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1 ionally dependent on CDK7, a transcriptional cyclin-dependent kinase.
2 proteins, could potentially be substrates of cyclin-dependent kinases.
3 c transcription may be directly regulated by cyclin-dependent kinases.
4 orylation mediated by signaling pathways and cyclin-dependent kinases.
5 events premature mitotic entry by inhibiting cyclin-dependent kinases.
6 ks2 are adaptor-like proteins that bind many cyclin-dependent kinases.
7 a) polypeptides that bind to a subset of the cyclin-dependent kinases.
8 under physiological conditions, we show how cyclin-dependent kinase 1 (CDK1) activates the APC/C thr
9 effect of ATR ablation is not due to altered cyclin-dependent kinase 1 (CDK1) activity, DNA damage re
11 ba is phosphorylated in vitro and in vivo by cyclin-dependent kinase 1 (CDK1) at Ser(119) and Ser(175
13 l4 is phosphorylated in vitro and in vivo by cyclin-dependent kinase 1 (CDK1) during antimitotic drug
19 osphorylation of hundreds of proteins by the cyclin-dependent kinase 1 (Cdk1):cyclin B (CycB) complex
20 tein kinase kinase, ribosomal S6 kinase, and cyclin-dependent kinase 1/2 in combination with Bcl-XL i
26 we use single-cell time-lapse microscopy of Cyclin-Dependent Kinase 2 (CDK2) activity followed by en
27 E1 (CcnE1) is the regulatory subunit of the cyclin-dependent kinase 2 (Cdk2) and controls cell cycle
28 hase of cell cycle, elevation of Cylin E and Cyclin-dependent kinase 2 (CDK2) and downregulation of p
29 hibition of NF90 sensitized HCC cells to the cyclin-dependent kinase 2 (CDK2) inhibitor, roscovitine.
31 eracetylated, levels of p27 are reduced, and cyclin-dependent kinase 2 (CDK2) is activated upon SIRT1
32 ed a specific PTPN12-insert-loop harboring a cyclin-dependent kinase 2 (CDK2) phosphorylation site.
33 Here, we show that the cell cycle regulator, cyclin-dependent kinase 2 (CDK2), couples primary beta-c
35 E, in conjunction with its catalytic partner cyclin-dependent kinase 2 (CDK2), regulates cell cycle p
40 icity of protein tyrosine phosphatase N12 by cyclin-dependent kinase 2 phosphorylation orchestrating
43 phosphorylation is driven by the actions of cyclin-dependent kinases 2 and 4/6 at G1/S cell-cycle ch
46 f the mammalian two-hybrid assay showed that cyclin-dependent kinase 3 (CDK3) directly interacted wit
47 siRNA decreased the expression of cyclin D1, cyclin dependent kinase 4 and 6, and increased the expre
48 ed with induction of the INK4 (inhibitors of cyclin dependent kinase 4) locus leading to cell-cycle a
51 we aimed to analyze the participation of the cyclin-dependent kinase 4 (CDK4) in adipose tissue biolo
52 to target different immunogenic mutations in cyclin-dependent kinase 4 (CDK4) that naturally occur in
55 esult that may be due to an effect of p16 on cyclin-dependent kinase 4 levels and IL-12 secretion by
56 EGFR-amplified tumours and a combination of cyclin-dependent kinase 4/6 (CDK4/6) and EGFR inhibitors
57 rotoxicity, we show that the G1/S-regulating cyclin-dependent kinase 4/6 (CDK4/6) pathway is activate
58 (PD), an FDA-approved selective inhibitor of cyclin-dependent kinase 4/6 (CDK4/6), prevents radiation
59 ion phenotype was reversed by treatment with cyclin-dependent kinase 4/6 inhibitor, PD0332991/palboci
67 nd an untreated lobe (mean, 165.15 and 230.4 cyclin-dependent kinase 47-positive cells per x20 field,
71 ied in soluble form and is phosphorylated by cyclin-dependent kinase 5 (CDK5) as well as by CaMKII.
