ライフサイエンスコーパス: CDK5

1 hosphorylation by cyclin-dependent kinase 5 (Cdk5).

2 ptor 1 (ESR1) and cyclin-dependent kinase 5 (CDK5).

3 phosphorylated by cyclin-dependent kinase 5 (Cdk5).

4 n phosphatase 2A, but reduces p35 subunit of Cdk5.

5 unit 1a (cdk5r1a), an essential activator of Cdk5.

6 ic forms of tau, directly, and by activating cdk5.

7 as not been reported to be phosphorylated by Cdk5.

8 Ca(2+) homeostasis in SMA and activation of Cdk5.

9 iated downstream kinase cascade regulated by Cdk5.

10 This broad pro-tumorigenic role makes Cdk5 a promising drug target for the development of new

11 ere, we show that cyclin-dependent kinase 5 (Cdk5), a serine-threonine kinase that is highly active i

12 essed the contribution of the protein kinase Cdk5, a key neuronal signaling molecule, in cortico-stri

13 CDK5, a kinase active in G1/G0, primes NDE1 for FBW7-med

14 Here, we identify CDK5, a kinase active in post mitotic cells, as a new an

15 Here we identify CDK5, a predominantly cytoplasmic serine/threonine kinas

16 tely reverses the deleterious effects of the Cdk5 ablation.

17 or Cdk5, and expression of dominant negative Cdk5 abolishes the ability of dbcAMP or putrescine to en

18 Blocking Cdk5 action blocks Egr-1-induced tau phosphorylation but

19 3 restores most of the genes dysregulated by CDK5 action on PPARgamma in cultured adipocytes.

20 s caused calpain-dependent conversion of the Cdk5-activating cofactor p35 to p25.

21 which activator is responsible for enhancing Cdk5 activation and how the two distinct activators dire

22 MENT Accumulation of p25 results in aberrant Cdk5 activation and induction of numerous pathological p

23 ates the increased functional requirement of Cdk5 activation during neuronal differentiation.

24 mediated breakdown of cytoskeletal proteins, cdk5 activation, tau hyperphosphorylation, formation of

25 lopment, some of which may be independent of Cdk5 activation.

26 ssion of miR-23a, whereas overexpressing the CDK5 activator p35 attenuated both of these effects on N

27 responses, arguing that cooperation between Cdk5 activators maintains balanced Cdk5 signing, which i

28 rthermore, our data support a model in which Cdk5 activators play nonoverlapping and even opposing ro

29 Despite the robustly increased Cdk5 activity during neuronal differentiation, which act

30 tion, which underlies the robust increase of Cdk5 activity during rat and mouse neuronal differentiat

31 Although Cdk5 activity in donor T cells contributed to graft-vers

32 Increasing or decreasing Cdk5 activity in genetically engineered mice has severe

33 The loss of p39 attenuates overall Cdk5 activity in neurons and preferentially affects phos

34 clinical, murine, GVHD model, we reveal that Cdk5 activity is increased in key target organs early af

35 However, it was not clear whether p25/Cdk5 activity is necessary for the progression of these

36 Thus, targeting aberrant Cdk5 activity may serve as an effective treatment for st

37 These results demonstrate that CDK5 activity provides resistance to heat-induced apopto

38 d effector function, but the contribution of Cdk5 activity to the development of GVHD has not been ex

39 Selective inhibition of aberrant Cdk5 activity via genetic overexpression of Cdk5 inhibit

40 revented apoptosis under conditions in which CDK5 activity was inhibited.

41 at p35 expression, an activator of Cdk5, and Cdk5 activity were increased in metastatic tumor cells,

42 Inhibition of CDK5 activity with roscovitine-sensitized cells to heat

43 arch exploring the function of p35-dependent Cdk5 activity.

44 not been successful without affecting normal Cdk5 activity.

45 rough the insolubilization and inhibition of CDK5 activity.

46 v2.1 cellular localization via inhibition of Cdk5 activity.

47 Taken together, these results suggest that CDK5 acts as a crucial signaling hub in prostate cancer

48 iated dorsolateral striatal-specific loss of Cdk5 all impaired dopamine-facilitated LTP or D1-dopamin

49 c status of p21 through its interaction with Cdk5 and Abl enzyme substrate 1 (Cables1).

