ライフサイエンスコーパス: PLC-gamma

1 PLC gamma 1 contains a pair of Src homology 2 (SH2) doma

2 PLC gamma activity was dependent on the presence of Tyr(

3 PLC-gamma 1 also has mitogenic activity upon growth-fact

4 PLC-gamma has been well conserved throughout, although s

5 PLC-gamma is bound to CAIR-1/BAG-3 in unstimulated cells

6 PLC-gamma was immunoprecipitated, and associated protein

7 bl- and TCR-induced phospholipase C gamma 1 (PLC gamma 1) activation.

8 of TCR/CD3-induced phospholipase-C gamma 1 (PLC gamma 1) activity by the tyrosine kinase Emt/Itk/Tsk

9 ereas activation of phospholipase C gamma 1 (PLC gamma 1) by PAF was independent of G proteins but re

10 ngagement activates phospholipase C gamma 1 (PLC gamma 1) via a tyrosine phosphorylation-dependent me

11 phosphorylation of phospholipase C gamma 1 (PLC gamma 1) via activation of src-kinases.

12 lar-weight protein, phospholipase C gamma 1 (PLC gamma 1, M(r) 148,000) and a low-molecular-weight pr

13 Phospholipase C gamma 1 (PLC-gamma 1) hydrolyses phosphatidylinositol-4,5-bisphos

14 Phospholipase C-gamma 1 (PLC-gamma 1) is phosphorylated on three tyrosine residue

15 the association of phospholipase C-gamma 1 (PLC-gamma) with FGF receptor or with cytoskeleton.

16 g proteins such as phospholipase C-gamma(1) (PLC-gamma(1)), Grb2, and Gads.

17 rovessels as in cultured endothelium: Flk-1; PLC-gamma; and mitogen-activated protein kinase.

18 ates with Syk and phospholipase C-gamma 1/2 (PLC gamma 1/2).

19 ivated T cells, and phospholipase C gamma 2 (PLC gamma 2) are among the proteins tyrosine phosphoryla

20 n the regulation of phospholipase C gamma 2 (PLC gamma 2) downstream of the collagen receptor glycopr

21 n a central area and c-Cbl, p95(vav), Grb-2, PLC gamma, Fyn, and Lck distributed more uniformly acros

22 ith a larger amount of active receptors; (4) PLC-gamma and Akt are not directly sensitive to cell den

23 nstrated by the robust activation of ZAP-70, PLC-gamma, and Ras.

24 ore, 70Z/3 Cbl-induced activation of NFAT, a PLC gamma 1/Ca(2+)-dependent transcriptional event, requ

25 These studies are the first to define a PLC-gamma-associated protein that may be required for An

26 -gamma); genetic and biochemical tests for a PLC-gamma-SH3::Dos interaction were negative, indicating

27 PLC-3 is a PLC-gamma homolog and is expressed in contractile sheath

28 mediates Ca2+ release at fertilization via a PLC-gamma SH2 domain-mediated mechanism.

29 ues also contain a protein that can activate PLC-gamma in the presence of arachidonic acid.

30 d to cytosolic phospholipase A2 may activate PLC-gamma isozymes indirectly in the absence of tyrosine

31 eceptors coupled to PI 3-kinase may activate PLC-gamma isozymes indirectly, in the absence of PLC-gam

32 These results suggest that 70Z/3 Cbl and PLC gamma 1 form a TCR-, Lat- and Slp-76-independent com

33 CR/CD3-regulated association between Emt and PLC gamma 1 in both normal and leukemic T cells.

34 based on our studies with individual Emt and PLC gamma 1 SH2/SH3 domains, we propose a mechanism for

35 ribe a regulated interaction between Emt and PLC gamma 1, and based on our studies with individual Em

36 mast cells, Gab2 by interacting with Lyn and PLC gamma may have negative regulatory effects on Fc eps

37 The association of Gab2 with Lyn and PLC gamma were enhanced after receptor aggregation.

38 ed a reduction in rhodocytin-induced Syk and PLC gamma 2 tyrosine phosphorylation.

39 ma PH domain-mediated membrane targeting and PLC gamma activation.

40 c-Jun, and an association between Flk-1 and PLC-gamma.