73 ent requires tightly regulated activation of Cyclin-dependent kinase 5 (Cdk5) by two distinct cofacto
74 t of MAPKs and proline-directed kinases like cyclin-dependent kinase 5 (Cdk5) in cell-based as well a
75 We recently identified an essential role for cyclin-dependent kinase 5 (Cdk5) in T-cell activation an
79 the algorithm, we showed that inhibition of Cyclin-dependent kinase 5 (Cdk5) led to reduced branchin
82 CNS myelination, including the noncanonical cyclin-dependent kinase 5 (Cdk5) whose functions are reg
85 p35, is known to induce aberrant activity of cyclin-dependent kinase 5 (Cdk5), which is associated wi
86 factors, p35 and p39, independently activate Cyclin-dependent kinase 5 (Cdk5), which plays diverse ro
90 r ratios of p25/p35, indicative of increased cyclin-dependent kinase 5 activity as compared with wild
91 tion is enhanced by prior phosphorylation by cyclin-dependent kinase 5 and antagonized by Fyn phospho
92 purmorphamine treatment was shown to reduce cyclin-dependent kinase 5 in patient cells, suggesting a
93 using roscovitine and siRNA directed towards cyclin-dependent kinase 5) ameliorated the cilia phenoty
94 of histone modifications at the murine Cdk5 (cyclin-dependent kinase 5) locus, given growing evidence
95 ss is accompanied by generation of the Cdk5 (cyclin-dependent kinase 5)-activator p25, up-regulation
96 ion of DeltaFosB, prodynorphin, dynorphin A, cyclin-dependent kinase 5, and increased phosphorylation
100 highly conserved phosphorylation site and by cyclin-dependent kinase-5 (Cdk5) at a newly described si
102 STAT activation and downstream activation of cyclin-dependent kinase 6 (Cdk6) and MycNol3(-/-) MPN Th
103 fects may be mediated by targeting of HMGA2, cyclin-dependent kinase 6 (CDK6), and other predicted mi
105 s is because of the known ability of vCyclin/cyclin-dependent kinase 6 complex to resist p21 and p27
107 we show that the Mediator-associated kinases cyclin-dependent kinase 8 (CDK8) and CDK19 restrain incr
109 Here we identify the Skp2-macroH2A1 (mH2A1)-cyclin-dependent kinase 8 (CDK8) axis as a critical path
111 results in diminished CTCF binding, lack of cyclin-dependent kinase 8 (CDK8) recruitment, and an att
114 and the enhancer regions, and inhibition of cyclin-dependent kinase 9 (CDK9), that regulates these e
116 e inhibitors of the transcription regulating cyclin-dependent kinase 9 on the development and progres
117 horylated at an N-terminal serine cluster by cyclin-dependent kinase-9 (CDK9), which is recruited int
118 disruption of the core cell cycle regulator CYCLIN-DEPENDENT KINASE A;1 (CDKA;1) and that this repre
119 canonical two-step mechanism in which 1) the cyclin-dependent kinase activating kinase Cak1 phosphory
122 s activated by both the CDC7-Dbf4 kinase and cyclin-dependent kinase and via interactions with CDC45
123 reduced upregulation of p21, an inhibitor of cyclin-dependent kinases, and blocked G1 arrest after TB
124 dc55) prevents nucleolar release of the Cdk (Cyclin-dependent kinase)-antagonising phosphatase Cdc14
126 complexes are not phosphorylated properly by cyclin-dependent kinase/CDC7-Dbf4 kinase and exhibit red
127 model linking cell growth and two sequential cyclin dependent kinase (CDK) activities, and experiment
129 rosine kinase phosphorylates and inactivates cyclin-dependent kinase (Cdk) 1/2 in response to DNA dam
130 Palbociclib is a potent and specific oral cyclin-dependent kinase (CDK) 4/6 inhibitor that has str
134 ocess is controlled during the cell cycle by cyclin-dependent kinase (CDK) and Dbf4-dependent kinase
136 ty is further required to promote loading of cyclin-dependent kinase (CDK) and proliferating cell nuc
137 hanism demonstrated for other substrates, as cyclin-dependent kinase (CDK) binding-defective mutants
141 resume cycling after nutrient deprivation or cyclin-dependent kinase (CDK) inactivation express HO in
142 Re-establishing cell cycle control through cyclin-dependent kinase (CDK) inhibition has therefore e
145 is, we investigated the regulation of p21, a cyclin-dependent kinase (CDK) inhibitor encoded by CDKN1
149 p53-responsive downstream proteins, such as cyclin-dependent kinase (CDK) inhibitor p21, which promo
151 N1 stabilizes and increases the level of the cyclin-dependent kinase (CDK) inhibitor p27, which inhib
152 and, mTOR inhibition blunts the induction of cyclin-dependent kinase (CDK) inhibitors (CDKIs), includ
154 tagal) activity, increased expression of the cyclin-dependent kinase (CDK) inhibitors p16INK4A (CDKN2
155 pendent apoptotic cascades, up-regulation of cyclin-dependent kinase (CDK) inhibitors p21 and p27, an
159 atase and tensin homolog/AKT, retinoblastoma/cyclin-dependent kinase (CDK) N2A-p16(INK4A), and TP53/m
160 moting KMN network recruitment to CENP-C and cyclin-dependent kinase (CDK) regulating KMN network rec
162 hesis that dephosphorylation of four perfect cyclin-dependent kinase (Cdk) sites flanking the CHD pro
163 an initiation factor and essential target of Cyclin-Dependent Kinase (CDK), are targets of the checkp
164 e (UPR) in vivo accumulate p27(Cdkn1b), show cyclin-dependent kinase (Cdk)-1 inhibition, retain their
165 1's activation loop is phosphorylated by the cyclin-dependent kinase (CDK)-activating kinase (Cak1),
167 e we demonstrate that Ngn3 protein undergoes cyclin-dependent kinase (Cdk)-mediated phosphorylation o
169 on is activated during cell cycle transit by cyclin-dependent kinase (Cdk)-mediated Rb phosphorylatio
172 omain antagonist (BA) JQ1 attenuates MYC and cyclin-dependent kinase (CDK)4/6, inhibits the nuclear R
174 cells were highly sensitive to inhibitors of cyclin-dependent kinases (CDK), especially THZ1, a coval
175 s a novel potent small molecule inhibitor of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.