50 ers, enhances tau phosphorylation, activates Cdk5 and BACE-1, and accelerates amyloidogenic APP proce

51 in by respectively controlling activities of Cdk5 and BACE-1, suggesting that Egr-1 is a potential th

52 the PSD fraction, and its phosphorylation by CDK5 and CaMKII is differentially regulated by activatio

53 ultimeric complex that favors p35 binding to Cdk5 and catalysis.

54 nded t(1/2), promotes aberrant activation of cdk5 and causes abnormal hyperphosphorylation of tau, th

55 ons leads to the inappropriate activation of Cdk5 and contributes to hyperphosphorylation of tau and

56 ndrocyte development than simply the loss of Cdk5 and could not be rescued by Cdk5 overexpression.

57 switch in mediating the synaptic effects of Cdk5 and demonstrates that SynI is necessary and suffici

58 erences in the hydrogen bond network between Cdk5 and its activators.

59 ss existing and new strategies for targeting Cdk5 and its downstream mechanisms as anti-cancer treatm

60 corrected in cells depleted of both FBW7 or CDK5 and NDE1.

61 D2 receptor dependent persistent changes of CDK5 and PSD-95 protein levels specifically within the s

62 is sufficient to regulate the expression of Cdk5 and results in altered behavioral responses to coca

63 ter inhibition of cyclin-dependent kinase 5 (Cdk5) and ERK1/2.

64 rthermore, Cadm4, cyclin-dependent kinase 5 (Cdk5) and p39 mRNAs were significantly correlated with v

65 proteins from whole brain derived from E18.5 Cdk5+/+ and Cdk5-/- embryos, using an Immobilized Metal-

66 cally implicate D1-dopamine receptor, NMDAR, Cdk5, and CaMKII in cortico-striatal plasticity.

67 showed that p35 expression, an activator of Cdk5, and Cdk5 activity were increased in metastatic tum

68 or of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.

69 )-induced PD-L1 up-regulation on MB requires Cdk5, and disruption of Cdk5 expression in a mouse model

70 k inhibitor that has greater selectivity for Cdk5, and expression of dominant negative Cdk5 abolishes

71 n of the Cdk5 regulator p35, inactivation of Cdk5, and increased auto-dephosphorylation of Thr320 of

72 ion of p35, the neuron-specific activator of Cdk5, and rat DRG neurons transduced with HSV overexpres

73 phosphorylated by cyclin-dependent kinase 5 (CDK5) as well as by CaMKII.

74 The phosphorylation state of SynI by Cdk5 at site 7 is regulated during chronic modification

75 ation site and by cyclin-dependent kinase-5 (Cdk5) at a newly described site.

76 hosphorylation by cyclin-dependent kinase 5 (Cdk5) at Thr345.

77 Chronic [Ca2+]i dysregulation amplifies Cdk5-ATM signaling, possibly linking impaired glutamater

78 These data show that an ERK/Cdk5 axis controls PPARgamma function and suggest that M

79 We show that CDK5 binds and phosphorylates GIV at Ser1674 near its GE

80 ins that showed decreased phosphorylation at Cdk5-/- brains.

81 ted activation of Cyclin-dependent kinase 5 (Cdk5) by two distinct cofactors, p35 and p39.

82 yperactivation of Cyclin-dependent kinase 5 (Cdk5), by the production of its truncated activator p25,

83 dult Cdk5(-/-C) mice is identical to control Cdk5(+/+C) mice.

84 We then generated chimeric mice (Cdk5(+/+C) or Cdk5(-/-C)) using hematopoietic progenitor

85 However, transplantation of donor Cdk5(-/-C) bone marrow and T cells dramatically reduced

86 The immunophenotype of adult Cdk5(-/-C) mice is identical to control Cdk5(+/+C) mice.

87 then generated chimeric mice (Cdk5(+/+C) or Cdk5(-/-C)) using hematopoietic progenitors from either

88 Our findings suggest that Cdk5 can be considered a promising therapeutic target in

89 In cancer, these anti-oncogenic effects of CDK5 can provide selective pressure for the down-regulat

90 The failure of remyelination in Cdk5 cKO animals was associated with a reduction in sign

91 he lesion sites was significantly reduced in Cdk5 cKO compared with wild-type animals although the to

