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1 Fin1 and Dam1, and phosphorylation by cyclin-dependent kinase.
2 on mediated by signaling pathways and cyclin-dependent kinases.
3 peptides that bind to a subset of the cyclin-dependent kinases.
4 hich is controlled by the activity of cyclin-dependent kinases.
5 sphatidylinositol 3-kinase (PI3K) and cyclin-dependent kinases.
6 of ATR ablation is not due to altered cyclin-dependent kinase 1 (CDK1) activity, DNA damage responses
9 entry initiated by the activities of Cyclin-dependent kinase 1 (CDK1) and Polo-like kinase 1 (PLK1),
11 hosphorylated in vitro and in vivo by cyclin-dependent kinase 1 (CDK1) during antimitotic drug-induce
13 (Aurora A)/Polo-like kinase 1 (PLK1)/cyclin-dependent kinase 1 (CDK1) signaling pathway was the main
14 STING led to premature activation of cyclin-dependent kinase 1 (CDK1), early onset to S-phase and mi
15 totic activation of Gwl requires both cyclin-dependent kinase 1 (CDK1)-dependent phosphorylation and
19 uring mitosis through the activity of cyclin-dependent kinase 1 (CDK1)/cyclin B rather than through c
20 we identified a metabolic function of cyclin-dependent kinase 1 (CDK1)/cyclin B1-the activation of mi
21 l inositol-3-kinase (PI3K), phosphoinositide-dependent kinase 1 (PDK1 or PDPK1), and protein kinase B
22 at inhibition of the G(2)/M regulator cyclin-dependent kinase 1 decreases BMP (bone morphogenetic pro
24 ion with decreased phosphorylation of cyclin-dependent kinase 1 staining by immunohistochemistry afte
25 nase kinase, ribosomal S6 kinase, and cyclin-dependent kinase 1/2 in combination with Bcl-XL inhibiti
27 1) exists as 2 isoforms that regulate cyclin-dependent kinase-1 activation and chromosome condensatio
28 were sufficient to activate phosphoinositide-dependent kinase-1 to phosphorylate AKT on Thr-308 but i
29 CPH1 isoforms are phosphorylated in a cyclin-dependent kinase-1-dependent manner in mitosis and ident
31 LIP and ChIP-seq, we found that human cyclin-dependent kinase 11 (CDK11) associates with RNA and chro
35 orylation (activation) of calcium/calmodulin-dependent kinase 2 (CaMKII) and also that inhibition of
36 nE1) is the regulatory subunit of the cyclin-dependent kinase 2 (Cdk2) and controls cell cycle re-ent
38 -181c significantly inhibited phospho-cyclin-dependent kinase 2 (CDK2) and cyclin-A expression, arres
39 thway reversed quiescence by inducing cyclin-dependent kinase 2 (CDK2) and reducing p21(CIP1) and NEU
44 y, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zes
45 e show that the cell cycle regulator, cyclin-dependent kinase 2 (CDK2), couples primary beta-cell dys
46 ed with Cell Division Cycle 6 (CDC6), Cyclin-dependent kinase 2 (CDK2), Cyclins D1 and D3, indicating
48 onjunction with its catalytic partner cyclin-dependent kinase 2 (CDK2), regulates cell cycle progress
49 ted cell division cycle 7 (CDC7)- and cyclin-dependent kinase 2 (CDK2)-dependent reactivation of the
52 he approach is illustrated by mapping cyclin-dependent kinase 2, which successfully identifies orthos
53 orylation is driven by the actions of cyclin-dependent kinases 2 and 4/6 at G1/S cell-cycle checkpoin
54 lammatory signaling pathway driven by cyclin-dependent kinase 4 (CDK4) and CDK6 and the methyltransfe
55 regulated in malignant cells, such as cyclin-dependent kinase 4 (CDK4) and CDK6, have attracted consi
59 on that results in hyperactivation of cyclin-dependent kinase 4 and 6 (CDK4/6), rather than by the hu
61 ny older women will be treated with a cyclin-dependent kinase 4/6 (CDK4/6) inhibitor and an aromatase
