ライフサイエンスコーパス: MAP2

1 CREB), and microtubule associated protein 2 (MAP2).

2 n state of microtubule-associated protein-2 (MAP2).

3 GFAP), oligodendroglia (CNPase), or neurons (MAP2).

4 P), and/or microtubule-associated protein 2 (MAP2).

5 f neuronal cells (beta-III tubulin, NeuN and MAP2).

6 physin and microtubule-associated protein 2 (MAP2).

7 sections of the brainstem immunolabeled with MAP2.

8 ncrease in dendrite growth markers, KLK8 and MAP2.

9 ression of neuronal markers, Hu antigen, and MAP2.

10 likely via the spatial access of calpain to MAP2.

11 tric oxide are not involved in the damage to MAP2.

12 l cells by regulating the phosphorylation of MAP2.

13 A treatment induces the dephosphorylation of MAP2.

14 ratio of phosphorylated to dephosphorylated MAP2.

15 f three specific sites of phosphorylation on MAP2.

16 synapsin 1 was associated most strongly with MAP2.

17 ted a reduction in PSD-95, synaptophysin and MAP2.

18 recipitates with and directly interacts with MAP2.

19 mosphere packaging (MAP1: 50% N2/50% CO2 and MAP2: 80% N2/20% CO2) for up to 15 days at 4 degrees C w

20 he expression of the mature neuronal markers Map2 a/b and neurofilament was increased.

21 tin, neuron-specific class III beta-tubulin, Map2 a/b, and neurofilament), and photoreceptor-specific

22 Microtubule-associated protein 2 (MAP2), a neuron-specific protein, stabilizes microtubule

23 mpal formation and that they colocalize with MAP2, a dendritic and/or postsynaptic marker.

24 ntibody to microtubule-associated protein 2 (MAP2, a dendritic marker), or SV2 (an antibody to a prot

25 We showed previously that MAP2, a neuron-specific protein that stabilizes microtub

26 pines, and microtubule-associated protein 2 (MAP2), an overall dendritic marker.

27 The nuclear P-STAT3 colocalized with MAP2 and Bcl-2 within the peri-infarct zone.

28 MAP2 and cyclophilin mRNA did not differ between the gro

29 th increased expression of the neural marker MAP2 and decreased expression of chemokines, including s

30 res for the evaluation of the performance of MAP2 and existing multiple alignment programs.

31 MAP2 and MAP1B polypeptides are hypophosphorylated in Jn

32 -binding signature motifs in eukaryotic Tau, MAP2 and MAP4 proteins.

33 These included microtubule-related MAP2 and MAPT, as well as WNT3 and MICB, all implicated

34 Our data indicate that SE-induced Map2 and microglial changes parallel each other's spatio

35 y a potential association between SE-induced Map2 and microglial changes, a spatiotemporal profile of

36 sion of the neuronal differentiation markers MAP2 and NeuN and downregulates the expression of the ce

37 degradation and may account for the loss of MAP2 and neuronal damage observed in the brain of AIDS p

38 lso downregulates cyclin D1 while increasing MAP2 and p27 protein levels.

39 Whereas Map2 and synapsin1 staining are little altered, there is

40 Decreased expression of the neuronal marker MAP2 and synaptic markers PSD95 and synaptophysin in AD

41 ce showed a longer, thicker and more intense MAP2 and synaptophysin positive signal in the CNS, with

42 MAP2 and tau are abundant microtubule-associated protein

43 MAP2 and tau exhibit microtubule-stabilizing activities

44 contribute to functional differences between MAP2 and tau in neurons.

45 Surprisingly, even though the MAP2 and tau MTBDs share high sequence homology and poss

46 minant brain microtubule-associated proteins MAP2 and tau play a critical role in microtubule cytoske

47 ggest that PP2A/Balpha is part of segregated MAP2 and tau signaling scaffolds that can coordinate the

48 To investigate how MAP2 and tau stabilize microtubules, we calculated 3D ma

49 rylated epitopes in neurofilaments (NFs) and MAP2 and tau were used in immunohistochemical and immuno

50 proline-rich RTPPKSP motif conserved in both MAP2 and tau, inhibits the interaction of PP2A/Balpha wi

51 nd the microtubule (MT)-associated proteins, MAP2 and Tau, is stronger for multimers than for monomer

52 : the dendrite-specific cytoskeletal protein MAP2 and the alpha-subunit of CAMKII.

