ライフサイエンスコーパス: CDK5

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

2 the C terminus by cyclin-dependent kinase 5 (Cdk5).

3 ucose-responsive kinases GSK3, PKA, PKC, and CDK5.

4 branching by expressing a dominant negative Cdk5.

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

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

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

8 iated downstream kinase cascade regulated by Cdk5.

9 alled Pef1, whose closest human homologue is CDK5.

10 ed in HEK293 cells are regulatory targets of Cdk5.

11 entified phosphorylation sites downstream of Cdk5.

12 Here, we identify TRIM59 as a substrate of CDK5.

13 We report that CDK5, 14-3-3epsilon, and CDK5 cofactor KIAA0528 together

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

15 ere, we show that cyclin-dependent kinase 5 (Cdk5), a protein kinase that regulates cell migration an

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

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

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

19 We demonstrate that CDK5, a kinase primarily functional in post-mitotic neur

20 ese effects were mediated by a mechanism for Cdk5: A liquid chromatography-tandem mass spectrometry-b

21 tely reverses the deleterious effects of the Cdk5 ablation.

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

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

24 hese findings are confirmed by inhibition of CDK5-activated TRIM59 activity that results in suppressi

25 day 7 (P7) mice to ethanol generates p25, a CDK5-activating peptide, in a time- and CB1R-dependent m

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

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

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

29 editing uncovered a female-specific role of Cdk5 activation in attenuating fear memory retrieval.

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

31 he molecular mechanisms acting downstream of Cdk5 activation.

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

33 btypes, regulates cdk5 kinase by binding the cdk5 activator p35.

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

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

36 Pharmacological inhibition of CDK5 activity before ethanol exposure prevented accumula

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

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

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

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

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

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

43 Cdk5 activity is induced by the repulsive guidance cue S

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

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

46 at CEP85L highlights a complex that controls CDK5 activity to promote neuronal migration.

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

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

49 related, Rac1, gene expression in a CB1R and CDK5 activity-dependent manner, which persisted to adult

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

51 not been successful without affecting normal Cdk5 activity.

52 regulation of p25/Cyclin-dependent kinase 5 (Cdk5) activity leads to the hyperphosphorylation of Tau

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

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

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

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

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

58 nes involved in learning and memory, such as cdk5 and chrna7, indicating effects of chronic unpredict

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

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

61 ng its cleavage to p25, which hyperactivates CDK5 and interferes with the GSK3beta-induced degradatio

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

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

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

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

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

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

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

69 contextual fear conditioning, expression of CDK5, and enrichment of histone modifications of the Cdk

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

71 is based on preferential scaffolding of DCX, cdk5, and p35 by nestin.

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

73 ing by transcriptional regulation of BACE-1, CDK5, and tau gene expression via the upregulation of FO

74 as preventing CAP1 from accessing its kinase CDK5 appears to underlie CAP1 dephosphorylation induced

75 Our results establish CDK5 as a regulator of 53BP1 recruitment.

76 e-like behaviors in HD and aimed to validate Cdk5 as a target for depression treatment.

77 the inhibition of cyclin-dependent kinase 5 (Cdk5) as a promising combination strategy to improve sor

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

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

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

81 Chemical inhibition of CDK5 blocks the metastatic spread of patient-derived mel

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

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 We report that CDK5, 14-3-3epsilon, and CDK5 cofactor KIAA0528 together promote NudEL phosphoryl

89 However, we observed that ablation of CDK5 completely abrogated the metastasis, revealing that

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

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

92 CDK5 contributes to neuronal cell death while beta-caten

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

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

95 2 peptide, but not alpha-Synuclein, enhances Cdk5-dependent phosphorylation of S437-Acn.

96 Finally, we show that biomarkers of Cdk5-dependent tumors effectively predict response to an

97 EGFR-activated CDK5 directly binds to and phosphorylates TRIM59, a ubiq

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

99 identified beta-adducin phosphorylation as a Cdk5 downstream mechanism potentially mediating structur

100 in functions in immature neurons to modulate cdk5 downstream of the Sema3a response.

101 serve as biomarkers and effectively pinpoint Cdk5-driven tumors.

102 Here, we show that Cdk5 drives growth in subgroups of patients with multipl

103 Taken together, we found that CDK5 drives nuclear entry of PER2, which is critical for

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

105 dose-dependent manner, whereas depletion of Cdk5 enhances fibronectin secretion.

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

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

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

109 Likewise, Cdk5 expression was upregulated after SNL in the DRG.

110 pecific epigenetic activation of hippocampal Cdk5 expression.