62 We aimed to develop a radiolabeled cyclin-dependent kinase 4/6 (CDK4/6) inhibitor for breast cance
65 trant is combined with palbociclib (a cyclin-dependent kinase 4/6 inhibitor), adding periodic cycles
69 thality between decreased activity of cyclin-dependent kinases 4 and 6 (CDK4/6) and VHL inactivation
75 HER2-targeted therapy, inhibitors of cyclin-dependent kinases 4 and 6, angiogenesis inhibitors, poly
77 dies suggest that deregulation of p25/Cyclin-dependent kinase 5 (Cdk5) activity leads to the hyperpho
79 Here we investigate the inhibition of cyclin-dependent kinase 5 (Cdk5) as a promising combination str
81 and upregulates Ca(V)3.2 channels and cyclin-dependent kinase 5 (Cdk5) in dorsal root ganglia (DRG) a
82 ntly identified an essential role for cyclin-dependent kinase 5 (Cdk5) in T-cell activation and effec
84 cell signals for CAP1, we found that cyclin-dependent kinase 5 (CDK5) phosphorylates both Ser307 and
88 known to induce aberrant activity of cyclin-dependent kinase 5 (Cdk5), which is associated with neur
90 phamine treatment was shown to reduce cyclin-dependent kinase 5 in patient cells, suggesting a conver
91 glycogen synthetase kinase 3beta and cyclin-dependent kinase 5 is required to prevent P301L-induced
92 glycogen synthetase kinase 3beta and cyclin-dependent kinase 5 prevents tau mislocalization to dendr
93 7j is highly effective in preventing cyclin-dependent kinase 5-mediated phosphorylation of PPARgamma
96 novel treatment strategy that targets cyclin-dependent kinase 7 (CDK7) in HER2 inhibitor-resistant (H
97 ings demonstrate that pharmacological cyclin-dependent kinase 7 (CDK7) inhibitors can evoke anticance
100 ocks glucose consumption by targeting cyclin-dependent kinase 7 (CDK7) similar to other CDK7 inhibito
102 inery and especially to inhibition of cyclin-dependent kinase 7 (CDK7), which is essential for the tr
104 odule that includes the MED13, MED12, cyclin-dependent kinase 8 (CDK8), and cyclin C (CCNC) subunits.
105 The activity of its catalytic core, cyclin-dependent kinase 8 (CDK8), is controlled by Cyclin C and
106 ic process: a new replication factor, cyclin-dependent kinase 8/19-cyclinC (Cdk8/19-cyclin C), binds
108 We found that SIRT2 deacetylates cyclin-dependent kinase 9 (CDK9) in a type I IFN-dependent mann
110 rylation of elongation factor Spt5 by cyclin-dependent kinase 9 (Cdk9) occur during transcription by
111 Mechanistically, BRD4 is required for cyclin-dependent kinase 9 (CDK9) recruitment and phospho-Ser 2
112 K9ac) and 56 (H3K56ac), activation of cyclin-dependent kinase 9 (CDK9)-that phosphorylates NELF and t
115 as a substrate for the P-TEFb kinase cyclin-dependent kinase 9, which triggers release of polymerase
116 ed at an N-terminal serine cluster by cyclin-dependent kinase-9 (CDK9), which is recruited into GC-in
117 tion of the core cell cycle regulator CYCLIN-DEPENDENT KINASE A;1 (CDKA;1) and that this repression i
118 al two-step mechanism in which 1) the cyclin-dependent kinase activating kinase Cak1 phosphorylaytes
119 uggest that stimulation of autophagy by cAMP-dependent kinase activation might conceivably rescue the
120 aryote Saccharomyces cerevisiae, Cln3-cyclin-dependent kinase activity enables Start, the irreversibl
121 cursor to NAD(+) Cell lysates possess an ATP-dependent kinase activity that efficiently converts NRH
122 his study was to evaluate the role of an AMP-dependent kinase (AMPK) activator, 5-aminoimidazole-4-ca
123 yme, we obtain the first structure of an ADP-dependent kinase (AncMsPFK) with F6P at its active site.
