ライフサイエンスコーパス: GAP-43

1 5 (PSD-95) and growth-associated protein-43 (GAP-43).

2 M), and growth-associated phosphoprotein-43 (GAP-43).

3 etinal terminals in the dLGN, do not contain GAP 43.

4 related to inhibited PKC phosphorylation of GAP-43.

5 T projections to forebrain in the absence of GAP-43.

6 tes, a process that required the presence of GAP-43.

7 rowth by ECM in P19s occurs independently of GAP-43.

8 nt that induces outgrowth independently from GAP-43.

9 d by immunohistochemistry with antibodies to GAP-43.

10 ephalic wall and like RGC axons also express GAP-43.

11 es and express the growth-associated protein GAP-43.

12 s downstream effectors CREB, synapsin I, and GAP-43.

13 N-terminus and the basic effector domain of GAP-43.

14 actions with acylated basic proteins such as GAP-43.

15 lation mixtures co-purified with full-length GAP-43.

16 with the pro-plasticity/regeneration protein GAP-43.

17 sed OMP, whereas approximately 10% expressed GAP-43.

18 erve increased growth-associated protein-43 (GAP-43), a marker for axonal growth, in wild-type but no

19 5 (PGP9.5) and growth-associated protein 43 (GAP-43), a marker of regenerating nerve axons, was perfo

20 t the level of growth-associated protein-43 (GAP-43), a palmitoylated neuronal protein, is elevated i

21 ong evidence that growth-associated protein (GAP-43), a protein found only in the nervous system, reg

22 mTOR activity is linked to the expression of GAP-43, a crucial component of axonal outgrowth.

23 The present study examined whether GAP-43, a growth-associated protein expressed on growing

24 GAP-43, a marker of axonal growth and elongation, showed

25 ranscription factor Brn-3b and expression of GAP-43, a protein associated with axon growth.

26 Neuronal markers; including PGP9.5, GAP-43, acetylated tubulin, and neurofilaments; revealed

27 This resemblance and the fact that GAP-43 also has been proposed to regulate calmodulin ava

28 ed the role of growth-associated protein 43 (GAP-43; also known as neuromodulin and B-50) in axonal s

29 , serving as nonlearning controls, showed no GAP-43 alterations, nor did D2 mice subjected to either

30 almitoylated domain, which resembles that of GAP-43 and also mediates axonal targeting.

31 The levels of GAP-43 and BDNF mRNAs were significantly elevated in pat

32 o-expressing two major growth cone proteins, GAP-43 and CAP-23, can elicit long axon extension by adu

33 owth in vivo, e.g. , increased expression of GAP-43 and certain cell surface glycoproteins.

34 critical roles in neurotransmitter release (GAP-43 and dynamin) or glutamatergic neurotransmission (

35 The results demonstrate that GAP-43 and L1 coexpressed in Purkinje cells can act syne

36 Purkinje cells expressing both GAP-43 and L1 showed more extensive axonal sprouting and

37 CX1 silencing prevented Akt phosphorylation, GAP-43 and MAP2 overexpression, and neurite elongation.

38 oforms, the subsequent loss of activation of GAP-43 and MARCKS, and the established role of PKCs in s

39 Systematic mutagenesis of the GAP-43 and PSD-95 palmitoylation motifs indicates that t

40 GAP-43 and synaptophysin expression did not differ betwe

41 nstrated strong colocalization compared with GAP-43 and synaptophysin, which showed much less colocal

42 blocked the consumption of both full-length GAP-43 and the co-purified GAP-43 fragments.

43 red to that of the growth-associated protein GAP-43 and the results indicated colabeling of most axon

44 tly at the location of the glial wedge, both GAP-43 (-/-) and GAP-43 (+/+) cortical axons were still

45 pregulation of growth-associated protein-43 (GAP-43) and enhanced Fluoro Ruby uptake by the small-dia

46 expression of growth-associated protein 43 (GAP-43) and the cell adhesion molecule L1 has been corre

47 in, MAP-2, the growth-associated protein-43 (GAP-43) and the dendritic spine marker, drebrin.