41 tative role in regulating actin assembly and PLC-gamma 1 signaling in light of its unique interaction

42 l coupling of AT1 receptors to PLC-beta1 and PLC-gamma, as well as dual coupling of AT1 receptors to

43 Although the PH domains of PLC-delta and PLC-gamma have been studied, the comparable domains of t

44 activated TrkB and downstream AKT, ERK, and PLC-gamma signaling in TNBC cells, increasing their inva

45 n contrast, ANG induced ORF73 expression and PLC-gamma and AKT phosphorylation.

46 cided with transient dissociation of Fyn and PLC-gamma.

47 , causes recruitment of beta(3) integrin and PLC-gamma to adhesion contacts and induces stable associ

48 way dependent on protein tyrosine kinase and PLC-gamma activation in hematopoietic progenitors.

49 horylated Src-family kinases (pSFK), LAT and PLC-gamma over T cell receptor (TCR) alone.

50 on, including PYK2, p130(Cas), paxillin, and PLC-gamma.

51 dc42/Rac/RhoG protein family, MAPK, PI3K and PLC-gamma, thereby affecting both development and functi

52 or both phosphoinositide 3-kinase (PI3K) and PLC-gamma.

53 Moreover, direct interaction of PYK2 and PLC-gamma can be induced by either adhesion or M-CSF, su

54 ptor led to a rapid increase in receptor and PLC-gamma phosphorylation, and a slower increase in the

55 trate a direct association between c-Src and PLC-gamma, we hypothesized that a linker protein mediate

56 ntibodies against PLC-beta1, but not by anti-PLC-gamma and -delta antibodies.

57 Moreover, electropor-ation of anti-PLC-gamma antibody markedly inhibited the IP3 production

58 unoprecipitated with PLC-gamma 1 antibodies, PLC-gamma 1, actin, and vinculin were coprecipitated in

59 sequent to triggering of motility-associated PLC gamma activity attenuates the EGFR mitogenic respons

60 lysates from EGF-treated cells did not bind PLC-gamma as was seen in intact cells.

61 8059 and U0126, two MAPK inhibitors, blocked PLC-gamma 1-induced expression of MDR1.

62 To gain insight into both PLC-gamma evolution and structure-function relationships

63 -783 favored over Tyr-1253, before the bound PLC-gamma 1 was released, and phosphorylation at the two

64 f downstream signaling processes mediated by PLC gamma, Shc, and Grb2.

65 Sustained signaling by PLC-gamma provides a means for differential neuronal gen

66 cules, including Shc, Grb2, phospholipase C (PLC-gamma), and phosphatidylinositol 3 kinase.

67 servations, activation of PI 3-kinase causes PLC gamma PH domain-mediated membrane targeting and PLC

68 NG silencing inhibited phospholipase Cgamma (PLC-gamma) and AKT phosphorylation, and in contrast, ANG

69 s sufficient to induce phospholipase Cgamma (PLC-gamma) phosphorylation and NFAT (nuclear factor of a

70 the binding sites for phospholipase Cgamma (PLC-gamma), RasGTPase-activating protein, phosphatidylin

71 After activation of phospholipase Cgamma (PLC-gamma), TRPC1 mediated Ca(2+) entry and triggered pr

72 Consequently, PLC-gamma isozymes link phosphorylation to phospholipase

73 In contrast, PLC-gamma isozymes (PLC-gamma1 and -gamma2) are structur

74 ssion, since treatment with the conventional PLC-gamma inhibitor U73122 also showed similar results.

75 were negative, indicating that if Drosophila PLC-gamma binds to Dos, it must do so indirectly or thro

76 function relationships within the Drosophila PLC-gamma encoded by small wing (sl), we cloned and sequ

77 lts indicate that an endogenous starfish egg PLC-gamma interacts with an egg SFK and mediates Ca2+ re

78 Immunoprecipitations of sea urchin egg PLC-gamma using an affinity-purified antibody directed a

79 e induced tyrosine phosphorylation of either PLC gamma 1 SH2(N) or SH2(C) domain mutants to a level c

80 from receptor-mediated activation of either PLC-gamma or PLC-beta.

81 receptors capable of associating with either PLC-gamma or PI3K relayed a growth signal that was compa

82 domain was crucial for the constitutive Emt/PLC gamma 1 association; however, upon TCR/CD3 engagemen

83 more efficient in mediating the enhanced Emt/PLC gamma 1 interaction.

84 se at fertilization, an oocyte cDNA encoding PLC-gamma was isolated from the starfish Asterina miniat

85 increased ability to phosphorylate exogenous PLC-gamma in vitro.