124 karyotes and, despite lacking obvious cyclin-dependent kinase and cyclin homologs, has an ordered euk
125 entified kenpaullone, an inhibitor of cyclin-dependent kinases and glycogen synthase kinase 3, as a m
127 regulators of the G(1) phase, such as cyclin-dependent kinases and pRb (retinoblastoma protein), are
128 eted by the kinases protein kinase C, cyclin-dependent kinase, and mitogen-activated protein kinase s
129 upregulation of p21, an inhibitor of cyclin-dependent kinases, and blocked G1 arrest after TBI there
132 how they led to the identification of cyclin-dependent kinases as core to these cell cycle controls.
133 se synchronisation of the activity of cyclin dependent kinases at distinct stages of the cell cycle,
134 ted: inhibition of the autoactivated calcium-dependent kinase (calmodulin kinase II [CaMKII]) via the
135 of phagophore formation requires the calcium-dependent kinase CaMKKbeta and AMPK, which increase the
136 Activation of MutSgamma requires the Dbf4-dependent kinase Cdc7 (DDK), which directly phosphorylat
139 of the retinoblastoma (RB) protein by cyclin-dependent kinase (CDK) 4/6 and increased G1-S progressio
140 represents the downstream target for cyclin-dependent kinase (CDK) 4/6 inhibitors that are in clinic
141 alog 24), which selectively inhibited cyclin-dependent kinase (CDK) 5 over CDK2 in cancer cell lines.
143 g kinase (CAK), a complex composed of cyclin-dependent kinase (CDK) 7, cyclin H, and MAT1, is a criti
146 urther required to promote loading of cyclin-dependent kinase (CDK) and proliferating cell nuclear an
147 demonstrated for other substrates, as cyclin-dependent kinase (CDK) binding-defective mutants are cap
148 Cip1) /p27(Kip1) ) inhibit cyclin and cyclin-dependent kinase (CDK) complex that promotes fibrosis an
149 p27) tumor suppressor inhibits cyclin/cyclin-dependent kinase (CDK) complexes and halts cell cycle pr
151 ilizes and increases the level of the cyclin-dependent kinase (CDK) inhibitor p27, which inhibits cel
152 psis (Arabidopsis thaliana) encodes a cyclin-dependent kinase (CDK) inhibitor that plays a central ro
153 er cell lines(3-5), we identify CR8-a cyclin-dependent kinase (CDK) inhibitor(6)-as a compound that a
154 OR inhibition blunts the induction of cyclin-dependent kinase (CDK) inhibitors (CDKIs), including p16
155 activity, increased expression of the cyclin-dependent kinase (CDK) inhibitors p16INK4A (CDKN2A) and
156 in chordoma, and that transcriptional cyclin-dependent kinase (CDK) inhibitors targeting CDK7/12/13 a
160 n host cells because the HCMV-encoded cyclin-dependent kinase (CDK) ortholog pUL97 extensively phosph
161 t of anaphase, is mediated by mitotic cyclin-dependent kinase (CDK) phosphorylation of the GTPase's d
163 multisite phosphorylation networks of cyclin-dependent kinase (CDK) targets have opened a new level o
164 e master regulator of the cell cycle, cyclin-dependent kinase (CDK), temporally coordinates an array
165 ivation loop is phosphorylated by the cyclin-dependent kinase (CDK)-activating kinase (Cak1), and Y20
170 isordered protein (IDP) that inhibits cyclin-dependent kinase (Cdk)/cyclin complexes (e.g., Cdk2/cycl
172 e, we described that the complex Clb2-cyclin-dependent kinase (Cdk)1, one of the master regulators of
175 ere highly sensitive to inhibitors of cyclin-dependent kinases (CDK), especially THZ1, a covalent inh
177 otein kinase Wee1, which inhibits the cyclin-dependent kinase Cdk1 in yeast through human cells.
