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1 ptor, Neuropilin 1 (NRP1), and activation of cyclin dependent kinase 5.
2 ndent on prior phosphorylation of Ser-778 by cyclin-dependent kinase 5.
3 nerated CAD cells results from activation of cyclin-dependent kinase 5.
4 EB enhanced the overactivation of cyclin-dependent kinase 5.
5 ing with the phosphatase PP2A and the kinase cyclin-dependent kinase 5.
6 tor erythroid 2-related factor 2, notch, and cyclin-dependent kinase 5.
7 lcineurin, and was opposed by the actions of cyclin-dependent kinase 5.
8 , leads to tau phosphorylation by activating cyclin-dependent kinase 5.
11 a novel interaction between muskelin and the cyclin-dependent kinase 5 activator p39 and suggest that
12 ss is accompanied by generation of the Cdk5 (cyclin-dependent kinase 5)-activator p25, up-regulation
14 r ratios of p25/p35, indicative of increased cyclin-dependent kinase 5 activity as compared with wild
15 using roscovitine and siRNA directed towards cyclin-dependent kinase 5) ameliorated the cilia phenoty
16 tion is enhanced by prior phosphorylation by cyclin-dependent kinase 5 and antagonized by Fyn phospho
17 ncreased phosphorylation of ezrin at T235 by cyclin-dependent kinase 5 and consequent dissociation of
18 mutations abolished Thr21 phosphorylation by cyclin-dependent kinase 5 and external signal regulated
19 lens library for proteins that interact with cyclin-dependent kinase 5 and its regulators, p35 and p3
21 AD, glycogen synthase kinase-3 beta (GSK3B), cyclin-dependent kinase-5 and dual specificity tyrosine-
23 including glycogen synthase kinase 3beta and cyclin-dependent kinase-5 and its activators p25 and p35
24 lycogen synthase kinase-3 beta (GSK-3 beta), cyclin-dependent kinase 5, and c-Jun NH(2)-terminal kina
25 ion of DeltaFosB, prodynorphin, dynorphin A, cyclin-dependent kinase 5, and increased phosphorylation
27 e homolog-1, glycogen synthase kinase 3beta, cyclin-dependent kinase 5, and tau protein phosphatase 2
28 he cytoplasmic serine/threonine kinase Cdk5 (cyclin-dependent kinase 5) are both required for normal
29 ave now identified the neuronal kinase Cdk5 (cyclin-dependent kinase 5) as an important regulator of
30 kinase, CaM kinase II, casein kinase II, or cyclin-dependent kinase 5, at concentrations 50 or more
31 s associated with a significant elevation in cyclin dependent kinase-5 but not other kinases that hav
32 ntrast, inhibiting protein tyrosine kinases, cyclin-dependent kinase 5, Ca(2+)/calmodulin-dependent k
44 ent studies suggest that deregulation of p25/Cyclin-dependent kinase 5 (Cdk5) activity leads to the h
47 th a significant increase in activity of the cyclin-dependent kinase 5 (cdk5) and accumulation of its
48 ent time- and dose-dependent stimulations of cyclin-dependent kinase 5 (cdk5) and calcium/calmodulin-
49 g pharmacologic inhibitors of PI3K, Akt, and cyclin-dependent kinase 5 (cdk5) and constitutively acti
51 by sequential phosphorylation by the kinases cyclin-dependent kinase 5 (Cdk5) and glycogen synthase k
53 ivation of proline-directed kinases, such as cyclin-dependent kinase 5 (Cdk5) and glycogen synthase k
54 es responsible for these phosphorylations as cyclin-dependent kinase 5 (CDK5) and glycogen synthase k
55 ed amyloid beta (Abeta)-induced decreases in cyclin-dependent kinase 5 (Cdk5) and increases in CXCL1
60 ients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and its activator p35.
67 reover, A-705253 decreased the activation of cyclin-dependent kinase 5 (CDK5) and thereby diminished
70 ied in soluble form and is phosphorylated by cyclin-dependent kinase 5 (CDK5) as well as by CaMKII.