92 Moreover, Cdk5 CKO dramatically reduced infarctions following MCAO

93 Cre;Cdk5(fl/fl) conditional knock-out mouse (Cdk5 cKO), myelin repair was delayed significantly in re

94 he three-dimensional structure of the p39 AD-Cdk5 complex and found differences in the hydrogen bond

95 the p25 (p35 C-terminal region including AD)-Cdk5 complex, we simulated the three-dimensional structu

96 Testing this hypothesis, inhibition of Cdk5 (comprising a molecule central to the processes des

97 Pharmacological Cdk5 inhibition, brain-wide Cdk5 conditional knockout, or viral-mediated dorsolatera

98 role of histone modifications at the murine Cdk5 (cyclin-dependent kinase 5) locus, given growing ev

99 tion of Drp1 (dynamin-related protein 1) and Cdk5 (cyclin-dependent kinase 5), targets known to contr

100 d stress is accompanied by generation of the Cdk5 (cyclin-dependent kinase 5)-activator p25, up-regul

101 nction, and reduction of tau pathology via a cdk5-dependent mechanism.

102 Cdk5-dependent NR2B phosphorylation is regulated by neur

103 2 peptide, but not alpha-Synuclein, enhances Cdk5-dependent phosphorylation of S437-Acn.

104 d from AR signaling, further corroborated by CDK5-dependent proliferation of AR null cells.

105 aturation and axonal elongation, revealing a Cdk5-dependent regulation of SynIII function.

106 l signaling lipid PI3,5P2 We show that Pho85/CDK5 directly phosphorylates and positively regulates th

107 This inhibition is a consequence of Cdk5 disruption in neural cells because remyelination in

108 Inhibition of aberrant Cdk5 during ischemia protected dopamine neurotransmissio

109 from either embryonic day 16.5 Cdk5(+/+) or Cdk5(-/-) embryos to enable analyses of the role of Cdk5

110 m whole brain derived from E18.5 Cdk5+/+ and Cdk5-/- embryos, using an Immobilized Metal-Ion Affinity

111 udy provides evidence for the causal role of Cdk5 epigenetic remodeling in NAc in Cdk5 gene expressio

112 Our results reveal a central role of Cdk5 expressed in PV interneurons in gating inhibitory n

113 ation on MB requires Cdk5, and disruption of Cdk5 expression in a mouse model of MB results in potent

114 t kinase 5) locus, given growing evidence of Cdk5 expression in nucleus accumbens (NAc) influencing r

115 (PDE4) by cyclin-dependent protein kinase 5 (Cdk5) facilitated cAMP degradation and homeostasis of cA

116 hanisms can control ciliary length through a CDK5-FBW7-NDE1 pathway.

117 In CNP-Cre;Cdk5(fl/fl) conditional knock-out mouse (Cdk5 cKO), myel

118 n-expressing cells and their progeny require Cdk5 for proper development during the early postnatal p

119 ovide a novel strategy to selectively target Cdk5 for the treatment of Alzheimer's disease.

120 Collectively, our findings show that Cdk5-Foxc2 interaction represents a critical regulator o

121 st opposing roles of p39 and p35 in synaptic Cdk5 function and epileptic responses, arguing that coop

122 that reductions in synaptic transmission and Cdk5 function are related to decreases in voluntary runn

123 Despite the well-known p35-dependent Cdk5 function, why postnatal neurons express abundant p3

124 5, reduces S437-Acn phosphorylation, whereas Cdk5 gain-of-function increases pS437-Acn levels.

125 In particular, epigenetic regulation of the Cdk5 gene alters responses to cocaine and stress in mous

126 es of the role of Cdk5 in GVHD, as germ line Cdk5 gene deletion is embryonically lethal.

127 When Cdk5 gene deletion was induced in nestin-expressing cell

128 role of Cdk5 epigenetic remodeling in NAc in Cdk5 gene expression and in the control of reward and st

129 s are sufficient to bidirectionally regulate Cdk5 gene expression via enrichment of their respective

130 remodel histone proteins specifically at the Cdk5 gene.