53 tochemistry to determine the distribution of Map2 and the microglia marker IBA1 in the hippocampus af

54 gulation of the phosphorylation of MAP1b and MAP2 and their biological activities.

55 al markers microtubule-associated protein 2 (MAP2) and Bcl-2 using immunohistochemistry.

56 he related microtubule-associated protein 2 (MAP2) and MAP4.

57 Microtubule-associated protein 2 (MAP2) and tau, which is involved in Alzheimer's disease,

58 adation of microtubule-associated protein 2 (MAP2) and the collapse of cytoskeletal filaments.

59 ptophysin, microtubule-associated protein 2 (MAP2), and calbindin.

60 Tau, MAP2, and MAP4 are members of a microtubule-associated p

61 CMs expressed neuronal markers such as Tuj1, Map2, and NCAM.

62 Multiple sites in NFs, MAP2, and tau were hyperphosphorylated as early as 4 wee

63 on of microtubule-associated proteins MAP1B, MAP2, and tau.

64 labeled against GABA and the neuronal marker MAP2, and the percentage of neurons that were GABA-posit

65 ncreased expression of neuronal markers Dcx, Map2, and Tubb3.

66 Reductions in MAP2- and NeuN-positive neurons were detected at day 1 a

67 In this work, we used a phospho-specific MAP2 antibody (Ab 305) that recognizes epitopes close to

68 ted that, like Rp1, phospho-JNKs and phospho-MAP2 are present in outer segments of photoreceptors.

69 yclonal to microtubule-associated protein 2 (MAP2) as Ran-SPION-rIgP/cIgY-MAP2, or to rhodopsin (Rho)

70 not of PP2B also induced phosphorylation of MAP2 at multiple sites and impaired its microtubule bind

71 activation leads to the dephosphorylation of MAP2 at sites recognized by Ab 305 in a dose-dependent m

72 describe a multiple alignment program named MAP2 based on a generalized pairwise global alignment al

73 we took a strategy of identifying potential MAP2 binding partners.

74 a model system, this study demonstrated that MAP2 breakdown occurs very early after OGD, with the fir

75 tor activation plays a prominent role in the MAP2 breakdown.

76 bule-binding regions (MTBRs) of both Tau and MAP2 can undergo self-assembly into straight filaments (

77 ssessed by microtubule-associated protein 2 (MAP2), class III beta-tubulin TUJ1, synapsin-1, VGluT, a

78 Here, we provide evidence that MAP2 co-purifies with and is dephosphorylated by endogen

79 Tau and MAP2 compete for binding to and dephosphorylation by PP2

80 onding to Ser1270, Ser1274, and Ser1779) and MAP2 (corresponding to Thr350, Ser1702, and Ser1706) wer

81 fy dendrite structure via the NMDA receptor--MAP2-cytoskeletal protein pathway, but this pathway does

82 It involves proteasome-mediated MAP2 degradation and may account for the loss of MAP2 an

83 )-Ca(2+) exchanger of mitochondria, triggers MAP2 degradation.

84 meruli, UEA(+) processes interdigitated with MAP2(+) dendrites, some of which likely originate from i

85 nd reduced microtubule-associated protein 2 (MAP2) dendrites in human neurons.

86 MAP2 phosphorylation or in the NMDA-induced MAP2 dephosphorylation response.

87 static disease-free survival than those with MAP2- disease.

