ライフサイエンスコーパス: phospholipase C gamma

1 ed zeta signaling chain, the PTK ZAP-70, and phospholipase C gamma.

2 docking site of the Gab adaptor proteins and phospholipase C gamma.

3 f tyrosine 785 is required for activation of phospholipase C-gamma.

4 d not detect interactions with Grb2, SHC, or phospholipase C-gamma.

5 e hypothesis that it is a partner protein of phospholipase C-gamma.

6 equired for FcR-dependent phosphorylation of phospholipase C-gamma.

7 ding phosphatidylinositol 3-kinase, Shc, and phospholipase C-gamma.

8 he full activation of TrkB and of downstream phospholipase C-gamma.

9 kinases (RTK), such as Shc, Grb2, FRS2, and phospholipase C-gamma.

10 feration, IL-2 production, and activation of phospholipase C-gamma.

11 ptor binding protein 2, Sos, p85, SHP-2, and phospholipase C-gamma.

12 requirements for 70Z/3 Cbl- and TCR-induced phospholipase C gamma 1 (PLC gamma 1) activation.

13 lls, actin polymerization was independent of phospholipase C gamma 1 (PLC gamma 1) activity, because

14 tein-coupled receptor, whereas activation of phospholipase C gamma 1 (PLC gamma 1) by PAF was indepen

15 TCR engagement activates phospholipase C gamma 1 (PLC gamma 1) via a tyrosine pho

16 activity was dependent on phosphorylation of phospholipase C gamma 1 (PLC gamma 1) via activation of

17 e, we chose a high-molecular-weight protein, phospholipase C gamma 1 (PLC gamma 1, M(r) 148,000) and

18 Phospholipase C gamma 1 (PLC-gamma 1) hydrolyses phospha

19 Phospholipase C Gamma 1 (PLCG1) is frequently mutated in

20 identified an allelic series of mutations in phospholipase c gamma 1 (plcg1).

21 s and lacks the final exon that includes the phospholipase C gamma 1 (PLCgamma1) binding site.

22 ctor receptor-associated factors (TRAFs) and phospholipase C gamma 1 (PLCgamma1) enhanced cytotoxicit

23 Phospholipase C gamma 1 (Plcgamma1) has been implicated

24 (MAPK), phosphoinositol-3 kinase (PI3K) and phospholipase C gamma 1 (PLCgamma1) pathways.

25 r activation of T cells (LAT), and activated phospholipase C gamma 1 (PLCgamma1), which all localize

26 binds the SH2 domain of Grb2 correlates with phospholipase C gamma 1 activation and suggest that such

27 Phospholipase C gamma 1 appears to be abundant in cytopl

28 Phospholipase C gamma 1 associated with cytoskeleton was

29 er, TCR-mediated tyrosine phosphorylation of phospholipase C gamma 1 remains intact in the Jurkat cel

30 eceptor-mediated tyrosine phosphorylation of phospholipase C gamma 1 still occurs.

31 te with the activated PDGF beta R, including phospholipase C gamma 1, SHP2, and phosphoinositol-3-kin

32 struct containing the SH2 and SH3 domains of phospholipase C gamma 1.

33 Phospholipase C-gamma 1 (PLC-gamma 1) is phosphorylated

34 gic inhibitors to examine the association of phospholipase C-gamma 1 (PLC-gamma) with FGF receptor or

35 nhibits the phosphorylation of LAT, Vav, and phospholipase C-gamma 1 and decreases NFAT (nuclear fact

36 Phospholipase C-gamma 1 and phosphatidylinositol 3-kinas

37 thereby activate regulatory enzymes such as phospholipase C-gamma 1 and phosphatidylinositol 3-kinas

38 increase in the tyrosine phosphorylation of phospholipase C-gamma 1 and phospholipase C-gamma 2 and

39 regation induced tyrosine phosphorylation of phospholipase C-gamma 1 and phospholipase C-gamma 2, an

40 e kinases, phosphorylation and activation of phospholipase C-gamma 1, and activation of protein kinas

41 tyrosine kinase-catalyzed phosphorylation of phospholipase C-gamma 1, we used wild-type and CD45-defi

42 c-FOS, and the phosphorylation of ZAP70 and phospholipase C-gamma 1.