131 In a targeted screen, Cdk5 genetically interacted with Acinus (Acn), a primari

132 levels of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphata

133 Collectively, our findings show that Cdk5 has an important functional role in the regulation

134 Recently, CDK5 has been implicated in a number of different cancer

135 However Cdk5 has been recently implicated in the development and

136 Recently, cyclin-dependent kinase 5 (Cdk5) has been shown to function as a major regulator of

137 ouse that is deficient in p25 generation and Cdk5 hyperactivation.

138 To date, strategies to specifically inhibit Cdk5 hyperactivity have not been successful without affe

139 Collectively, our data implicate Cdk5 in allogeneic T-cell responses after HCT and as an

140 MARCKS is known to be phosphorylated by Cdk5 in chick neural cells while Grin1 has not been repo

141 Selective loss of Cdk5 in dorsolateral striatum increased locomotor activi

142 his mouse model to elucidate the role of p25/Cdk5 in FTD mutant tau-mediated pathology.

143 -) embryos to enable analyses of the role of Cdk5 in GVHD, as germ line Cdk5 gene deletion is embryon

144 Our finding highlights a central role for Cdk5 in immune checkpoint regulation by tumor cells.

145 d apoptosis indicating a protective role for CDK5 in inhibiting heat-induced apoptosis.

146 Also, a knock down of Cdk5 in jck cells using small interfering RNA results in

147 contribute to the pro-oncogenic activity of CDK5 in lung adenocarcinoma.

148 hese data demonstrate a crucial role for p25/Cdk5 in mediating tau-associated pathology and suggest t

149 dk5 inhibitors, whereas specific deletion of Cdk5 in OLs inhibits myelin repair.

150 to study the cancer-promoting mechanisms of CDK5 in prostate cancer.

151 ere, we demonstrate that genetic ablation of Cdk5 in PV interneurons in mouse brain leads to an incre

152 In contrast, overexpression of Cdk5 in sheep (Ovis aries) only produces brown patches o

153 Here, to address the role of p25/Cdk5 in tauopathy, we generated double-transgenic mice b

154 To further validate the role of p25/Cdk5 in tauopathy, we used frontotemporal dementia patie

155 In search for novel substrates of Cdk5 in the brain we performed quantitative phosphoprote

156 Finally, conditional inactivation of Cdk5 in the jck mice significantly attenuates cystic dis

157 scription factor Foxc2 as a key substrate of Cdk5 in the lymphatic vasculature, mechanistically linki

158 , the role of its phosphorylation by PKA and Cdk5 in the modulation of this process is unknown.

159 mma) at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimulates insulin resistance, b

160 cted kinases like cyclin-dependent kinase 5 (Cdk5) in cell-based as well as in vitro kinase assays an

161 ies implicate the cyclin-dependent kinase 5 (Cdk5) in regulating oligodendrocyte (OL) development and

162 ssential role for cyclin-dependent kinase 5 (Cdk5) in T-cell activation and effector function, but th

163 Conversely, phosphorylation by CDK5 increases r-synGAP's HRas GAP activity by 98% and i

164 to phosphorylate Kv2.1, with pharmacological Cdk5 inhibition being sufficient to decluster channels.

165 is a hallmark of myeloma, and specifically, cdk5 inhibition can enhance the activity of proteasome i

166 Instead, CDK5 inhibition increased NOXA mRNA and protein levels b

167 The effects of Cdk5 inhibition on the size and depletion kinetics of th

168 The increased abundance of NOXA by CDK5 inhibition was not a result of changes in NOXA prot

169 Pharmacological Cdk5 inhibition, brain-wide Cdk5 conditional knockout, o

170 agonist propyl pyrazole triol (10 nm) or the CDK5 inhibitor roscovitine (28 mum) on day 30 of withdra

171 Intriguingly, intra-NAc injection of the Cdk5 inhibitor roscovitine, dose-dependently decreased w

172 n contrast, treatments with roscovitine, the Cdk5 inhibitor, resulted in an opposite effect on serine

173 milar branching defects as those observed in Cdk5 inhibitor-treated larvae.