86 t AHNAK molecule contains multiple sites for PLC-gamma activation.

87 pase A2 can act as an additional trigger for PLC-gamma activation, constituting an alternative mechan

88 Although structures of isolated domains from PLC-gamma isozymes are available, these structures are i

89 y identified site for phospholipase C gamma (PLC gamma) activation, were not.

90 omitant activation of phospholipase C gamma (PLC gamma) and phosphatidylinositol (PI) 3-kinase.

91 in the regulation of phospholipase C gamma (PLC gamma) isoforms by immuno-tyrosine-based activation

92 pathways, which were phospholipase C gamma (PLC gamma), C-Src, SH2-containing protein (SHC), and mit

93 itol 3-kinase (PI3K), phospholipase C gamma (PLC gamma), the GTPase-activating protein (GAP), and Syp

94 ase 2, Grb2, Lyn, and phospholipase C gamma (PLC gamma).

95 r ability to activate phospholipase C-gamma (PLC gamma).

96 the downstream enzyme phospholipaseC-gamma (PLC gamma) and a mitosis-associated response pathway.

97 through Syk kinase to phospholipase C-gamma (PLC-gamma) activated the expressed TRPC3 channels in bot

98 hate formation due to phospholipase C-gamma (PLC-gamma) activation, PDGF-BB induced phosphoinositol h

99 g pathways, including phospholipase C-gamma (PLC-gamma) and Akt cascades, crucial for endothelial pro

100 ns of both receptors, phospholipase C-gamma (PLC-gamma) and phosphatidylinositol 3'-kinase.

101 that coactivation of phospholipase C-gamma (PLC-gamma) and phosphoinositide 3-kinase (PI3-kinase) by

102 ssential role for the phospholipase C-gamma (PLC-gamma) binding site, but not the Shc binding site, f

103 studies suggest that phospholipase C-gamma (PLC-gamma) contributes to regulation of sodium/hydrogen

104 ome contains a single phospholipase C-gamma (PLC-gamma) homolog, encoded by small wing (sl), that act

105 (2+) or inhibition of phospholipase C-gamma (PLC-gamma) inhibited Vav activation (85 and 70%, respect

106 Stimulation of phospholipase C-gamma (PLC-gamma) is a critical event in angiotensin II (Ang II

107 e recently shown that phospholipase C-gamma (PLC-gamma) is activated by tau, a neuronal cell-specific

108 Phospholipase C-gamma (PLC-gamma) is stimulated by epidermal growth factor via

109 Phospholipase C-gamma (PLC-gamma) is typical of proteins that appeared at this

110 Phospholipase C-gamma (PLC-gamma) isozymes are thought to be activated by recep

111 was due to defective phospholipase C-gamma (PLC-gamma) phosphorylation and activation.

112 t through calcium and phospholipase C-gamma (PLC-gamma) signal transduction.

113 indirectly activates phospholipase C-gamma (PLC-gamma) to produce IP3, which triggers Ca2+ release f

114 e kinase to stimulate phospholipase C-gamma (PLC-gamma) which increases inositol 1,4,5-trisphosphate

115 so called LET-23) and phospholipase C-gamma (PLC-gamma), diacylglycerol-binding proteins, and regulat

116 en known to stimulate phospholipase C-gamma (PLC-gamma), internal Ca2+ mobilization does not play a s

117 nase, PI 3-kinase and phospholipase-C-gamma (PLC-gamma).

118 sp70/Hsc70 and latent phospholipase C-gamma (PLC-gamma).

119 eceptor activation of phospholipase C-gamma (PLC-gamma).

120 Syk/ZAP-70, Vav, and phospholipase C-gamma (PLC-gamma); and is thought to be important for interleuk

121 for mammalian Gab is phospholipase C-gamma (PLC-gamma); genetic and biochemical tests for a PLC-gamm

122 tor (EGFR), Shc, and phospholipase-C gamma1 (PLC gamma), and growth factor receptor binding protein 2

123 plexes between activated EGFR and SOS, Grb2, PLC gamma, and SHC that can be precipitated with antibod

124 Here we investigate how PLC-gamma may be activated, by using the PLC-gamma SH2 d

125 To identify PLC-gamma-associated proteins, RASM cells were labeled w

126 2 treatment caused induction of prostin-1 in PLC gamma competent cells.