48 orm (MAP1B-P), growth-associated protein 43 (GAP-43), and polysialylated neural cell-adhesion molecul

49 er protein (OMP), growth-associated protein (GAP-43), and synaptophysin.

50 ges, CD31+ blood vessels, and CGRP+, NF200+, GAP-43+, and TH+ nerve fibers in the synovium, as well a

51 X1 colocalized and coimmunoprecipitated with GAP-43, and NCX1 silencing prevented NGF-induced effects

52 se of the well known marker of growth cones, GAP-43; and an enhancement of endoplasmic reticulum (ER)

53 ansplanted animals, numerous neurofilament-, GAP-43-, anti-calcitonin gene-related peptide (CGRP)-, a

54 The GAP-43 antisense vector, in contrast, decreased neuropil

55 Ubiquitinated GAP-43 appeared to be the source of the fragments in the

56 Instead, GAP-43 appears to mediate RGC axon interaction with guid

57 Together, these results suggest GAP-43 as a key factor promoting epileptogenesis, a poss

58 ly increased membrane phospholipids, tau and GAP-43, as well as APP holoprotein and secreted APPs.

59 on of the growth-associated neuronal protein GAP-43 at Ser(41) was observed.

60 rat neuronal growth-associated protein B-50 (GAP-43) at serines 191/192 and threonines 88, 89 and/or

61 tamatergic neurons in the cerebellar cortex (GAP-43, BDNF, and GABA OLE_LINK2>(A)-delta subunit) in t

62 l cells that express little or no endogenous GAP-43, but only in the absence of a tissue-specific rep

63 of several known hnRNP K RNA targets (NF-M, GAP-43) by compromising their efficient nuclear transpor

64 rence approach, we found that downregulating GAP-43 causes a significant increase in the turnover of

65 INCL cells with a green fluorescent protein-GAP-43 cDNA construct shows abnormal localization of thi

66 ific enolase (NSE) promoter and either a rat GAP-43 cDNA or the corresponding antisense sequence.

67 ell genes, including GLUR1, GABA-B1a, NMDA1, GAP-43, ChAT, BDNF, nestin, BMP-2, BMP-4, and EGR1, was

68 on of the glial wedge, both GAP-43 (-/-) and GAP-43 (+/+) cortical axons were still repulsed by Slit-

69 Reduced growth is not observed when GAP-43-deficient axons are cultured with optic chiasm, c

70 show that, compared to wild-type RGC axons, GAP-43-deficient axons exhibit reduced growth in the pre

71 xons to a similar extent and does not affect GAP-43-deficient axons more so.

72 medium inhibits growth of both wild-type and GAP-43-deficient axons to a similar extent and does not

73 teral diencephalon optic tract entry zone in GAP-43-deficient embryo preparations results in robust R

74 revious studies have shown that RGC axons in GAP-43-deficient mice initially fail to grow from the op

75 mediated neurite outgrowth was unaffected by GAP-43 deletion.

76 cted in GAP-43 null embryos, indicating that GAP-43-dependent guidance at this site is RGC axon speci

77 Depalmitoylation of membrane-bound GAP-43 did not release the protein from the membrane, im

78 ffects on both axon populations suggest that GAP-43 does not mediate pathfinding specifically for one

79 sic residues within the N-terminal domain of GAP-43 dramatically reduced membrane localization of GAP

80 To identify the function of GAP-43 during activity-dependent increases in Ca2+ level

81 almodulin may act as a negative regulator of GAP-43 during periods of low activity in the neurons.