174 emyelination in slice cultures is blocked by Cdk5 inhibitors, whereas specific deletion of Cdk5 in OL

175 Cdk5 activity via genetic overexpression of Cdk5 inhibitory peptide (CIP) reduces pathologic changes

176 Adeno-associated virus 9-mediated Cdk5 inhibitory peptide reverses pathologic changes and

177 The various mechanisms by which Cdk5 inhibits and promotes neurodegeneration are still p

178 Pharmacological inhibition of Cdk5 inhibits repair of lysolecithin lesions.

179 an lymphoid cell line to hyperthermia causes CDK5 insolubilization and loss of tyrosine-15 phosphoryl

180 Disrupting NR2B-Cdk5 interaction via a small interfering peptide (siP) i

181 Cdk5 is a post-mitotic kinase with complex roles in main

182 the aberrant activity of the protein kinase Cdk5 is a principal cause of neuronal death in rodents d

183 In this study, we show that Cdk5 is also an important regulator of remyelination.

184 CDK5 is an atypical cyclin-dependent kinase family membe

185 Cdk5 is an atypical cyclin-dependent kinase that is well

186 l cycle-associated cyclin-dependent kinases, CDK5 is best known for its regulation of signaling proce

187 Together, these data suggest that Cdk5 is critical in regulating the transition of adult o

188 We observed that CDK5 is necessary for proliferation of several prostate

189 Phosphorylation of SynI by Cdk5 is physiologically regulated and enhances its bindi

190 Our data indicate that Cdk5 is required to maintain the protective role of basa

191 Additional data indicate that, in neurons, CDK5 is the kinase responsible for phosphorylating kines

192 Cyclin-dependent kinase 5 (Cdk5) is a brain-specific membrane-bound protein kinase

193 Cyclin-dependent kinase 5 (Cdk5) is a proline-directed serine/threonine kinase whic

194 ere, we show that cyclin-dependent kinase 5 (Cdk5) is an essential regulator of lymphatic vessel deve

195 e first time that cyclin-dependent kinase 5 (Cdk5) is an essential regulator of MITF and PAX3.

196 ce indicates that cyclin-dependent kinase 5 (Cdk5) is inappropriately activated in several neurodegen

197 Here we show that cyclin-dependent kinase 5 (Cdk5) is required for dbcAMP and putrescine to overcome

198 ncreased in metastatic tumor cells, and that Cdk5 kinase activity is responsible for talin1 phosphory

199 dy, cyclin E1 was found to restrict neuronal Cdk5 kinase activity.

200 The CDK5 kinase phosphorylates four serines in DLC1 located

201 ified TFP5, a truncated fragment of p35, the Cdk5 kinase regulatory protein, which inhibits Cdk5/p35

202 Endothelial-specific Cdk5 knockdown causes congenital lymphatic dysfunction a

203 Cdk5 knockdown in mice causes a lightened coat color, a

204 xpression of Keratin 10 (K10) resulting from Cdk5 knockdown may be responsible for an abnormal epider

205 hat inhibition of Cyclin-dependent kinase 5 (Cdk5) led to reduced branching in the intrahepatic bilia

206 nscriptional repression, specifically to the Cdk5 locus in NAc in vivo We found that Cdk5-ZFP transcr

207 ig2(+) cells) was increased, suggesting that Cdk5 loss perturbs the transition of early OL lineage ce

208 Our results suggest that CDK5 may regulate ciliary length by affecting tubulin dy

209 growth-promoting effect was due to specific CDK5-mediated AKT activation.

210 active recycling pool and contributes to the Cdk5-mediated homeostatic responses.

211 is an essential downstream effector for the Cdk5-mediated homeostatic scaling.

212 dicating that TRPV1 is strongly modulated by Cdk5-mediated phosphorylation at position threonine-407(

213 studies have found WAVE1 to be inhibited by Cdk5-mediated phosphorylation in brain and to play a rol

214 E1 in human embryonic kidney cells prevents Cdk5-mediated phosphorylation of Kv2.1, and cyclin E1 ov

215 Cdk5-mediated phosphorylation of T406 can be regarded as

216 Together, our study reveals Cdk5-mediated phosphorylation of talin1 leading to beta1

217 Functional studies confirmed that inhibiting CDK5-mediated RALB activation with a clinically relevant

218 ng with p35, serine phosphorylation in their Cdk5 motifs was found to be increased.