43 lls, and PKC mu co-precipitates with Syk and phospholipase C-gamma 1/2 (PLC gamma 1/2).

44 Modulation of TCR/CD3-induced phospholipase-C gamma 1 (PLC gamma 1) activity by the ty

45 f Syk, linker for activation of T cells, and phospholipase C gamma(1), critical signals for calcium r

46 g sites for other signaling proteins such as phospholipase C-gamma(1) (PLC-gamma(1)), Grb2, and Gads.

47 "split" pleckstrin homology (PH) domain from phospholipase C-gamma(1) to the TRPC3 ion channel.

48 We find that y10 encodes phospholipase C gamma-1 (plcg1), a known effector of rec

49 we previously identified increased levels of phospholipase C gamma-1 (PLCgamma1) immunoreactivity spe

50 icient for artery specification, such as the phospholipase C gamma-1 (plcgamma1) mutant, fail to spec

51 GE(2) interfered with the phosphorylation of phospholipase C gamma-1 and extracellular signal-regulat

52 calcium entry into primary B lymphocytes via phospholipase C gamma-1-mediated activation of TRPC3 cha

53 The EGF caused recruitment of Grb2, phospholipase C-gamma-1 (PLCgamma1), Shc, and Src to EGF

54 at activation of tropomyosin kinase B (TrkB)-phospholipase-C-gamma-1 (PLCgamma1) signaling induced by

55 Syk, linker for activated T cells, and phospholipase C gamma 2 (PLC gamma 2) are among the prot

56 plays an important role in the regulation of phospholipase C gamma 2 (PLC gamma 2) downstream of the

57 Pathogenic variants of phospholipase C gamma 2 (PLCG2) cause 2 related forms of

58 ts in SH3BP2, which appear to signal through phospholipase C gamma 2 (PLCG2) to cause excessive osteo

59 eam of the gene encoding the B cell-specific phospholipase C gamma 2 (PLCG2), a B cell-specific enzym

60 Inhibition of the phospholipase C gamma 2 (PLCG2)/inositol 1,4,5-trisphosp

61 Here, we demonstrate an important role for phospholipase C gamma 2 (PLCgamma2) in Src activation in

62 Phospholipase C gamma 2 (PLCgamma2) plays important role

63 Mutations in BTK or phospholipase C gamma 2 (PLCgamma2), a signaling molecul

64 ons in PLCG2 can cause autoinflammation with phospholipase C gamma 2-associated antibody deficiency a

65 gnetic fields (EMF) results in activation of phospholipase C-gamma 2 (PLC-gamma2), leading to increas

66 osphorylation of phospholipase C-gamma 1 and phospholipase C-gamma 2 and no detectable increase in in

67 Tyrosine phosphorylation and activity of phospholipase C-gamma 2 and Syk protein tyrosine kinase

68 en tyrosine kinase) and p-PLCgamma2 (phospho-phospholipase C-gamma 2) in Mcu(plt)(-/)(-) platelets.

69 osphorylation of phospholipase C-gamma 1 and phospholipase C-gamma 2, an increase in intracellular fr

70 uced tyrosine phosphorylations of ZAP-70 and phospholipase C-gamma 2, the formation of phospho-zeta/Z

71 disclosed many mutations in PLCG2, encoding phospholipase C-gamma(2) (PLCgamma(2)).

72 e split pleckstrin homology (spPH) domain of phospholipase C-gamma(2) (PLCgamma(2)).