82 GAP-43 expressed in either PC12 or COS-1 cells was acety

83 In septum, injections of the GAP-43 expressing vector also caused aberrant clusters o

84 We show that mice lacking GAP-43 expression (-/-) fail to establish the ordered wh

85 vides an additional mechanism for regulating GAP-43 expression and function and may be critical for n

86 NGF regulates GAP-43 expression by altering the half-life of its mRNA.

87 Inhibition of GAP-43 expression by shRNA significantly reduced seizure

88 Our findings suggest that reduced GAP-43 expression can alter the fine-tuning of a cortica

89 However, GAP-43 expression decreased by day 15 post-seizure in co

90 An acute seizure increased GAP-43 expression in both CD and control rats.

91 e eye, Muller cell activation, and increased GAP-43 expression in ganglion cells across the entire re

92 ) line P19 is accompanied by upregulation of GAP-43 expression in neuroepithelial precursor cells.

93 ostaining for beta-gal and concurrent OMP or GAP-43 expression in P2-IRES-tauLacZ mice.

94 on the lens, causes only a minimal change in GAP-43 expression in RGCs and a minimal activation of th

95 novel approach for modulating intraneuronal GAP-43 expression in the adult brain.

96 Our results indicate that GAP-43 expression is critical for the normal establishme

97 Together with evidence of enhanced local GAP-43 expression not seen in controls, these findings s

98 t of GABA and glutamate in the modulation of GAP-43 expression was corroborated by Northern hybridiza

99 Baseline GAP-43 expression was higher in CD animals compared to c

100 In contrast, when upregulation of GAP-43 expression was prevented in 3 independent P19 lin

101 1 silencing prevented NGF-induced effects on GAP-43 expression, Akt phosphorylation, and neurite outg

102 glutamate are involved in the modulation of GAP-43 expression, cultured cerebellar granule cells wer

103 In agreement with their deficient GAP-43 expression, pDuH cells failed to grow neurites in

104 and induced a concomitant down-regulation of GAP-43 expression.

105 owed increased growth associated protein 43 (GAP-43) expression in brain samples resected from patien

106 In one purification protocol, the GAP-43 fragments formed in translation mixtures co-purif

107 Cleavage yielded 12 N-terminally labelled GAP-43 fragments that could be resolved by SDS/PAGE.

108 both full-length GAP-43 and the co-purified GAP-43 fragments.

109 lation of neurite outgrowth by NCAM requires GAP-43 function and that GAP-43 phosphorylation in isola

110 c tract development requires cell autonomous GAP-43 function in RGC axons and not in cellular element

111 These data suggest that GAP-43 function is required for commitment to a neuronal

112 ses Gap-43 mRNA translation and consequently GAP-43 function.

113 xit from the midline region does not require GAP-43 function.

114 ntaining the first 20 amino acid residues of GAP-43 fused to beta-galactosidase was targeted to DRMs

115 ing pathway(s) controlling activation of the GAP-43 gene after CNS injury differ in at least one key

116 th in similar neurons from mice in which the GAP-43 gene had been deleted by homologous recombination

117 gnaling pathways to modulate activity of the GAP-43 gene in neurons, without also causing inappropria

118 der regulation of a 1 kb fragment of the rat GAP-43 gene, a fragment that contains a number of evolut

119 so accompanied by enhanced expression of the GAP-43 gene, known to be regulated mainly posttranscript

120 In mice with targeted disruption of the GAP-43 gene, retinal ganglion cell (RGC) axons fail to p

121 moter from the growth-associated protein 43 (GAP-43) gene and found that it uses both of these mechan

122 ement from the growth-associated protein 43 (GAP-43) gene that can contribute to neuron-specific gene

123 not observed otherwise; and (3) resulted in GAP-43/ GFP-positive axons that were traced to the stria

124 GAP-43 has been implicated in axonal pathfinding and spr

125 rk has shown that mouse embryos deficient in GAP-43 have an enlarged optic chiasm within which RGC ax

126 dase (CO) histochemistry to demonstrate that GAP-43 heterozygous (+/-) mice develop larger than norma

127 ense vector, in contrast, decreased neuropil GAP-43 immunoreactivity compared to controls in the SNc.