88 element (DTE) corresponding to the mammalian MAP2 DTE is not contained in the 3' untranslated region

89 s to examine experience-dependent changes in MAP2 expression during postnatal development of the olfa

90 eractivation of BRAF-MEK signaling activates MAP2 expression in melanoma cells by two independent mec

91 of MAP2 on melanoma progression showed that MAP2 expression in metastatic melanoma cell lines leads

92 Previously, we showed that MAP2 expression is (a) activated in cutaneous primary me

93 ons, we have demonstrated this alteration in MAP2 expression is due to an increase in the non-phospho

94 Here, we show that in melanoma cells MAP2 expression is induced by the demethylating agent 5-

95 Decreased spinophilin but unchanged MAP2 expression provides molecular evidence for a hippoc

96 trate that immunoreactivity reflecting total MAP2 expression reaches a maximal level by postnatal day

97 othesized that BRAF signaling is involved in MAP2 expression.

98 orm of MAP2, rather than a decrease in total MAP2 expression.

99 Dephosphorylated MAP2 favours elongation by promoting microtubule polymer

100 by MAP2 on six simulated data sets show that MAP2 found the boundaries between similar and different

101 re as Module-A and Module-B) between Tau and MAP2 from a number of organisms.

102 thereby providing a regulated mechanism for MAP2 function within distinct cytoskeletal domains.

103 sed Isl-1, microtubule associated protein-2 (MAP2), gamma-synuclein, and NeuN, whereas Brn3 transcrip

104 wever, molecular mechanisms of regulation of MAP2 gene expression in melanoma are not understood.

105 elanoma progression, and HES1 play a role in MAP2 gene regulation during melanoma progression.

106 , astrocytic and microglial differentiation (MAP2, GFAP and CD68, respectively) showed many of the ce

107 ibose) and microtubule-associated protein 2 (MAP2), glial fibrillary-acidic protein (GFAP), CD68, A b

108 In hippocampus, MAP2 has been reported to be dephosphorylated by activat

109 Microtubule-associated protein 2 (MAP2) has been implicated in activity-dependent structur

110 date, only two MAP family members, MAP1A and MAP2, have been well characterized and studied in mammal

111 The microtubule associated protein 2 (Map2) helps stabilize microtubules of the dendritic cyto

112 The major antigenic protein 2 (MAP2) homolog of Ehrlichia chaffeensis was cloned and ex

113 sintegrate were maintained, as determined by MAP2 immunocytochemistry and Nissl staining.

114 frozen brain sections, that was confirmed by MAP2 immunohistochemistry.

115 Using microtubule-associated protein 2 (MAP2) immunohistochemistry, we detected a higher concent

116 We investigated MAP2-immunoreactive dendrites using a novel method of hi

117 We found a decline in Map2 immunoreactivity in the CA1 area that reached minim

118 s as determined by the reflective change and MAP2 immunoreactivity was 0.96+/-0.03 (n=5).

119 Areas not occupied by OMP or MAP2 immunoreactivity were either immunoreactive for GFA

120 reactivity was accompanied by a reduction of MAP2 immunoreactivity.

121 ivity, and microtubule associated protein-2 (MAP2) immunoreactivity, respectively, in rats subjected

122 easures of microtubule associated protein-2 (MAP2) immunostained dendrites indicated an enhancement o

123 stimulation (30 trains) caused a decrease in MAP2 immunostaining in the lamina in which the activated

124 ether, this study indicates a novel role for MAP2 in LTP mechanisms and suggests that MAP2 participat

125 etic mechanisms are involved in silencing of MAP2 in melanoma.

126 We also showed that ectopic expression of MAP2 in metastatic melanoma cells inhibits cell growth b

127 Ran-SPION-rIgP/cIgY-MAP2 or SPION-rIgP/cIgY-MAP2 in normal C57black6 mice (n = 3 each, 40 mug/kg, i.

128 expectedly found that NRG-2 colocalizes with MAP2 in proximal primary dendrites of hippocampal neuron

129 a progressive decrease in synaptophysin and MAP2 in the CA3 area of hippocampus compared with contro

130 a two-stage alteration in immunostaining for MAP2 in the dendritic laminae.

131 g domain to investigate the possible role of MAP2 in the Xenopus visual system.