73 Phospholipase C gamma-2 (PLCgamma2)-dependent calcium (C

74 Phospholipase C-gamma-2 (PLCG2) is selectively expressed

75 FR autophosphorylation, comparable levels of phospholipase C gamma activation as measured by inositol

76 ontact requiring CD58 costimulation revealed phospholipase C-gamma activation matching cytotoxicity w

77 cal regulators of TCR signaling required for phospholipase C-gamma activation.

78 e phosphorylation of paxillin, Shc, Raf, and phospholipase C-gamma after AngII stimulation.

79 te tyrosine phosphorylation of Shc, Raf, and phospholipase C-gamma after angiotensin II stimulation.

80 itiate Ca(2+) release by a pathway requiring phospholipase C gamma and a Src family kinase.

81 ognized as an essential requirement for both phospholipase C gamma and C beta isozymes to hydrolyze p

82 mics depend on both receptor tyrosine kinase/phospholipase C gamma and G protein-coupled receptor/pho

83 Phospholipase C gamma and phosphatidylinositol 3-kinase,

84 Importantly, the SH3 domains of Grb2, phospholipase C gamma and spectrin all failed to exert a

85 ilon RI-mediated tyrosine phosphorylation of phospholipase C-gamma and a dramatic enhancement of hist

86 tyrosine phosphorylation of syk, c-cbl, and phospholipase C-gamma and activates phosphatidylinositol

87 n of EGFR and two major downstream effectors phospholipase C-gamma and erk mitogen-activated protein

88 Defects were also seen in the activity of phospholipase C-gamma and in signals downstream of this

89 In contrast, inhibition of phospholipase C-gamma and LAT (linker for activation of

90 T cell receptor (TCR)-induced activation of phospholipase C-gamma and mitogen-activated protein kina

91 hances the phosphorylation and activation of phospholipase C-gamma and the early phase of Ca(2+) mobi

92 (EGFR)-signaling pathways to cell migration (phospholipase-C gamma) and/or mitogenesis (extracellular

93 transducer and activator of transcription 3, phospholipase C gamma, and focal adhesion kinase, in mul

94 MAPK, phospholipase C gamma, and Stat3 were activated to the s

95 betaCD-induced phosphorylation of EGFR, SHC, phospholipase C-gamma, and Gab-1 as well as MAPK activat

96 p72(Syk), B-cell linker protein (BLNK), and phospholipase C-gamma, and greater activation of the Ig

97 he downstream effector molecules IRS-1, Shc, phospholipase C-gamma, and phosphatidylinositol 3-kinase

98 hosphatidylinositol 3-kinase, RasGAP, SHP-2, phospholipase C-gamma, and Src are not necessary for LRP

99 These data provide evidence for a VEGF-R2-, phospholipase C-gamma-, and PKCalpha/epsilon-mediated cy

100 e was observed in the cellular expression of phospholipase C-gamma between controls and glycolipid-de

101 amino acid position 764, a site required for phospholipase C gamma binding and activation, whereas th

102 growth factor-beta receptor at Tyr(1021), a phospholipase C-gamma binding site, involving the requir

103 ines, and in particular, loss of the primary phospholipase C-gamma-binding tyrosine had a significant

104 s also found to result in phosphorylation of phospholipase C-gamma but reduced phosphorylation of c-S

105 e C-gamma or the downstream IP3 receptors of phospholipase C-gamma, but not by inhibition of MAP kina

106 The measurement of cellular activity of phospholipase C-gamma, by myo-inositol 1,4,5-trisphospha

107 osine phosphorylation and the recruitment of phospholipase C-gamma, Cbl, SHP2, and Shc to that recept

108 alone resulted in efflux of (45)Ca(2+) by a phospholipase C-gamma-dependent pathway.