128 vels 2-fold compared to controls; (2) led to GAP-43 immunoreactivity in neuronal perikarya, axons, an

129 reases (p</=0.001; 1.5-4.0-fold increase) in GAP-43-immunoreactivity (IR) in these regions of the ros

130 ressed in 25 of 25 (100%) and CD56/N-CAM and GAP-43 in 23 of 25 (92%) nevi, predominantly in type C n

131 urite outgrowth and rapid phosphorylation of GAP-43 in isolated growth cones required the first three

132 cord, where they were also co-expressed with GAP-43 in neurons and axons.

133 Moreover, forced expression of GAP-43 in PPT1-deficient cells results in the abnormal a

134 e whether the phenotype results from loss of GAP-43 in RGCs or in diencephalon components such as CD4

135 Our findings show the requirement of GAP-43 in sustaining synaptic stability and promoting th

136 rat model of CD to examine the regulation of GAP-43 in the brain and serum over the course of epilept

137 Expression of GAP-43 in the cerebellum and selected regions of the bra

138 tore levels of the growth-associated protein GAP-43 in the hippocampus, though not in the cerebral co

139 eric G protein Go, which may be regulated by GAP-43 in vitro, was also enriched in DRMs from PC12 cel

140 ar identity of the fatty acid(s) attached to GAP-43 in vivo.

141 3 (STX-3) and the growth-associated protein (GAP-43) in the adult rat hippocampus region.

142 ylase (TH) and growth associated protein-43 (GAP-43) in the L5 DRG 1 week after L5 spinal nerve ligat

143 Modulation of endocytosis by GAP-43, in association with rabaptin-5, may constitute a

144 to calmodulin, we sought proteins with which GAP-43 interacts in the presence of Ca2+.

145 tion, raft association may aid in sorting of GAP-43 into axonally directed vesicles in the trans-Golg

146 Alterations in GAP-43-IR following chronic cystitis may suggest a reorg

147 In contrast to significant increases in GAP-43-IR in specific regions of the rostral lumbar and

148 y 100%) of bladder afferent cells expressing GAP-43-IR was unchanged following CYP-induced urinary bl

149 Changes in GAP-43-IR were not observed at the L5 segmental level.

150 audal lumbosacral spinal cord, no changes in GAP-43-IR were observed in the L1, L2 or L6, S1 dorsal r

151 Changes in GAP-43-IR were restricted to those segmental levels exam

152 cells in the L1, L2 and L6, S1 DRG expressed GAP-43-IR.

153 bel within the visual thalamus suggests that GAP 43 is confined to type I corticothalamic terminals a

154 These results suggest that GAP-43 is a key regulator in normal pathfinding and arbo

155 GAP-43 is a neuronal protein that regulates actin dynami

156 GAP-43 is an abundant intracellular growth cone protein

157 GAP-43 is an abundant protein in axonal growth cones of

158 GAP-43 is bound by calmodulin when Ca2+ levels are low,

159 GAP-43 is expressed in proliferating neuroblasts in vivo

160 The membrane phosphoprotein GAP-43 is involved in axon growth and synaptic plasticit

161 GAP-43 is palmitoylated at Cys-3 and Cys-4.

162 that in the adult rat, plasticity related to GAP-43 is present in primary and secondary sensory corte

163 the data show that a functional threshold of GAP-43 is required for commissure formation and suggests

164 ng to dendrites, the palmitoylation motif of GAP-43 is sufficient for axonal targeting and can redire

165 The growth-associated protein GAP-43 is thought to be one determinant of such plastici

166 Growth-associated protein 43 (GAP 43) is a presynaptic protein that has been proposed

167 Growth-associated protein-43 (GAP-43) is a major growth cone protein whose phosphoryla

168 The possibility that GAP-43, is differentially affected as a function of stra

169 fragment from a well characterized GAP gene, GAP-43, is sufficient to activate expression in both dev

170 targeted to DRMs even more efficiently than GAP-43 itself.

171 extension; these phenotypes were rescued by GAP-43 knockdown.

172 We have previously shown that GAP-43 knockout (-/-) mice fail to develop whisker-relat

173 sing vector also caused aberrant clusters of GAP-43 labelled fibers in terminal fields, i.e., fornix

174 0% developed chronic epilepsy with increased GAP-43 levels in their serum.