182 ed using a bioinformatics strategy as cyclin-dependent kinases CDK2 and CDK9 inhibitors, which play c
183 st when bound in ternary complex with cyclin-dependent kinase (Cdk2) and cyclins (e.g., Cdk2/Cyclin A
185 , we show that CNTD1 interacts with a cyclin-dependent kinase, CDK2, which also accumulates in crosso
186 d in most human cancers, and specific cyclin-dependent kinase Cdk4/6 inhibitors are approved or in cl
187 te the RB pathway using inhibitors of cyclin-dependent kinases CDK4 and CDK6 are effective in some ca
188 th transcriptomic analysis identifies cyclin-dependent kinases CDK4 and CDK6 as regulators of metasta
191 ibitors of mTOR and inhibitors of the cyclin-dependent kinases CDK4 and CDK6 substantially improve pr
197 irmed high selectivity of 4.35 toward cyclin-dependent kinases (CDKs) 2, 5, and 9, and the cocrystal
198 is strictly controlled by a number of cyclin-dependent kinases (CDKs) and CDK inhibitors (CKIs), the
200 c) kinase subunit (CKS) proteins bind cyclin-dependent kinases (CDKs) and play important roles in cel
201 controlled by the conserved family of cyclin-dependent kinases (CDKs) and their partner cyclins.
203 Increasing evidence suggests that cyclin-dependent kinases (Cdks) are inappropriately activated i
206 r of PAH pathobiology, and identified cyclin-dependent kinases (CDKs) as overactivated kinases in spe
208 , cyclin-specific docking motifs help cyclin-dependent kinases (CDKs) phosphorylate different substra
211 signaling, restricts the activity of cyclin-dependent kinases (CDKs) that promote cell division.
214 Mcm2 promotes the stable recruitment of Dbf4-dependent kinase (DDK) to Mcm2-7 double hexamers, which
216 otein-E2F binding specificity and how cyclin-dependent kinases differentially regulate pocket protein
217 inal domain that is phosphorylated by cyclin-dependent kinases during the transition from initiation
218 ated kinase-ribosomal S6 PK-phosphoinositide-dependent kinase (ERK-RSK-PDK) complex is an excellent e
219 changes in substrate specificity during ADP-dependent kinase evolution along with the structural det
220 ypanosoma brucei CRK9 is an essential cyclin-dependent kinase for the parasite-specific mode of pre-m
221 n assay, we determine that execution of Dbf4-dependent kinase function, including Cdc45 loading, resu
222 he Arabidopsis (Arabidopsis thaliana) cyclin-dependent kinase G1 (CDKG1) is necessary for recombinati
223 oted the activation of the Ca(2+)/calmodulin-dependent kinase II (CaMKII) and the phosphorylation of
227 nduced calcium signaling, calcium/calmodulin-dependent kinase II (CaMKII) phosphorylates OGT, which i
229 ch as fibroblast growth factors (FGF) or CaM-dependent kinase II (CaMKII)) that can also modify chann
230 xpressing myocytes caused calcium/calmodulin-dependent kinase II activation and altered myocyte bioen
231 naptic cell surface, in a calcium/calmodulin-dependent kinase II and protein kinase G-dependent manne
233 phosphorylated at Ser133, calcium-calmodulin-dependent kinase II phosphorylated at Thr286, and brain-
236 cre mouse line driven by calcium/calmodulin-dependent kinase IIalpha promoter also eliminated cocain
237 Sex-dependent associations involve cyclin-dependent kinases in bladder cancer, the MAPK signaling
238 gnized convergence of Shh agonism and cyclin-dependent kinase inhibition as potential therapeutic tar
239 in cellular ATP synthesis, activation of AMP-dependent kinase, inhibition of mTOR signaling, and indu
241 el of resistance to a pharmacological cyclin-dependent kinase inhibitor (CDKi), we show that this ass