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

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

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

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

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

116 We confirm that loss of Cdk5 function significantly impairs radial migration, bu

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

118 5, reduces S437-Acn phosphorylation, whereas Cdk5 gain-of-function increases pS437-Acn levels.

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

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

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

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

123 remodel histone proteins specifically at the Cdk5 gene.

124 d enrichment of histone modifications of the Cdk5 gene.

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

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

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

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

129 However Cdk5 has been recently implicated in the development and

130 Cyclin-dependent kinase 5 (Cdk5) has been involved in processes associated with anx

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

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

133 ork shows that the exacerbated expression of Cdk5 in a preclinical model of neuropathic pain increase

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

135 the impact of pharmacological inhibition of Cdk5 in depressive-like and anxiety-like behaviors in Hd

136 Selective loss of Cdk5 in dorsolateral striatum increased locomotor activi

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

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

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

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

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

142 Specific inhibition of CDK5 in mitosis abrogates PP4R3beta phosphorylation and

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

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

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

146 This study evaluated the involvement of Cdk5 in the development and prevalence of depressive-lik

147 We applied epigenetic editing of Cdk5 in the hippocampus and examined the regulation of f

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

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

150 These results point to Cdk5 in the nucleus accumbens as a critical contributor

151 Knock-down of Cdk5 in the suprachiasmatic nuclei (SCN), the main coord

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

153 )3.2 channels and cyclin-dependent kinase 5 (Cdk5) in dorsal root ganglia (DRG) and spinal dorsal hor

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

155 Combination of sorafenib with Cdk5 inhibition (genetic knockdown by short hairpin RNA

156 Cdk5 inhibition by roscovitine infusion prevented depres

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

158 metry-based proteomic approach revealed that Cdk5 inhibition interferes with intracellular traffickin

159 Thereby, Cdk5 inhibition offers a comprehensive approach to globa

160 Conclusion: Cdk5 inhibition represents an effective approach to impr

161 Cdk5 inhibition resulted in an accumulation of enlarged

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

163 xycycline inducible cell lines, we show that CDK5 inhibitor 24 selectively modulates Mcl-1 function w

164 l-xL in pancreatic cancer cell lines using a CDK5 inhibitor analog 24 that reduced Mcl-1 levels and 4

165 CC, and with Dinaciclib, a clinically tested Cdk5 inhibitor is readily available.

166 Consequently, the Cdk5 inhibitor olomoucine affected the compound action p

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

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

169 endocrine cancer are responsive to selective Cdk5 inhibitors and biomimetic nanoparticles are effecti

170 new transgenic mouse line that overexpresses Cdk5 inhibitory peptide (CIP) in motor neurons with the

171 In order to evaluate the influence of CDK5 inhibitory peptide (CIP) on Human alphaherpesvirus

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

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

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

175 A Cdk5 involvement in motor neuron degeneration is support

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

177 Notably, Cdk5 is an addressable target frequently overexpressed i

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

179 Taken together, it appears that CDK5 is critically involved in the regulation of the cir

180 of highly metastatic melanoma, we found that CDK5 is dispensable for the growth of primary tumors.

181 ely abrogated the metastasis, revealing that CDK5 is essential for the metastatic spread.

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

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

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

185 Cyclin-dependent kinase 5 (CDK5) is known to underlie both fear memory and stress b

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

187 er intermediate filament subtypes, regulates cdk5 kinase by binding the cdk5 activator p35.

188 ted by an upregulation of 5-lipoxygenase via cdk5 kinase pathway activation.

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

190 Endothelial-specific Cdk5 knockdown causes congenital lymphatic dysfunction a

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

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

193 eatic cancer cell lines, we show that either CDK5 knockdown or expression of a dominant negative CDK5

194 Using conditional CDK5 knockout mice and a mouse model of highly metastati

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

196 r proteins required for migration, including CDK5, LIS1, NDE1, KIF2A, and DYNC1H1.