175 Serum GAP-43 levels were significantly higher in CD rats that

176 (NGF) is accompanied by a marked increase in GAP-43 levels.

177 st that in both relay and association nuclei GAP 43 may be used to augment the cortical control of th

178 sults suggest that modulation of hippocampal GAP-43 may be important for contextual learning and that

179 ning and that strain-specific alterations in GAP-43 may be part of a disrupted pathway in D2 mice tha

180 Individual GAP-43 (+/-) mice could be assigned to two groups based

181 Likewise, 100% of GAP-43 (+/-) mice with one disrupted allele also showed

182 atosensory areas or primary visual cortex of GAP-43 (+/-) mice.

183 Here we show that 100% of homozygote GAP-43 (-/-) mice failed to form the anterior commissure

184 s of identifiable whisker territories in the GAP-43 -/- mouse cortex.

185 inase C (PKC)-dependent stabilization of the GAP-43 mRNA and neuronal differentiation.

186 leading to an increase in the levels of the GAP-43 mRNA and protein.

187 e of full-length, capped, and polyadenylated GAP-43 mRNA and that this effect was caused in part by a

188 re to GABA decreased the cellular content of GAP-43 mRNA by 21% whereas exposure to glutamate resulte

189 of HuD protein in PC12 cells stabilizes the GAP-43 mRNA by delaying the onset of mRNA degradation an

190 Analysis of the levels of GAP-43 mRNA by in situ hybridization indicated that a 7-

191 Thus, modulation of GAP-43 mRNA by these neurotransmitters may influence gra

192 Here, we show that the 3'UTR of GAP-43 mRNA can deplete axons of endogenous beta-actin m

193 This stabilization was specific for GAP-43 mRNA containing the HuD binding element in the 3'

194 This study examined GAP-43 mRNA expression and distribution in primary and s

195 siRNA-mediated depletion of overall GAP-43 mRNA from dorsal root ganglia (DRGs) decreased th

196 in ovo electroporation of axonally targeted GAP-43 mRNA increased length and axonally targeted beta-

197 GAP-43 vector in this region: (1) increased GAP-43 mRNA levels 2-fold compared to controls; (2) led

198 There are more of these GAP-43 mRNA positive corticothalamic cells in layer 5 of

199 , ARPP-19 bound to a region in the 3' end of GAP-43 mRNA previously found to be important for regulat

200 tudies have identified factors that regulate Gap-43 mRNA stability and localization, but it remains u

201 Analysis of GAP-43 mRNA stability demonstrated that the mRNA had a s

202 In correlation with the effect of HuD on GAP-43 mRNA stability, we found that HuD binds GAP-43 mR

203 rts axon branching and axonal translation of GAP-43 mRNA supports elongating growth.

204 x structure in the 5' untranslated region of Gap-43 mRNA that directly interacts with hnRNP-Q1 as a m

205 We conclude that HuD stabilizes the GAP-43 mRNA through a mechanism that is dependent on the

206 nd have demonstrated that hnRNP-Q1 represses Gap-43 mRNA translation and consequently GAP-43 function

207 localization, but it remains unclear whether Gap-43 mRNA translation is also regulated.

208 Therefore hnRNP-Q1-mediated repression of Gap-43 mRNA translation provides an additional mechanism

209 nteracts with hnRNP-Q1 as a means to inhibit Gap-43 mRNA translation.

210 In the six cortical areas studied, GAP-43 mRNA was expressed predominantly in layers 5 and

211 The GAP-43 mRNA was stabilized in these cells, leading to an

212 Localization of GAP-43 mRNA within granule cells of the immature and mat

213 r granule cell model, suggest that levels of GAP-43 mRNA, in vivo, are modulated by input from both e

214 ticothalamic cells in layers 5 and 6 express GAP-43 mRNA.

215 onstruct linked to the critical 3' region of GAP-43 mRNA.

216 marily by promoting the stabilization of the GAP-43 mRNA.

217 n the 3' untranslated region (3' UTR) of the GAP-43 mRNA.