132 specific silencing of high-molecular-weight MAP2 in vivo abolished induction of long-term potentiati

133 dy against microtubule-associated protein 2 (MAP2) in hatchlings showed that some Kv1.1 remained as c

134 s imposed by the microtubule-binding protein MAP2, indicating that MAP2 is the dominant AKAP in neuro

135 ve cells co-labeled with an antibody against MAP2, indicating that the proliferating cells were neuro

136 osa cells with antisense oligonucleotides to MAP2 inhibited the phosphorylation of cAMP-response elem

137 We tested for MAP2 interaction with SH3 domain-containing proteins.

138 gorized each SZ subject as having either low MAP2-IR (SZ MAP2-IR(low)) or normal MAP2-IR (SZ MAP2-IR(

139 ther low MAP2-IR (SZ MAP2-IR(low)) or normal MAP2-IR (SZ MAP2-IR(normal)).

140 = 20; control subjects, n = 20), we measured MAP2-IR and dendritic spine density and spine number in

141 irm that low density of small spines and low MAP2-IR are robust SZ phenotypes and suggest that MAP2-I

142 mGluR1a-ir was tightly clustered along large MAP2-ir dendrites.

143 y and confocal microscopy to measure DSD and MAP2-IR in A1 deep layer 3.

144 s not been explored in previous studies, and MAP2-IR loss has not been investigated in the primary au

145 These findings demonstrate that MAP2-IR loss is closely linked to dendritic spine pathol

146 We then tested the hypothesis that MAP2-IR mediates the effect of SZ on DSD in a cohort of

147 IR are robust SZ phenotypes and suggest that MAP2-IR mediates the effect of SZ on DSD.

148 This staining did not colocalize with MAP2-ir or SV2-ir and was not altered by decortication o

149 The relationship between MAP2-IR reduction and lower dendritic spine density, whi

150 Moreover, MAP2-IR statistically mediated small spine differences,

151 mediated small spine differences, with lower MAP2-IR values associated with fewer small spines.

152 Based on the distribution of MAP2-IR values in NPC subjects, we categorized each SZ s

153 In 12 (60%) subjects with Sz, MAP2-IR values were lower than the lowest values in cont

154 nsistent with previous studies, both DSD and MAP2-IR were lower in SZ subjects.

155 The reductions in MAP2-IR were not associated with neuron loss, loss of MA

156 SZ subject as having either low MAP2-IR (SZ MAP2-IR(low)) or normal MAP2-IR (SZ MAP2-IR(normal)).

157 However, mean DSD did not differ between SZ MAP2-IR(normal) and NPC subjects.

158 2-IR (SZ MAP2-IR(low)) or normal MAP2-IR (SZ MAP2-IR(normal)).

159 ubule-associated-protein-2 immunoreactivity (MAP2-IR) in A1 deep layer 3 is lower, and positively cor

160 with Sz exhibited a significant reduction in MAP2-IR.

161 also were reduced in Sz and correlated with MAP2-IR.

162 MAP2 is a neuron-specific microtubule-associated protein

163 eutics provide resources for identifying how MAP2 is altered in Sz and possible leads to novel therap

164 However, it is unclear how MAP2 is associated with synaptic plasticity mechanisms.

165 MAP2 is degraded after ischemia and other metabolic insu

166 We showed that MAP2 is frequently activated in human cutaneous melanoma

167 The proteolysis of MAP2 is limited by endogenous calpain activity, likely v

168 hilst branching is more likely to occur when MAP2 is phosphorylated and microtubules are spaced apart

169 MAP2 is predominantly dendritic.

170 otubule-associated proteins (MAPs) MAP1b and MAP2 is regulated by the degree of their phosphorylation

171 of staining for phosphoindependent forms of MAP2 is relatively unaffected by blocking odorant passag

172 he typically robust immunoreactivity (IR) of MAP2 is significantly reduced across several cortical re

173 tubule-binding protein MAP2, indicating that MAP2 is the dominant AKAP in neurons.