127 collagen can activate platelets deficient in PLC gamma 2, G alpha q, or TxA2 receptors, as well as pl

128 The role of the PLC gamma 1 SH2 domains in PLC gamma 1 phosphorylation was explored by mutational a

129 -/- platelets exhibit a greater reduction in PLC gamma 2 phosphorylation than is seen in the absence

130 s to the Src homology 2 domains contained in PLC-gamma without interrupting binding of PLC-gamma to N

131 SH2 introns suggest that the SH2 domains in PLC-gamma are derived from an ancestral domain that was

132 The fenoldopam-induced increase in PLC-gamma and activity was mediated by protein kinase A

133 protein kinase (MAPK) was also increased in PLC-gamma 1-transfected cells.

134 orylation of Itk and its effectors including PLC-gamma, Akt, and extracellular signal-regulated kinas

135 bound to signaling intermediates, including PLC-gamma.

136 th phorbol 12-myristate 13-acetate increased PLC-gamma protein and activity, effects that were blocke

137 70Z/3 Cbl-induced PLC gamma 1 phosphorylation required Zap-70, as for the

138 0Z/3 Cbl did not eliminate 70Z/3 Cbl-induced PLC gamma 1 phosphorylation, suggesting that blockage of

139 70Z/3 Cbl-induced PLC gamma 1 tyrosine phosphorylation required, in additi

140 EGF-induced PLC gamma tyrosine phosphorylation and inositol 1,4,5-tr

141 mma PH domain prevents growth factor-induced PLC gamma activation.

142 he SH2(N) domain is required for TCR-induced PLC gamma 1 phosphorylation, presumably by participating

143 to Lat, a crucial interaction in TCR-induced PLC gamma 1 phosphorylation.

144 nce Syk is also required for the BCR-induced PLC-gamma 2 activation, our findings indicate that PLC-g

145 Urea-inducible PLC-gamma activation, in conjunction with the genistein-

146 -nitrocoumarin (3-NC), selectively inhibited PLC-gamma in Madin-Darby canine kidney cells without aff

147 m SH2 domains of AmPLC-gamma (which inhibits PLC-gamma activation) specifically inhibited Ca2+ releas

148 Confirming the SH3 interaction, PLC-gamma was pulled down by CAIR-1/BAG-3 PXXP-GST fusio

149 stral domain that was shuffled not only into PLC-gamma, but also into many other unrelated genes duri

150 induced apoptosis whilst TrkA mutated at its PLC-gamma binding site (Y785F) is capable of protecting

151 phosphorylation of 47-, 60-, 84-, and 97-kD PLC-gamma-associated proteins.

152 wn signaling pathways including PI-3 kinase, PLC-gamma, Ras or Stats.

153 e that resulted in reduced formation of LAT, PLC-gamma, and AKT microclusters.

154 ind to Src SH3-containing proteins Fyn, Lck, PLC-gamma, and Grb2, and mutated WASP, if expressed, was

155 t high-resolution structure of a full-length PLC-gamma isozyme and use it to underpin a detailed mode

156 s that could in theory still provide limited PLC-gamma function.

157 evealed no defects in Fc epsilon RI-mediated PLC gamma 1 activation.

158 fect on parameters of Fc epsilon RI-mediated PLC gamma activation, and had little effect on the initi

159 ivation of the downstream effector molecules PLC-gamma, STAT5, and phosphatidylinositol 3-kinase/AKT,

160 ed mitogenesis was not observed in three non-PLC gamma activating, nonmotility-responsive EGFR-expres

161 ial but redundant roles in the activation of PLC gamma 2 by GPVI.

162 and Vav2 are not required for activation of PLC gamma 2 in response to stimulation of the ITAM-coupl

163 ced activation of PKC mu, like activation of PLC gamma 2, requires Syk and is partially regulated by

164 rate eggs, SH2 domain-mediated activation of PLC gamma appears not to be required.

165 f a complex that promotes the association of PLC gamma 1 with a tyrosine kinase.

166 that the pleckstrin homology (PH) domain of PLC gamma binds to phosphatidylinositol 3,4,5-trisphosph

167 Signaling pathways downstream of PLC gamma 1 involved increase of intracellular Ca 2+ lev

168 The complete elimination of PLC gamma 1 phosphorylation required deleting the SH3 do

169 Pharmacological inhibition of PLC gamma (U73122) confirmed that PLC gamma signaling su

170 treatment induces an alternate mechanism of PLC gamma 1 phosphorylation.