218 amate agonist (ACPD), decreased the level of GAP-43 mRNA.

219 significantly lowered levels of granule cell GAP-43 mRNA.

220 ic RNA-binding proteins to the 3' UTR of the GAP-43 mRNA.

221 ave identified Growth-associated protein 43 (Gap-43) mRNA as a novel target of hnRNP-Q1 and have demo

222 region of the growth-associated protein-43 (GAP-43) mRNA.

223 depletes axons of endogenous beta-actin and GAP-43 mRNAs and attenuates both in vitro and in vivo re

224 cient for axonal transport of beta-actin and GAP-43 mRNAs and for regeneration of peripheral nerve.

225 'UTR competes with endogenous beta-actin and GAP-43 mRNAs for binding to ZBP1 and axonal localization

226 P-43 mRNA stability, we found that HuD binds GAP-43 mRNAs with long tails (A150) with 10-fold higher

227 ked palmitoylation at two cysteines near the GAP-43 N terminus has been implicated in directing membr

228 GAP-43 (+) nerve fiber density increased gradually from

229 rating spinal cord axons contain beta-actin, GAP-43, Neuritin, Reg3a, Hamp, and Importin beta1 mRNAs.

230 GAP-43 (neuromodulin) is a protein kinase C substrate th

231 brain neurogranin/RC3 (Ng) and neuromodulin/GAP-43 (Nm).

232 xons, wild-type, heterozygous, or homozygous GAP-43 null donor retinal tissues were grafted onto host

233 D44/SSEA axon trajectories are unaffected in GAP-43 null embryos, indicating that GAP-43-dependent gu

234 re we have found that the enlarged chiasm of GAP-43 null mouse embryos appears subsequent to a failur

235 s to innervate the cortex and hippocampus in GAP-43-null (GAP43-/-) mice.

236 the fact that Purkinje cells do not express GAP-43 or L1 in adult mammals or regenerate axons into p

237 Purkinje cells expressing GAP-43 or L1 showed minor enhancement of axonal sproutin

238 lesioned side; however, the percent of P2(+)/GAP-43(+) OSNs dramatically increased.

239 e [growth-associated protein of 43 kDa m.w. (GAP-43(+))] OSNs by assessing the expression of the P2 O

240 Approximately 35% of the N-terminal GAP-43 peptides were also modified by palmitate and/or s

241 Likewise, GAP-43 phosphorylation in isolated growth cones also was

242 th by NCAM requires GAP-43 function and that GAP-43 phosphorylation in isolated growth cones occurs v

243 r granule cells is associated with increased GAP-43 phosphorylation on serine-41.

244 memory and suggest an unheralded target, the GAP-43 phosphorylation site, for enhancing cognitive abi

245 D2 mice have slightly lower basal levels of GAP-43 phosphorylation than do B6 mice.

246 Both neurite outgrowth and NCAM-stimulated GAP-43 phosphorylation were inhibited by antibodies to t

247 c FGF or melittin also resulted in increased GAP-43 phosphorylation.

248 pregulation of the growth-associated protein GAP-43 primarily in large-diameter sensory profiles (whi

249 ansfected cells contained reduced amounts of GAP-43 protein and mRNA, and these levels remained low e

250 LY 294002 prevented Akt phosphorylation and GAP-43 protein expression rise in NCX1.4 overexpressing

251 duced an increase in Akt phosphorylation and GAP-43 protein expression.

252 Interestingly, alterations in hippocampal GAP-43 protein levels and phosphorylation state in respo

253 protein while increasing axonal synthesis of GAP-43 protein resulted in long axons with few branches.

254 protein while decreasing axonal synthesis of GAP-43 protein resulted in short highly branched axons.

255 GAP-43 protein was primarily located in excitatory neuro

256 inal palmitoylation signal, derived from the GAP-43 protein.

257 -resistant constructs encoding beta-actin or GAP-43 proteins, but only if the mRNAs were targeted for

258 tions of axonally synthesized beta-actin and GAP-43 proteins.