174 ing for phosphorylation-independent forms of MAP2 is unchanged by naris closure, the total amount of

175 Although MAP2 is widely used as a marker of neuronal differentiat

176 Microtubule-associated protein 2 (MAP2) is a neuron-specific cytoskeletal protein, enriche

177 Microtubule-associated protein 2 (MAP2) is a neuronal phosphoprotein that promotes net mic

178 Microtubule-associated protein 2 (MAP2) is a neuronal protein that plays a role in maintai

179 All neuronal MAP2 isoforms bound specifically to the SH3 domains of c

180 imally composed of the MAPK in series with a MAP2 kinase (MAP2K) and a MAP3K.

181 tin2 involves phosphorylation of JNK3 by the MAP2 kinase MKK4.

182 erine/threonine acetyl-transferase targeting MAP2 kinases.

183 The distribution of MAP2-labeled neurons in relation to the gray matter/whit

184 of the Schaffer collateral pathway promoted MAP2 labeling in spine heads of CA1 neurons.

185 OGD, with the first statistical decrease in MAP2 levels within the first 30 min after the insult.

186 mutations in UNC-70 beta-spectrin, PTL-1 tau/MAP2-like and MEC-7 beta-tubulin proteins in Caenorhabdi

187 A spatial correlation between Map2 loss and reactive microglia was also reported in hu

188 cts with the microtubule-associated proteins MAP2, MAP4, and tau, stimulates the microtubule- and dyn

189 n state of microtubule-associated protein 2 (MAP2) may play a key role in controlling dendritic elong

190 MAP2 (microtubule-associated protein 2) is a cytoskeleta

191 iscovered a widespread network of precocious MAP2 (microtubule-associated protein 2)-immunoreactive c

192 a single residue was adequate to disrupt the MAP2-microtubule interaction in HeLa cells.

193 pendent protein kinase activity disrupts the MAP2-microtubule interaction in living HeLa cells and pr

194 the JNK signaling cascades (i.e. JNK1, JNK2, MAP2, MKK4 and c-Jun) is reduced, whereas phospho-ERK an

195 ubstitutions of individual Tau residues into MAP2 Module-B likewise result in the formation of PHF-li

196 ontrast to mammalian MAP2 transcripts, avian MAP2 mRNA is lacking dendritic targeting competence.

197 s the transport of CPE-containing endogenous MAP2 mRNA to dendrites, whereas overexpression of a muta

198 in the 3' untranslated region (UTR) of avian MAP2 mRNA.

199 We found that in contrast to rodent MAP2 mRNAs, which are highly enriched in dendritic regio

200 esis to replace selected residues within the MAP2 MTBR by residues at corresponding positions in Tau.

201 Few MAP2/nestin-positive cells were seen in control cultures

202 occupancy of late target genes and enhanced Map2(+) neurite outgrowth.

203 rietal cortices had decreased mtDNA, reduced MAP2 (neuronal) and increased GFAP (astrocyte) mRNA, rel

204 ock of transitively similar regions and that MAP2 never produced a block of regions that are not tran

205 The major antigenic protein 2 (MAP2) of Ehrlichia canis was cloned and expressed.

206 Experimental results produced by MAP2 on four real sets of orthologous genomic sequences

207 f the mechanisms that underlie the effect of MAP2 on melanoma progression showed that MAP2 expression

208 Experimental results by MAP2 on six simulated data sets show that MAP2 found the

209 activity for antibody AP18, which recognizes MAP2 only when phosphorylated on Ser136.

210 When tau (but not MAP2 or MAP1b) is experimentally depleted from neurons,

211 e examined the uptake of Ran-SPION-rIgP/cIgY-MAP2 or SPION-rIgP/cIgY-MAP2 in normal C57black6 mice (n

212 synaptodendritic signaling proteins such as MAP2 or synaptophysin in the brains of human immunodefic

213 ated protein 2 (MAP2) as Ran-SPION-rIgP/cIgY-MAP2, or to rhodopsin (Rho) as anti-Rho-SPION-Ran.

214 re associated with tau hyperphosphorylation, MAP2 overexpression and reduction of synaptic proteins i

215 ng prevented Akt phosphorylation, GAP-43 and MAP2 overexpression, and neurite elongation.