197 Loss of CEP85L disrupts CDK5 localization and activation, leading to centrosome

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

199 Of note is that CDK5 may not exclusively phosphorylate PER2, but in addi

200 Sex-specific epigenetic regulation of Cdk5 may reflect differences in the effect of CDK5 on do

201 We also found that Cdk5 may regulate Ca(V)3.2 channel functional expression

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

203 This finding may be attributed to CDK5 mediated hyperphosphorylation of tau only in the fe

204 ze that such increasing utilization reflects CDK5-mediated NudEL phosphorylation, which increases the

205 d suggest that increased channel activity by Cdk5-mediated phosphorylation after SNL contributes nerv

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

207 Moreover, Cdk5-mediated phosphorylation down-regulates the activit

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

209 Mcl-1 is stabilized by CDK5-mediated phosphorylation in pancreatic ductal adeno

210 Cdk5-mediated phosphorylation of T406 can be regarded as

211 Cdk5-mediated phosphorylation regulates phosphatidylinos

212 hosphorylates PIPKIgamma90 at S453, and that Cdk5-mediated PIPKIgamma90 phosphorylation is essential

213 These data suggest that Cdk5-mediated PIPKIgamma90 phosphorylation regulates cel

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

215 Hence, inhibition of CDK5 might represent a very potent therapeutic strategy

216 ces in behavior and epigenetic regulation of Cdk5 occurred after long-term, but not short-term, fear

217 dk5 may reflect differences in the effect of CDK5 on downstream target proteins that regulate memory.

218 au, we avoid confounding neuronal effects of CDK5 on microtubules.

219 reversed through inhibition of GSK3beta and CDK5 or genetic deletion of tau.

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 The cyclin-dependent kinase 5 (CDK5), originally described as a neuronal-specific kinas

223 er with degradation selectivity for CDK2 and CDK5 over not only CDK1, but transcriptional CDKs (CDK7

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

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

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

227 The inhibition of CDK5/p25 activity before postnatal ethanol exposure resc

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

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

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

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

232 we tested the hypothesis that inhibition of Cdk5/p25 hyperactivation in vivo is a neuroprotective fa

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 nestin, which is known to bind the neuronal cdk5/p35 kinase, affects responses to axon guidance cues

239 e lissencephaly-linked doublecortin (DCX) by cdk5/p35, but the phosphorylation of other cdk5 substrat

240 cephaly-linked protein doublecortin (DCX) by cdk5/p35, but the phosphorylation of other cdk5 substrat

241 a selective scaffold for DCX with activated cdk5/p35.

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

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

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

245 CDK5 phosphorylated PER2 at serine residue 394 (S394) in

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

247 P1, we found that cyclin-dependent kinase 5 (CDK5) phosphorylates both Ser307 and Ser309 residues, wh

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

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

250 CDK5 plays a critical role in GBM and is a potential tar

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

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

253 targeted histone acetylation of hippocampal Cdk5 promoter attenuated fear memory retrieval and incre

254 roteins targeting histone acetylation to the Cdk5 promoter was paired with a quantification of learni

255 In mouse and human melanoma cells CDK5 promotes cell invasiveness by directly phosphorylat

256 However, the mechanism by which CDK5 promotes GBM tumorigenicity remains largely unknown

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

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

259 finding that targeted histone acetylation of Cdk5 regulates stress responsivity in male mice, we hypo

260 we show that the cyclin-dependent kinase 5 (CDK5) regulates the mammalian circadian clock involving

261 of preCGG young adult mice indicate abnormal Cdk5 regulation.

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

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

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

265 ockdown or expression of a dominant negative CDK5 results in synergistic induction of apoptosis.

266 hus, genetic or pharmacological targeting of CDK5 sensitizes pancreatic cancers to Bcl-2 inhibitors,

267 This CB1R-mediated activation of CDK5 signaling during active synaptic development may sl

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 responses to axon guidance cues upstream of cdk5, specifically, to Sema3a.

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

274 y cdk5/p35, but the phosphorylation of other cdk5 substrates is not affected by nestin.

275 y cdk5/p35, but the phosphorylation of other cdk5 substrates is not affected.

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

277 tin to interact with DCX, but not with other cdk5 substrates.

278 ethanol-induced CB1R-mediated activation of CDK5 suppresses Arc and Rac1 expression in the mouse bra

279 273 of PPARgamma in a robust manner and that Cdk5 suppresses ERKs through direct action on a novel si

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

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

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

283 protein-based diagnostic assay combined with Cdk5-targeted therapy is a rational treatment approach f

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

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

286 tumors effectively predict response to anti-Cdk5 therapy in patient-derived xenografts.

287 code that integrates signals from mTORC1 and Cdk5 to direct an insulin-stimulated, post-translational

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

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

290 Our findings suggest targeting CDK5/TRIM59 signaling axis as a putative strategy for tr

291 ted positively with serum insulin levels, of CDK5 tv1 positively with % HbA1c levels, while in contro

292 In patients, increased expression of CDK5 tv2, CDKN2A tv3 or THADA tv5 correlated positively

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

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

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

299 In conclusion, we demonstrate targeting CDK5 will sensitize pancreatic cancers to Bcl-2 protein

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