74 WAVE1 is phosphorylated at multiple sites by cyclin-dependent kinase 5 (Cdk5) both in vitro and in in
75 -type controls, resulting from activation of cyclin-dependent kinase 5 (CDK5) but not glycogen syntha
76 se in cyclin D1 attenuates the activation of cyclin-dependent kinase 5 (cdk5) by its neuronal activat
78 ent requires tightly regulated activation of Cyclin-dependent kinase 5 (Cdk5) by two distinct cofacto
79 Furthermore, stabilization of HIF1alpha by cyclin-dependent kinase 5 (CDK5) enabled it to promote t
80 discovered that phosphorylation of Dixdc1 by cyclin-dependent kinase 5 (Cdk5) facilitates its interac
81 hatase calcineurin (CNAalpha) and the kinase cyclin-dependent kinase 5 (CDK5) has a dramatic influenc
88 ated receptor gamma (PPARgamma) at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimu
90 duce the overexpression of neuronal-specific cyclin-dependent kinase 5 (Cdk5) in breast cancer-derive
91 t of MAPKs and proline-directed kinases like cyclin-dependent kinase 5 (Cdk5) in cell-based as well a
92 odynia and upregulates Ca(V)3.2 channels and cyclin-dependent kinase 5 (Cdk5) in dorsal root ganglia
93 Here, we demonstrate a novel role for p25/cyclin-dependent kinase 5 (Cdk5) in regulating APP proce
95 We recently identified an essential role for cyclin-dependent kinase 5 (Cdk5) in T-cell activation an
113 e with a targeted disruption in the gene for cyclin-dependent kinase 5 (cdk5) is abnormal in its stru
118 Here, we report for the first time that cyclin-dependent kinase 5 (Cdk5) is an essential regulat
126 pha(1)beta(1) integrin-induced activation of cyclin-dependent kinase 5 (cdk5) is involved in neurite
134 the algorithm, we showed that inhibition of Cyclin-dependent kinase 5 (Cdk5) led to reduced branchin
140 ulatory cell signals for CAP1, we found that cyclin-dependent kinase 5 (CDK5) phosphorylates both Ser
147 The proline-directed serine/threonine kinase cyclin-dependent kinase 5 (cdk5) plays an important role
154 ant brain tumors where type-II inhibition of cyclin-dependent kinase 5 (CDK5) stabilizing the DFG-out
155 r-activated receptor gamma) at serine 273 by cyclin-dependent kinase 5 (Cdk5) stimulates diabetogenic
156 ites that were mediated by the activation of cyclin-dependent kinase 5 (cdk5) through increased forma
157 mechanism by which phosphorylation of GIV by cyclin-dependent kinase 5 (CDK5) triggers GIV's ability
160 neural-specific activating subunit, p35, of cyclin-dependent kinase 5 (Cdk5) was recently reported t
163 CNS myelination, including the noncanonical cyclin-dependent kinase 5 (Cdk5) whose functions are reg
165 ry tangles (NFTs), it has been reported that cyclin-dependent kinase 5 (Cdk5), a critical neuronal ki
171 ns three consensus phosphorylation sites for cyclin-dependent kinase 5 (cdk5), a proline-directed ser
176 inction requires downregulation of Rac-1 and cyclin-dependent kinase 5 (Cdk5), and upregulation of p2
177 ycogen synthase kinase-3beta (GSK-3beta) and cyclin-dependent kinase 5 (Cdk5), as well as nonproline-
179 glycogen synthase kinase-3beta (GSK-3beta), cyclin-dependent kinase 5 (Cdk5), cAMP-dependent protein
181 ngly sensitised to PARP inhibitor, including cyclin-dependent kinase 5 (CDK5), MAPK12, PLK3, PNKP, ST
183 his pathway involves enzymatic activities of cyclin-dependent kinase 5 (CDK5), protein phosphatase 1
188 p35, is known to induce aberrant activity of cyclin-dependent kinase 5 (Cdk5), which is associated wi
189 factors, p35 and p39, independently activate Cyclin-dependent kinase 5 (Cdk5), which plays diverse ro
190 degradation of the p35 regulatory subunit of cyclin-dependent kinase 5 (Cdk5), with the resultant dec
192 e find that glutamate-dependent reduction in cyclin-dependent kinase 5 (Cdk5)-dependent RIIbeta phosp
193 sters that are not stabilized by agrin via a cyclin-dependent kinase 5 (Cdk5)-mediated mechanism, but
205 highly conserved phosphorylation site and by cyclin-dependent kinase-5 (Cdk5) at a newly described si
210 lycogen synthase kinase-3beta (GSK3beta) and cyclin-dependent kinase-5 (CDK5), are involved in the ne
211 uding glycogen synthase kinase 3 (GSK-3) and cyclin-dependent kinase-5 (Cdk5), to phosphorylate sever
215 as phosphorylation sinks where they mitigate cyclin-dependent kinase 5 dysregulation induced by mutan
219 purmorphamine treatment was shown to reduce cyclin-dependent kinase 5 in patient cells, suggesting a
220 phenomenon associated with the activation of cyclin-dependent kinase 5 in several neurodegenerative d
224 de of both glycogen synthetase kinase 3B and cyclin-dependent kinase 5 is required to prevent P301L-i
225 of both glycogen synthetase kinase 3beta and cyclin-dependent kinase 5 is required to prevent P301L-i
226 nd that c-Jun NH2-terminal kinase (JNK), not cyclin-dependent kinase 5, is required for APP phosphory
227 of histone modifications at the murine Cdk5 (cyclin-dependent kinase 5) locus, given growing evidence
228 ermore, 7j is highly effective in preventing cyclin-dependent kinase 5-mediated phosphorylation of PP
229 trations in which olomoucine is specific for cyclin-dependent kinases (5 microM), it reduced only ant
230 ddition, levels of the activation subunit of cyclin-dependent kinase 5, p25, are elevated significant
233 inase C phosphorylation site, and Thr-574, a cyclin-dependent kinase 5 phosphorylation site, regulate
235 that p35, the neuronal-specific activator of cyclin-dependent kinase 5, plays a key role in proper ne
236 of both glycogen synthetase kinase 3beta and cyclin-dependent kinase 5 prevents tau mislocalization t
237 de of both glycogen synthetase kinase 3B and cyclin-dependent kinase 5 prevents tau mislocalization t
240 PP1), and phosphorylation at Thr-75 by Cdk5 (cyclin-dependent kinase 5) results in inhibition of prot
243 r34 (protein kinase A site, Thr34A), Thr75, (cyclin-dependent kinase 5 site, Thr75A), Ser97 (kinase C
245 f Drp1 (dynamin-related protein 1) and Cdk5 (cyclin-dependent kinase 5), targets known to contribute
246 In contrast, Ser(67) phosphorylation by cyclin-dependent kinase 5 was unaffected by phospho-Ser(