216 for MAP2 in LTP mechanisms and suggests that MAP2 participates in activity-dependent synaptic plastic

217 ar signaling and neuronal cytoskeleton, with MAP2 perhaps acting as a molecular scaffold upon which c

218 In addition, our observations suggest that MAP2 phosphorylation by long-term activation of D1Rs (an

219 We also observed that the elevations in MAP2 phosphorylation in neuronal cultures in the presenc

220 The shift in MAP2 phosphorylation occurs even when deprivation is del

221 show no differences in the baseline level of MAP2 phosphorylation or in the NMDA-induced MAP2 dephosp

222 This indicates that D1Rs modulate MAP2 phosphorylation through PKA-associated intracellula

223 Moreover, MAP2 phosphorylation underwent a substantial increase be

224 neurons, D1R stimulation-induced increase in MAP2 phosphorylation was blocked by the protein kinase A

225 extension corresponded with an elevation in MAP2 phosphorylation.

226 owing manipulations with calcium, CaMKII and MAP2 phosphorylation.

227 here is an activity-dependent stimulation of MAP2 phosphorylation.

228 nesis into microtubule-associated protein 2 (MAP2)-positive neurons (-24%) and doublecortin (Dcx)-pos

229 ngs are consistent with the observation that MAP2-positive cells are not affected by the presence of

230 In NRG-1-treated cultures, many of the MAP2-positive cells co-labeled with an anti-nestin antib

231 ltures was due to increased proliferation of MAP2-positive cells rather than the regulation of cell s

232 cultures, the agrin-deficient neurons formed MAP2-positive dendrites and tau-1-positive axons.

233 ion (-17%) and neuronal differentiation into MAP2-positive neurons (-22%) and into Dcx-positive neuro

234 t microtubule-associated protein 2-positive (MAP2-positive) dendrite outgrowth, suggesting that Abl m

235 ed rapid translocation of a subpopulation of MAP2, present in dendritic shafts, to spines following L

236 rge nuclei, similar to those seen in vivo in MAP2+ primary melanomas cells.

237 ssion analysis, that patients diagnosed with MAP2+ primary melanomas have significantly better metast

238 The MAP2 program produces an ordered list of local multiple

239 Because MAP2 promoter activity levels in melanoma cell lines als

240 kdown of HES1 results in the upregulation of MAP2 promoter activity.

241 repressor, are involved in the regulation of MAP2 promoter activity.

242 In support of this, methylation of MAP2 promoter DNA in vitro inhibits its activity.

243 etastatic melanoma cells N-box region of the MAP2 promoter is occupied by endogenous HES1.

244 e demethylating agent 5-aza-2'-cytidine, and MAP2 promoter is progressively methylated during melanom

245 arative analysis of the mouse, rat and human MAP2 promoter sequences showed the presence of a conserv

246 MAP2D is the only MAP2 protein present in ovaries and is localized to gran

247 ere not associated with neuron loss, loss of MAP2 protein, clinical confounders, or technical factors

248 ecular weight splice variant of the neuronal MAP2 protein.

249 synthesis of the endogenous alphaCaMKII and MAP2 proteins induced by tetanic stimulations in hippoca

250 s of orthologous genomic sequences show that MAP2 rarely missed a block of transitively similar regio

251 n increase in the non-phosphorylated form of MAP2, rather than a decrease in total MAP2 expression.

252 changes may be important in the mechanism of MAP2 redistribution and breakdown after oxygen-glucose d

253 ss of the synaptic markers synaptophysin and MAP2, reduced the gliosis, and preserved the capacity to