242 how that polymersomes can deliver the cyclin-dependent kinase inhibitor (R)-roscovitine into human ne
243 the absence of Jdp2, a complex of the cyclin-dependent kinase inhibitor 1 (p21(Cip1)) and Nrf2 bound
244 and induces expression of p(21CIP1) (cyclin-dependent kinase inhibitor 1), and p(27KIP1) (cyclin-dep
245 CA2 DNA repair associated (BRCA2) and cyclin-dependent kinase inhibitor 1A (CDKN1A) interacting prote
247 hort-term NEUROG3 expression required cyclin-dependent kinase inhibitor 1A (CDKN1A)/p21(CIP1) express
248 nd p38 MAPK-dependent upregulation of cyclin-dependent kinase inhibitor 1A (Cdkn1a, encoding for p21(
249 genes, and we identified the mRNA of cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) as a direct
250 m was identified as downregulation of cyclin-dependent kinase inhibitor 1B (p27(Kip1)) via upregulati
251 t kinase inhibitor 1), and p(27KIP1) (cyclin-dependent kinase inhibitor 1B) expression, key cell cycl
252 fying the well-known tumor suppressor cyclin dependent kinase inhibitor 2A (Cdkn2a), whose alternativ
253 enes RB1 (retinoblastoma) and CDKN2a (cyclin-dependent kinase inhibitor 2a) are critical cell-cycle r
255 d 3-fold hypomethylation of the human cyclin-dependent kinase inhibitor 2B (CDKN2B or p15) gene promo
256 with reduced levels of the p21(Cip1) cyclin-dependent kinase inhibitor and tumor suppressor protein.
258 nd Enhancer of Split 1 (HES1) and the cyclin-dependent kinase inhibitor CDKN1C/p57 as novel targets o
260 e found that the expression of p21, a cyclin-dependent kinase inhibitor involved in cell cycle regula
261 orted to control the stability of the CYCLIN-DEPENDENT KINASE inhibitor KIP-RELATED PROTEIN (KRP), wh
262 ccompanied by increased expression of cyclin-dependent kinase inhibitor p21 and decreased expression
264 ease in the tumor protein p53 and the cyclin-dependent kinase inhibitor p21WAF1/CIP1, which are findi
265 liferation and elevated expression of cyclin-dependent kinase inhibitor P27 (P27KIP1) in a GEF-H1/RHO
269 ic upregulation of p57Kip2, a Cip/Kip cyclin-dependent kinase inhibitor, and we identified this induc
270 cally, encapsulation of dinaciclib, a cyclin-dependent kinase inhibitor, into PD-L1-targeted LNPs led
272 dy, we show that dinaciclib, a potent cyclin dependent kinase inhibitor, significantly increases the
273 of the Skp2-degradation target p27, a cyclin-dependent kinase inhibitor, which was confirmed as the m
274 fforts have led to the development of Cyclin-Dependent Kinase inhibitors (CDKi's) as small molecule d
275 cell cycle, decreasing expression of cyclin-dependent kinase inhibitors and upregulating pro-apoptot
276 isms, including YAP/TAZ signaling and cyclin-dependent kinase inhibitors, by blocking entry into quie
277 olymorphisms in the region of the calmodulin-dependent kinase isoform D (CaMK1D) gene are associated
289 ivated by phosphorylation - and their Ca(2+)-dependent kinase (PhK), are elevated in microsomal extra
294 issense variants in CDK19, encoding a cyclin-dependent kinase protein family member that predominantl
295 s process through expression of the NFkappaB-dependent kinase proviral integration site for Moloney m
297 (nuclear ubiquitous casein kinase and cyclin-dependent kinase substrate 1) is a chromatin-associated,
298 elected for cell fitness, enriched in Cyclin-dependent kinase substrates, and evolutionarily conserve
299 hat Magnaporthe oryzae CKS1 encodes a cyclin-dependent kinase subunit, which plays a significant role