171 ted in defective tyrosine phosphorylation of PLC gamma 1 in response to TCR/CD3 perturbation.

172 a rapid translocation and phosphorylation of PLC gamma 1, and subsequent inositol trisphosphate (IP3)

173 BB did stimulate tyrosine phosphorylation of PLC gamma 1, the phospholipase was strongly inhibited by

174 fect TCR-induced tyrosine phosphorylation of PLC gamma 1.

175 oduction despite tyrosine phosphorylation of PLC gamma 1.

176 Tyrosine phosphorylation of PLC gamma 2 by collagen and CRP is not altered in Tec-/-

177 h a reduction in tyrosine phosphorylation of PLC gamma 2.

178 established that tyrosine phosphorylation of PLC gamma is necessary for its activation, we show here

179 el such as spatial cytosolic polarization of PLC gamma towards an extrinsic chemotactic gradient.

180 ominant-negative mutant or the prevention of PLC gamma membrane targeting by overexpression of the PL

181 n observed with respect to the regulation of PLC gamma 2 in platelets.

182 functional role for Tec in the regulation of PLC gamma 2 in the absence of Btk.

183 gamma isozymes indirectly, in the absence of PLC-gamma tyrosine phosphorylation, through the generati

184 cells, which are required for activation of PLC-gamma and downstream pathways.

185 at sufficient levels and that activation of PLC-gamma and PKC plays a pivotal role in PDGF-betaR-med

186 ) generated by LET-23 mediated activation of PLC-gamma induces repetitive intracellular Ca(2+) releas

187 prolonged phosphorylation and activation of PLC-gamma signaling that is sustained for up to 2 h.

188 suggest that integrin-mediated activation of PLC-gamma to initiate phosphoinositide signaling and int

189 he activity of Src, a proximate activator of PLC-gamma in other cells, with peaks at 1 and 9 min in a

190 t dependent on the phospholipase activity of PLC-gamma 1, but requires an SH3 domain.

191 holine and, had no effect on the activity of PLC-gamma.

192 in PLC-gamma without interrupting binding of PLC-gamma to NHE3, was used to probe a non-lipase-depend

193 The binding of PLC-gamma(1) and Syk to tyrosyl-phosphorylated CD22 was

194 r studies provided evidence that blockage of PLC-gamma activation by neomycin appears to be mediating

195 cues, one of which requires coactivation of PLC-gamma and PI3-kinase pathways.

196 s mediated by the NH2-terminal SH2 domain of PLC-gamma(1) and the COOH-terminal SH2 domain of Syk, re

197 sates bound selectively to the SH3 domain of PLC-gamma, but not its N-SH2 or C-SH2 domains.

198 PtdIns(3,4,5)P3 through a combined effect of PLC-gamma 1 activation and preferential profilin binding

199 pression of a dominant negative (DN) form of PLC-gamma, the PLC-z fragment, in HBMEC inhibits PLC-gam

200 n translocation of a significant fraction of PLC-gamma from the cytosol to the membrane compartment o

201 ith Trk mutants, drug-mediated inhibition of PLC-gamma activity also blocks PN1 induction by NGF.

202 Inhibition of PLC-gamma by 3-NC was associated with an increase in tig

203 y ID5 were not affected by the inhibition of PLC-gamma.

204 3-NC), which was inactive as an inhibitor of PLC-gamma, also had no effect on tight junction permeabi

205 uld be reproduced by a specific inhibitor of PLC-gamma, we propose that a balance between the activit

206 cent work has demonstrated that injection of PLC-gamma SH2 domain fusion proteins into starfish eggs

207 Involvement of PLC-gamma activation is suggested by using a PLC inhibit

208 of adhesion, consistent with involvement of PLC-gamma.

209 differentially couple to the two isoforms of PLC-gamma.

210 phosphorylated proteins, PtdIns(3,4,5)P3] of PLC-gamma; the PH domain [PtdIns(4,5)P2] and C2 domain (

211 al, because both tyrosine phosphorylation of PLC-gamma and G protein-dependent PLC-beta activation pa

212 indicating that tyrosine phosphorylation of PLC-gamma contributes mainly to the later phase of PLC a

213 ranslocation and tyrosine phosphorylation of PLC-gamma in the basolateral membrane (BLM).

