not prevent Akt dependent accumulation of mature SREBP, 284–285 genetic deletion of both S6K1 and S6K2 does not prevent accumulation of mature SREBP, 285, 287– 288 Subtype-specific role, of phospholipase C-b via differential interactions with PDZ domain proteins, 138–148 domain structures and the regulation of PLC-b subtypes by G proteins, 140 NHERF, 142–143 Par-3, 145 PDZ-binding motif, 141 potential PDZ domain proteins that interact with PLC-b subtypes and GPCRs, 146–147 PSD-95, 145–146 role of PDZ domain proteins in subtype-specific role of PLC-b in GPCR-mediated signaling, 141–142 Shank2, 143–145
Subject Index / Advances in Enzyme Regulation 51 (2011) 320–329
Temporal order of DNA replication, reside in the epigenetic code specified by chromosomal proteins, 266–269 Thrombosis, weeble chimeric mice have propensity for, 104 Transcription, and gene loops, control of eukaryotic gene expression, 118–124 characteristics of, 120–121 chromosome conformation capture, 120 dependent upon components of promoter and terminator complexes, 121 genetic suppression and discovery of, 118–119 Ssu72 is an integral component of the CPF 30 -end processing complex, 120 Ssu72 is a Pol II CTD phosphatase, 119–120 TFIIB at the terminator, 121–122 Transcriptional regulators, A-type lamins and associated proteins bind to chromatin and, 246, 249 Transcription factor II B (TFIIB), role in gene loops and transcriptional memory, 119–123 Tumor suppressor, PTEN is haploinsufficient for, 37–38, 40, 42, 44 Tumor suppressor proteins, Nit proteins also appear to behave as, 215
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