219 Also, the nonphosphorylatable Cdk5 mutant was unable to rescue the neurite elongation

220 c progenitors from either embryonic day 16.5 Cdk5(+/+) or Cdk5(-/-) embryos to enable analyses of the

221 Loss of Cdk5, or its required cofactor p35, reduces S437-Acn pho

222 ne receptor-specific conditional knockout of Cdk5, or ventral striatum infusion of a small interferin

223 types compared with those reported here upon Cdk5 overexpression or knockdown, demonstrating the impo

224 the loss of Cdk5 and could not be rescued by Cdk5 overexpression.

225 Here we show selective inhibition of Cdk5/p25 -hyperactivation by TFP5/TP5 peptide, which ide

226 which inhibits Cdk5/p35 and the hyperactive Cdk5/p25 activities in test tube experiments.

227 f p67 protects Cdk5/p35 and has no effect on Cdk5/p25 activity in the presence of TFP5.

228 To account for the selective inhibition of Cdk5/p25 activity, we propose that the "p10" N-terminal

229 mice, the peptide specifically inhibits the Cdk5/p25 complex and not the endogenous Cdk5/p35.

230 accumulation of the deregulated, hyperactive Cdk5/p25 complex in human brains has been implicated in

231 e show that TFP5/TP5 selective inhibition of Cdk5/p25 hyperactivation in vivo and in vitro rescues ni

232 to circumvent the formation of overreactive cdk5/p25.

233 th p67siRNA, we also show that TFP5 inhibits Cdk5/p35 activity, whereas in the presence of p67 the ac

234 that, in vitro, the addition of p67 protects Cdk5/p35 and has no effect on Cdk5/p25 activity in the p

235 k5 kinase regulatory protein, which inhibits Cdk5/p35 and the hyperactive Cdk5/p25 activities in test

236 erminal domain of p35, absent in p25, spares Cdk5/p35 because p10 binds to macromolecules (e.g., tubu

237 otein, one of many proteins copurifying with Cdk5/p35 in membrane-bound multimeric complexes.

238 the Cdk5/p25 complex and not the endogenous Cdk5/p35.

239 age-dependent loss in synaptic function and Cdk5/p39 activity in the NAc may be partially responsibl

240 specific epitopes, which was mediated by the cdk5 pathway.

241 Dysregulation of cyclin-dependent kinase 5 (cdk5) per relative concentrations of its activators p35

242 Cyclin-dependent kinase 5 (CDK5) phosphorylated DRP1 to increase its activity in BT

243 ered proliferation effects, we observed that CDK5 phosphorylates S308 on the androgen receptor (AR),

244 CDK5 phosphorylates synGAP primarily at two sites, Ser-7

245 ther familial PrP mutants are predisposed to Cdk5 phosphorylation and whether phosphorylation of fami

246 These results indicate that PKA and Cdk5 phosphorylation is required for the physiological a

247 Here we demonstrate that Cdk5 phosphorylation of SynI fine tunes the recruitment

248 tion is sensitive to neural activity through Cdk5 phosphorylation of Tomo1.

249 or PrP mutants did not convert into amyloid, Cdk5 phosphorylation rapidly converted these into Thiofl

250 CDK5 phosphorylation reduces this binding and orchestrat

251 Cyclin-dependent kinase 5 (Cdk5) phosphorylation of wild type PrP (pPrP) at serine

252 Our data suggest that p25/Cdk5 plays an important role in tauopathy in both mouse

253 s-tumor effects, pharmacologic inhibition of Cdk5 preserved leukemia-free survival.

254 inhibition or conditional knock-out (CKO) of Cdk5 prevented neuronal death in response to ischemia.

255 lectively targeted the regulation of PDE4 by Cdk5, produced analogous effects on stress-induced behav

256 in yeast, the cyclin-dependent kinase Pho85/CDK5 provides protection against hyperosmotic stress and

257 ere, we show that in Drosophila melanogaster Cdk5 regulates basal autophagy, a key mechanism suppress

258 We propose that targeting the Cdk5 regulation of PDE4 could be a new therapeutic appro

259 of preCGG young adult mice indicate abnormal Cdk5 regulation.