214 ng II stimulates tyrosine phosphorylation of PLC-gamma via activation of c-Src.

215 f beta-PDGFR and tyrosine phosphorylation of PLC-gamma, PI3Kp85 and Shc were detected only in PDGF-BB

216 ciation, and the tyrosine phosphorylation of PLC-gamma, specifically in the basal lateral membranes.

217 d fertilization-dependent phosphorylation of PLC-gamma.

218 ity accounts for the mitogenic properties of PLC-gamma 1.

219 Moreover, recruitment of PLC-gamma to TrkA is essential for NGF-mediated potentia

220 e the mechanism for the unique regulation of PLC-gamma isozymes by their X/Y linker.

221 kinase as a potential upstream regulator of PLC-gamma in the activation of starfish eggs.

222 esults indicate a lipase-independent role of PLC-gamma in the physiological agonist-induced activatio

223 used to probe a non-lipase-dependent role of PLC-gamma.

224 reover, the inhibitory effect of profilin on PLC-gamma 1-mediated PtdIns(4,5)P2 hydrolysis is overcom

225 to F4 cells had no effect on Grb2 binding or PLC gamma phosphorylation.

226 e DT40 deficient in either Syk, Lyn, Btk, or PLC gamma 2 revealed that BCR-induced activation of PKC

227 of conjugates that rearranged LAT, c-Cbl, or PLC gamma also exhibited cytoplasmic NF-AT migration to

228 te immune synapses containing LAT, c-Cbl, or PLC gamma.

229 ble to relocalize c-Cbl, LAT, CD3epsilon, or PLC gamma typically relocalized all four of these compon

230 icient activation in response to PLC-beta or PLC-gamma activation, which was independent of inositol

231 ular transformation, and that either PI3K or PLC-gamma are key initiators of such signal relay cascad

232 many tyrosine kinases directly phosphorylate PLC-gamma isozymes to enhance their lipase activity, the

233 ntribute to the activation of phosphorylated PLC-gamma 1.

234 lyphosphoinositide-phospholipase C-gamma (PI-PLC-gamma), a predominantly cytosolic isoform of PI-PLC,

235 th mutations eliminating activation of PI3K, PLC gamma, GAP, and Syp abolished the induction of type

236 Transfection of NIH 3T3 cells with a pMJ30-PLC-gamma 1 expression vector increased the activity of

237 urthermore, this study suggests that in pOCs PLC-gamma is a common downstream mediator for adhesion a

238 The resultant activation of signal proteins PLC gamma, SHC, MAPK, PI3K, and PDGF-beta receptor may p

239 bFGF) and activation of two signal proteins (PLC gamma and MAPK) in the tyrosine kinase pathways.

240 we show that PI(3,4,5)P3 activates purified PLC-gamma isozymes by interacting with their Src homolog

241 tyrosine residues function by reconstituting PLC-gamma(1) phosphorylation and recruitment to LAT.

242 Signaling cascades regulating PLC-gamma could, therefore, control a critical feature o

243 Cbl, which binds Zap-70, but did not require PLC gamma 1 binding to Lat, a crucial interaction in TCR

244 though fully active chimeras did not require PLC gamma, the responses of chimeras showing reduced act

245 Tec-induced NFAT activation requires PLC-gamma, but not the adapters LAT, SLP-76, and BLNK, w

246 ovide evidence for two genetically separable PLC-gamma-dependent pathways affecting the development o

247 Phosphorylation of Shp2, PLC-gamma, and MAPK was also stimulated by all three 'TD

248 r the first time that 1,25(OH)2D3 stimulates PLC-gamma as well as c-Src in rat colonocytes, and indic

249 PKA then stimulates PLC-gamma in cytosol and membrane via activation of PKC.

250 Complexes of either CD22/PTP-1C/Syk/PLC-gamma(1) could be isolated from B cells stimulated b

251 tein tyrosine phosphatase directly targeting PLC-gamma and counteracting the receptor-mediated signal

252 served introns in both the N- and C-terminal PLC-gamma SH2 domains that are present in SH2 domains in

253 ibition of PLC gamma (U73122) confirmed that PLC gamma signaling suppressed prostin-1 in that U73122

254 essary for its activation, we show here that PLC gamma is regulated additionally by the lipid product