109 t analysis revealed inhibition of downstream phospholipase C-gamma, extracellular signal-regulated pr

110 Given that PI 3-kinase and phospholipase C-gamma form multifunctional complexes dow

111 The substrates included: (i) a phospholipase C-gamma fragment (residues 530-850); (ii)

112 The assay involves immobilization of phospholipase C- gamma/glutathione S-transferase fusion

113 storing the binding sites for Grb2, Grb7, or phospholipase C-gamma had no effect on cellular growth o

114 ion is directed to the cell body and tail as phospholipase C-gamma hydrolyzes PIP(2) in the protrudin

115 -EtDO-P4 induced tyrosine phosphorylation of phospholipase C-gamma in a concentration-dependent manne

116 ssociation of an adaptor protein (pp36) with phospholipase C-gamma in NK cells.

117 lso show that ERK activation is dependent on phospholipase C-gamma, in keeping with its dependence on

118 The phosphorylation of phospholipase C-gamma induced by d-t-EtDO-P4 was abolish

119 s indicate that this inhibition depends on a phospholipase C-gamma-induced elevation of intracellular

120 Akt activation is abolished by the phospholipase C-gamma inhibitor U-73122, by the intracel

121 /mitogen-activated protein kinase (MAPK) and phospholipase C-gamma inhibitors, but not by an inhibito

122 cription (Stat) 1alpha,beta, Stat 3, Stat 5, phospholipase C-gamma, insulin receptor substrate 1, GTP

123 consistent with a specific glycosphingolipid-phospholipase C-gamma interaction.

124 Thus, the activation of phospholipase C-gamma is negatively regulated by membran

125 The substrate used in this system, phospholipase C-gamma, is one of several biologically im

126 eceptor (FcepsilonR1) leads to activation of phospholipase C gamma isoforms via tyrosine kinase- and

127 We also identify p95(vav) and phospholipase C-gamma isoforms as binding partners of 3B

128 Direct activation of the human phospholipase C-gamma isozymes (PLC-gamma1, -gamma2) by

129 ceptor tyrosine kinase signaling, triggering phospholipase C-gamma-mediated calcium release from the

130 apable of eliciting 45Ca efflux responses (a phospholipase C-gamma-mediated mechanism) after stimulat

131 eceptors to signaling molecules that include phospholipase C-gamma, mitogen-activated protein kinases

132 injected with the Src-homology 2 domains of phospholipase C gamma or of the Src family kinase Fyn (w

133 he MEK-ERK1/2 and p38 MAPK pathways, but not phospholipase C gamma or phosphatidylinositol 3-kinase,

134 by inhibition of phosphoinositide-3 kinase, phospholipase C-gamma or the downstream IP3 receptors of

135 ignal-regulated kinase (ERK) activation; the phospholipase C-gamma pathway, which causes calcium mobi

136 distinct early signaling pathways, including phospholipase C gamma, phosphatidylinositol 3-kinase, Sr

137 thropoietin (Epo) receptor complexes include phospholipase C-gamma, phosphatidylinositol 3-kinase, SH

138 a number of downstream effectors, including phospholipase C-gamma, phosphoinositol 3'-kinase, RAS, a

139 The phospholipase C-gamma phosphorylation was maximally enha

140 re, we examined whether polyphosphoinositide-phospholipase C-gamma (PI-PLC-gamma), a predominantly cy

141 Tyr(766), the previously identified site for phospholipase C gamma (PLC gamma) activation, were not.

142 tly results in the concomitant activation of phospholipase C gamma (PLC gamma) and phosphatidylinosit

143 av3 play a crucial role in the regulation of phospholipase C gamma (PLC gamma) isoforms by immuno-tyr

144 in the tyrosine kinase pathways, which were phospholipase C gamma (PLC gamma), C-Src, SH2-containing

145 ion of phosphatidylinositol 3-kinase (PI3K), phospholipase C gamma (PLC gamma), the GTPase-activating

146 luding phosphatidylinositol 3-kinase (PI3K), phospholipase C gamma (PLC gamma), the GTPase-activating

147 otein tyrosine phosphatase 2, Grb2, Lyn, and phospholipase C gamma (PLC gamma).