260 d to proteasome-dependent degradation of the Cdk5 regulator p35, inactivation of Cdk5, and increased

261 We generated larvae carrying a mutation in cdk5 regulatory subunit 1a (cdk5r1a), an essential activ

262 creates interfaces for efficient binding to CDK5 regulatory subunit-associated protein 2 (CDK5RAP2)

263 Down-regulation of CDK5 repressed AKT phosphorylation by altering its intra

264 Loss of Cdk5 results in persistent expression of the PD-L1 trans

265 locomotion and possible interaction with the Cdk5/RhoA pathway.

266 AP activity toward inactivation of Rap1, and CDK5 shifts the relative activity toward inactivation of

267 Cells depleted of FBW7 or CDK5 show enhanced levels of NDE1 and a reduction in cil

268 g and even opposing roles to govern balanced Cdk5 signaling in the postnatal brain.

269 ng hormone signaling, GNRH signaling, and/or CDK5 signaling pathways for those newly-identified loci.

270 n and how the two distinct activators direct Cdk5 signaling to govern neuronal network formation and

271 n between Cdk5 activators maintains balanced Cdk5 signing, which is crucial for postnatal brain funct

272 hosphorylation, we created mice that ablated Cdk5 specifically in adipose tissues.

273 at serine 273 by cyclin-dependent kinase 5 (Cdk5) stimulates diabetogenic gene expression in adipose

274 ults presented here identify Grin 1 as novel Cdk5 substrate and confirm previously identified MARCKS

275 In support, the Cdk5 substrate, ATM, is upregulated by 1.5- to 2-fold at

276 reviously identified MARCKS as a a bona fide Cdk5 substrate.

277 or activation, adds GIV to the repertoire of CDK5 substrates, and defines a mechanism by which this u

278 273 of PPARgamma in a robust manner and that Cdk5 suppresses ERKs through direct action on a novel si

279 Moreover, these defects in Cdk5(-/-) T-cell function are associated with altered CC

280 of this epigenetic remodeling and found that Cdk5-targeted H3K9/14ac increased cocaine-induced locomo

281 Conversely, Cdk5-targeted H3K9me2 attenuated both cocaine-induced lo

282 ficiency results in dysregulation of p35 and Cdk5 targets in synapses.

283 entially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impa

284 In mice, loss of Cdk5 throughout the forebrain elevated cAMP levels and i

285 mphatic vasculature, mechanistically linking Cdk5 to lymphatic development and valve morphogenesis.

286 Here we review the contribution of Cdk5 to molecular mechanisms that confer upon tumors the

287 we demonstrated that p39 selectively directs Cdk5 to phosphorylate protein substrates essential for a

288 ylation of GIV by cyclin-dependent kinase 5 (CDK5) triggers GIV's ability to bind and activate Galpha

289 a reduction in the activity of GSK3beta and CDK5, two of the major tau kinases.

290 onophthisis by pharmacological inhibition of CDK5 using either R-roscovitine or S-CR8 is accompanied

291 apid protection mechanism regulated by Pho85/CDK5 via signaling from the vacuole/lysosome, which is d

292 there was considerable growth promotion when CDK5 was overexpressed.

293 Cyclin-dependent kinase-5 (Cdk5) was reported to downscale neurotransmission by seq

294 Recently, cyclin-dependent kinase 5 (Cdk5) was shown to phosphorylate Kv2.1, with pharmacolog

295 Cyclin-dependent kinase 5 (Cdk5), which binds to and is activated by p35, phosphory

296 rrant activity of cyclin-dependent kinase 5 (Cdk5), which is associated with neurodegenerative disord

297 endently activate Cyclin-dependent kinase 5 (Cdk5), which plays diverse roles in normal brain functio

298 ase, is one of the presynaptic substrates of Cdk5, which phosphorylates it in its C-terminal region a

299 the noncanonical cyclin-dependent kinase 5 (Cdk5) whose functions are regulated by its activators p3

300 the Cdk5 locus in NAc in vivo We found that Cdk5-ZFP transcription factors are sufficient to bidirec