259 d N-Ras but not myristoylated G (alphai1) or GAP-43, proteins with N-terminal palmitoylation motifs.

260 y for GAP-43 was observed at 5d post-PH, and GAP-43 (+) PTs percentage increased thereafter with a pe

261 We demonstrate that GAP-43 regulates endocytosis and synaptic vesicle recycl

262 titute a common molecular mechanism by which GAP-43 regulates membrane dynamics during its known role

263 In contrast, GAP-43 remained up-regulated in CD rats, and over 50% de

264 These findings suggest that the GAP-43 repressive element plays an important role in all

265 ated H-Ras and growth-associated protein-43 (GAP-43), respectively.

266 depalmitoylating their substrates H-Ras and GAP-43, respectively, remained largely unknown.

267 ocalmodulin-binding proteins neurogranin and GAP-43, resulting in a low level of free calmodulin in t

268 nerve fibers), growth-associated protein 43 (GAP-43; sprouted nerve fibers), tyrosine hydroxylase (TH

269 At the ultrastructural level, the GAP 43 staining was restricted to small-diameter myelina

270 Finally, the older S100B animals showed more GAP-43 staining than the control animals, suggesting tha

271 gens and the neuritic markers neurofilament, GAP-43, synapsin-1, and CNPase--and on the perikarya of

272 culocyte lysate translation mixture used for GAP-43 synthesis, which suggested that the fragments wer

273 repressive element located downstream of the GAP-43 TATA box.

274 for multiple pathfinding abnormalities among GAP-43 (+/-) TCAs.

275 in the presence of ATP, and nonubiquitinated GAP-43 the source in the absence of ATP.

276 rexpression of the growth-associated protein GAP-43, the axonal protein kinase C substrate, dramatica

277 othalamic terminals, which appear to contain GAP 43 throughout the visual thalamus, and the large typ

278 tandem palmitoylated Cys residues can target GAP-43 to DRMs, defining a new signal for DRM targeting.

279 Targeting of GAP-43 to rafts may function to facilitate signaling thr

280 lls constitutively express L1 or both L1 and GAP-43 under the Purkinje cell-specific L7 promoter, and

281 ociated with an impaired cell-body response (GAP-43 upregulation was equivalent for both immediate an

282 Transduction with the GAP-43 vector in this region: (1) increased GAP-43 mRNA

283 he thalamus, immunocytochemical staining for GAP 43 was examined in a relay nucleus, the dorsal later

284 By 48 hours postinjury, GAP-43 was elevated bilaterally within the inner molecul

285 We found that GAP-43 was enriched in detergent-resistant membranes (DR

286 The expression of GAP-43 was modulated genetically in the adult rat nigros

287 If the overexpressed GAP-43 was mutated by a Ser --> Ala substitution to prec

288 At 6 m post-PH, immunoreactivity for GAP-43 was not detectable.

289 In contrast, immunoreactivity for GAP-43 was observed at 5d post-PH, and GAP-43 (+) PTs pe

290 BA/2J (D2) mice in the amount of hippocampal GAP-43 was observed, but naive D2 mice have slightly low

291 In control animals, expression of GAP-43 was present in specific regions of the gray matte

292 ed on the amount that PKC phosphorylation of GAP-43 was reduced in neocortical neurons.

293 tinated growth-associated protein of 43 kDa (GAP-43) was attacked by purified reticulocyte 20S protea

294 d genes, such as SPRR1A, but not others like GAP-43, was increased in the non-injured neurons.

295 expression of growth-associated protein 43 (GAP-43) were examined in lower urinary tract micturition

296 high level of growth-associated protein-43 (GAP-43), which is known to undergo palmitoylation.

297 with polybasic cytoplasmic proteins, such as GAP-43, which bind to rafts via their acylated N-termini

298 phosphorylation of the cytoskeletal element GAP-43, which promotes actin polymerization, is reduced

299 To determine the location of GAP 43 within the synaptic circuitry of the thalamus, im

300 ramatically reduced membrane localization of GAP-43 without affecting palmitoylation.