254 MAP2 regulates microtubule stability in a phosphorylatio

255 MAP2 regulates the assembly of cytoskeletal proteins suc

256 Little is known about MAP2 regulation or its interaction with the cytoskeleton

257 This study determined that MAP2 resides in a complex with the NMDA receptor, sugges

258 Disruption of microtubule dynamics by MAP2 resulted in multipolar mitotic spindles, defects in

259 Ubiquitous deletion of the MetAP-2 gene (MAP2) resulted in an early gastrulation defect, which is

260 Double labeling for OMP and MAP2 revealed two distinctive subcompartments within glo

261 The recombinant MAP2 (rMAP2) was tested in an ELISA format using 141 ser

262 The recombinant MAP2 (rMAP2) was used in an ELISA format with 60 blinded

263 iours, and microtubule-associated protein 2 (Map2, rs13475902) was associated with cognitive performa

264 This specific MAP2/SH3 domain interaction was inhibited by phosphoryla

265 Because MAP2 shares substantial sequence, regulatory, and functi

266 Targeted deletion of MAP2 specifically in the hemangioblast lineage resulted

267 A receptors specifically in the neurons with MAP2 spine translocation.

268 The mechanism of Tat action on MAP2 stability involved Tat-mediated translocation of th

269 ression of ILK, PINCH, PI3K, GSK-3beta, tau, MAP2, synaptophysin and drebrin in the lumbar spinal cor

270 ll markers (ATOH7, POU4F2, beta-III tubulin, MAP2, TAU, NEUROD1 and SIX3), formed synapses and showed

271 Tau, a member of the MAP2/tau family of microtubule-associated proteins, stab

272 MAP2/tau family proteins are characterized by three to f

273 icrotubule-associated proteins (MAPs) of the MAP2/Tau family, but also contribute to the assembly of

274 ion, catalytic subunits dissociated from the MAP2-tethered regulatory subunits and rapidly became enr

275 cently, we reported a substantial decline in Map2 that coincided with robust microglia accumulation i

276 those of other substrates such as fodrin or MAP2 that may be "natural" substrates for the calpains,

277 y against the microtubule-associated protein MAP2 to label interstitial white matter neurons in the a

278 We compared the responses of MAP2 to NMDA treatment in animals with high binocular pl

279 There is a dramatic redistribution of MAP2 to the somata of pyramidal neurons, particularly ne

280 in dendritic regions of the retina, chicken MAP2 transcripts are virtually absent from such areas an

281 blished the somato-dendritic distribution of MAP2 transcripts in vivo.

282 stion, the dendritic targeting competence of MAP2 transcripts was examined in chicken, mouse and rat.

283 sults indicate that in contrast to mammalian MAP2 transcripts, avian MAP2 mRNA is lacking dendritic t

284 Using a battery of antibodies (OMP, MAP2, TuJ1, calretinin, calbindin, parvalbumin, TH, and

285 ); we found retention of Ran-SPION-rIgP/cIgY-MAP2 using molecular contrast-enhanced MRI in vivo and v

286 l imaging showed that spine translocation of MAP2 was coupled with LTP-induced spine enlargement.

287 n of the phosphorylation levels of MAP1b and MAP2 was examined by Western blots using several phospho

288 en NAA/Cr and neuronal counts, calbindin, or MAP2 was found.

289 motif of the microtubule-associated protein MAP2 was identified in VP40.

290 To further characterize MAP2, we took a strategy of identifying potential MAP2 b

291 gulation of the phosphorylation of MAP1b and MAP2, we used okadaic acid and cyclosporin A to selectiv

292 The alterations in immunostaining for MAP2 were diminished, but not eliminated, by inhibiting

293 enriched in dendrites and co-localizes with MAP2, whereas RIIbeta is concentrated in axons.

294 ns such as microtubule-associated protein 2 (MAP2), which can interact with both cytoskeletal compone

295 fforded by microtubule-associated protein 2 (MAP2), which has a tau-like microtubule-binding domain,

296 ently different from hydrolysis of fodrin or MAP2, which are much less accessible as substrates for p

297 microtubule-associated protein (MAP) 1, and MAP2, which results in the inhibition of microtubule ass

298 y further revealed a significant decrease in MAP2 with predominant cytoplasmic 20S in cortical neuron

299 his phosphorylation-regulated association of MAP2 with proteins of intracellular signal transduction

300 lation states may enhance the interaction of MAP2 with the actin cytoskeleton, thereby providing a re