148 Phospholipase C-gamma (PLC gamma) is required for EGF-in

149 s that differed in their ability to activate phospholipase C-gamma (PLC gamma).

150 eceptors (BCR) coupled through Syk kinase to phospholipase C-gamma (PLC-gamma) activated the expresse

151 rease in inositol phosphate formation due to phospholipase C-gamma (PLC-gamma) activation, PDGF-BB in

152 gers different signaling pathways, including phospholipase C-gamma (PLC-gamma) and Akt cascades, cruc

153 tyrosine phosphorylations of both receptors, phospholipase C-gamma (PLC-gamma) and phosphatidylinosit

154 onal analysis indicates that coactivation of phospholipase C-gamma (PLC-gamma) and phosphoinositide 3

155 on sites indicates an essential role for the phospholipase C-gamma (PLC-gamma) binding site, but not

156 Multiple studies suggest that phospholipase C-gamma (PLC-gamma) contributes to regulat

157 The Drosophila genome contains a single phospholipase C-gamma (PLC-gamma) homolog, encoded by sm

158 ion of intracellular Ca(2+) or inhibition of phospholipase C-gamma (PLC-gamma) inhibited Vav activati

159 Stimulation of phospholipase C-gamma (PLC-gamma) is a critical event in

160 We have recently shown that phospholipase C-gamma (PLC-gamma) is activated by tau, a

161 Phospholipase C-gamma (PLC-gamma) is stimulated by epide

162 Phospholipase C-gamma (PLC-gamma) is typical of proteins

163 cytes activates protein tyrosine kinases and phospholipase C-gamma (PLC-gamma) isoforms.

164 Phospholipase C-gamma (PLC-gamma) isozymes are thought t

165 rosine kinases and immune receptors activate phospholipase C-gamma (PLC-gamma) isozymes at membranes

166 effect was specific and was due to defective phospholipase C-gamma (PLC-gamma) phosphorylation and ac

167 elial exocytosis in part through calcium and phospholipase C-gamma (PLC-gamma) signal transduction.

168 (SFK) that directly or indirectly activates phospholipase C-gamma (PLC-gamma) to produce IP3, which

169 tivation of Src tyrosine kinase to stimulate phospholipase C-gamma (PLC-gamma) which increases inosit

170 lation of receptor components, activation of phospholipase C-gamma (PLC-gamma), and increases in intr

171 ed by neuronal EGFR (also called LET-23) and phospholipase C-gamma (PLC-gamma), diacylglycerol-bindin

172 PtdIns(3,4,5)P3 has been known to stimulate phospholipase C-gamma (PLC-gamma), internal Ca2+ mobiliz

173 ternary complex with Hsp70/Hsc70 and latent phospholipase C-gamma (PLC-gamma).

174 regulator of antigen receptor activation of phospholipase C-gamma (PLC-gamma).

175 n lymphocytes; binds to Syk/ZAP-70, Vav, and phospholipase C-gamma (PLC-gamma); and is thought to be

176 A major partner for mammalian Gab is phospholipase C-gamma (PLC-gamma); genetic and biochemic

177 yrosine kinase required for full TCR-induced phospholipase C-gamma (PLC-gamma1) activation, exhibit d

178 ays regulated by MAP kinase, PI 3-kinase and phospholipase-C-gamma (PLC-gamma).

179 teins (phosphatidylinositol 3-kinase [PI3K], phospholipase C gamma [PLC gamma], C-Src, SHC, and mitog

180 Phospholipase C-(gamma) (PLC-(gamma)) is activated in ma

181 Moreover, Tregs with defective phospholipase C gamma (PLCgamma) activation due to a Y14

182 The high-affinity binding site for phospholipase C gamma (PLCgamma) on the activated fibrob

183 a-estradiol (E2) activates the UPR through a phospholipase C gamma (PLCgamma)-mediated opening of EnR