255 Here, we demonstrate that PLC-gamma 1 acts as a guanine nucleotide exchange factor

256 We demonstrate here that PLC-gamma binds directly to the C terminus of NHE3 and e

257 We report here that PLC-gamma isoforms are required for agonist-induced Ca2+

258 mma 2 activation, our findings indicate that PLC-gamma 2 activation is regulated by Btk and Syk throu

259 c-Src in rat colonocytes, and indicate that PLC-gamma is a direct substrate of secosteroid-activated

260 In summary, these data indicate that PLC-gamma is required for growth factor-induced activati

261 elease in response to sperm, indicating that PLC-gamma is necessary for Ca2+ release at fertilization

262 utation, these results strongly suggest that PLC-gamma activation regulates Ras activation in these c

263 receptor potential channel and suggest that PLC-gamma may play a common role in regulating the cell-

264 The PLC gamma and MAPK were activated at these time points.

265 In addition, the PLC gamma 1 SH2(N) domain mutant failed to associate wit

266 3 Cbl, consistent with 70Z/3 Cbl binding the PLC gamma 1 SH3 domain.

267 Furthermore, the PLC gamma 1-SH3 domain, but not the two PLC gamma 1-SH2

268 The role of the PLC gamma 1 SH2 domains in PLC gamma 1 phosphorylation w

269 membrane targeting by overexpression of the PLC gamma PH domain prevents growth factor-induced PLC g

270 Here we report evidence that the PLC gamma 1-dependent pathway of Fc epsilon RI-mediated

271 are consistent with the conclusion that the PLC gamma-dependent component of Fc epsilon RI-mediated

272 phosphorylation required, in addition to the PLC gamma 1 N-terminal SH2 domain, the C-terminal SH2 an

273 The PLC-gamma inhibitor, 3-NC, but not the inactive analog,

274 The PLC-gamma-binding site in NHE3 was identified (amino aci

275 Hsp70/Hsc70 was brought down by the PLC-gamma SH3 construct equally from native and EGF-trea

276 model also explains why mutant forms of the PLC-gamma isozymes found in several cancers have a wide

277 small wing (sl), we cloned and sequenced the PLC-gamma homologs from Drosophila pseudoobscura and D.

278 how PLC-gamma may be activated, by using the PLC-gamma SH2 domain fusion protein as an affinity matri

279 tivity or of the Src family protein with the PLC-gamma SH2 domains.

280 Furthermore, binding of p36-38 to PLC gamma 1 was not abrogated by mutations of the SH2(C)

281 and Slp-76-independent complex that leads to PLC gamma 1 phosphorylation and activation.

282 -beta1 via a heterotrimeric G protein and to PLC-gamma via a downstream tyrosine kinase; 2) the initi

283 because when it is mutated, NHE3 binding to PLC-gamma as well as NHERF2 is lost.

284 We show that CAIR-1/BAG-3 binds to PLC-gamma and Hsp70/Hsc70 through separate and distinct

285 ch are required for Btk and Itk to couple to PLC-gamma.

286 a concentration range that was inhibitory to PLC-gamma.

287 The effect of tau and AA was specific to PLC-gamma isozymes in the presence of submicromolar conc

288 tumor cells, showing that TIL are triggered, PLC gamma-1, LAT, and ZAP70 are not activated and LFA-1

289 the PLC gamma 1-SH3 domain, but not the two PLC gamma 1-SH2 domains, contributed to formation of the

290 NG for its advantage via a so-far-unexplored PLC-gamma pathway for maintaining its latency.

291 clasts in the absence of c-Src, possibly via PLC-gamma.

292 ons and that the receptors can use whichever PLC-gamma isoform is preferentially expressed in a cell

293 cellular calcium levels that correlated with PLC gamma activation.

294 previously been recognized to interact with PLC gamma 1, Grb2, and other molecules involved in TCR s

295 t Src family tyrosine kinases associate with PLC-gamma SH2 domains in a fertilization-dependent manne

296 time period which temporally correlated with PLC-gamma tyrosine phosphorylation in response to Ang II

297 ndothelial cells was immunoprecipitated with PLC-gamma 1 antibodies, PLC-gamma 1, actin, and vinculin

298 stable association of beta(3) integrin with PLC-gamma, phosphatidylinositol 3-kinase, and PYK2.

299 ture and predicted amino acid sequences with PLC-gamma homologs in other animals.

300 physical association of activated c-Src with PLC-gamma.