184 naling, it is shown that soc-1/Gab1 inhibits phospholipase C-gamma (PLCgamma) and phosphatidylinosito

185 phosmin-anaplastic lymphoma kinase (NPM-ALK)/phospholipase C-gamma (PLCgamma) complex also appears to

186 Phospholipase C-gamma (PLCgamma) has been implicated in

187 sponse was also blocked by pretreatment with phospholipase C-gamma (PLCgamma) inhibitor U71322 and pr

188 Phospholipase C-gamma (PLCgamma) is a key regulator of i

189 Phospholipase C-gamma (PLCgamma) is the isozyme of PLC p

190 ptors have previously been shown to activate phospholipase C-gamma (PLCgamma), protein kinase C (PKC)

191 to the membrane by diacylglycerol (DAG) in a phospholipase C-gamma (PLCgamma)-dependent manner.

192 the SH3 domains from Src, Fyn, Grb2, GAP, or phospholipase C-gamma (PLCgamma).

193 phosphoinositol-3 kinase (PI3K); Ras-MEK and phospholipase C-gamma (PLCgamma).

194 hatidylinositol 4,5-bisphosphate (PIP(2)) by phospholipase C-gamma (PLCgamma1) represents a critical

195 d that phosphatidylinositol 3-kinase/AKT and phospholipase C gamma/protein kinase C alpha activation

196 (i.e. phosphatidylinositol 3-kinase/AKT and phospholipase C gamma/protein kinase C alpha) are obliga

197 that interact with PDGF receptors including phospholipase C gamma, Ras GTPase-activating protein, an

198 these proteins in TCR-mediated activation of phospholipase C-gamma, recent data indicate that Tec fam

199 n, phosphatidylinositol 3-kinase (PI3K), and phospholipase C-gamma, respectively--in fibroblasts and

200 k and causes the tyrosine phosphorylation of phospholipase C-gamma, resulting in the Ca2+- and protei

201 ggers endothelial exocytosis in part through phospholipase C-gamma signal transduction.

202 NKL-induced expression of NFATc1 by blocking phospholipase C-gamma signaling, which, in turn, inhibit

203 n of selected tyrosine sites on ERK1/2, p38, phospholipase C-gamma, Src homology 2 domain-containing

204 ing networks via enhanced phosphorylation of phospholipase C-gamma/Src homology 2 domain-containing t

205 MC signaling mediators such as Lyn, Syk, and phospholipase C gamma; thus, a role for this adaptor in

206 e base line, and an increased sensitivity of phospholipase C-gamma to bradykinin stimulation.

207 ses neither receptor autophosphorylation nor phospholipase C-gamma transphosphorylation.

208 VEGF-D induced KDR and phospholipase C-gamma tyrosine phosphorylation more slow

209 ylation of total cellular proteins, Syk, and phospholipase C-gamma was also enhanced by Cbl-b deficie

210 Phosphorylation of the EGFR substrate phospholipase C-gamma was decreased by coexpression of G

211 dendritic growth, whereas the activation of phospholipase C-gamma was found to be responsible for sp

212 alization of anaplastic lymphoma kinase; and phospholipase C-gamma was identified as a molecular targ

213 In addition, phospholipase C-gamma was not tyrosine phosphorylated vi

214 3K)-Akt signaling (but not signaling through phospholipase C-gamma) was initiated and directly led to

215 ak1) and the TCR (TCR-zeta, CD3-epsilon, and phospholipase C-gamma) were minimally affected.

216 mily substrates whereas others (for example, phospholipase C-gamma) were not.

217 cules such as the receptor subunits, Syk and phospholipase C-gamma which resulted in faster release o

218 t Tyr-1316 is involved in phosphorylation of phospholipase C-gamma, which is, however, not important

219 naling pathways, including the activation of phospholipase C-gamma, which promotes the release of dia

220 binding sites for PI3-K (Y708, Y719) and for phospholipase C-gamma (Y977, Y989) in PDGF-mediated Bcr