176 the protein kinase Wee1, which inhibits the cyclin-dependent kinase Cdk1 in yeast through human cell
182 tral carbon metabolism are controlled by the cyclin-dependent kinase (Cdk1), a major cell cycle regul
185 ivator of transcription (Tat) as well as the cyclin-dependent kinases CDK13 and CDK11 and positive tr
186 nthesized using a bioinformatics strategy as cyclin-dependent kinases CDK2 and CDK9 inhibitors, which
187 the decrease in KAP expression activates the cyclin-dependent kinase, Cdk2, and this directly promote
189 py; inhibitors of mTOR and inhibitors of the cyclin-dependent kinases CDK4 and CDK6 substantially imp
191 cyclins (D1, D2 and D3) and their associated cyclin-dependent kinases (CDK4 and CDK6) are components
193 hese functions by binding to, and activating cyclin-dependent kinase, CDK7, which regulates transcrip
198 l phosphorylation by the "early" cyclins and cyclin-dependent kinases (cdks) (d-cyclins cdk4/6) and t
199 991) is an oral, small-molecule inhibitor of cyclin-dependent kinases (CDKs) 4 and 6 with preclinical
200 ammals is strictly controlled by a number of cyclin-dependent kinases (CDKs) and CDK inhibitors (CKIs
204 govern eukaryotic cell cycle progression are cyclin-dependent kinases (CDKs) and their partners.
213 ant retinoblastoma-related (RBR) proteins by cyclin-dependent kinases (CDKs) is well documented, but
218 Leishmania mexicana has a large family of cyclin-dependent kinases (CDKs) that reflect the complex
219 , toxicity is blocked by compounds targeting cyclin-dependent kinases (CDKs), as well as by dominant-
225 ASE PROMOTING COMPLEX SUBUNIT 10 (APC10) and CYCLIN-DEPENDENT KINASE D (CDKD) proteins from the proli
226 cket protein-E2F binding specificity and how cyclin-dependent kinases differentially regulate pocket
228 gene, dicer, and a probable uncharacterized cyclin dependent kinase in honey bees, we utilized RNAi
231 gehog (Shh) pathway agonist purmorphamine or cyclin-dependent kinase inhibition (using roscovitine an
232 unrecognized convergence of Shh agonism and cyclin-dependent kinase inhibition as potential therapeu
233 genes phosphatase and tensin homolog (PTEN), cyclin dependent kinase inhibitor 2A (CDKN2A), LKB1, and
235 g a model of resistance to a pharmacological cyclin-dependent kinase inhibitor (CDKi), we show that t
236 e, we show that polymersomes can deliver the cyclin-dependent kinase inhibitor (R)-roscovitine into h
237 l-cycle genes, and we identified the mRNA of cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) as a
238 ad markedly decreased quiescence and reduced cyclin-dependent kinase inhibitor 1b/c (Cdkn1b/1c) expre
239 tions of knockdowns of the tumor suppressors cyclin-dependent kinase inhibitor 2A (Cdkn2a), transform
240 sistent microbial insult (e.g. LPSs) induces cyclin-dependent kinase inhibitor 2A (CDKN2A/p16(INK4a))
241 d III transcription, and thyroxine decreased cyclin-dependent kinase inhibitor 2A (p16(ink4)) express
242 d by another major POAG risk gene, p16INK4a (cyclin-dependent kinase inhibitor 2A, isoform INK4a).
243 factor beta (TGFbeta) signaling in cultured cyclin-dependent kinase inhibitor 2B (CDKN2B)-deficient
244 mediates GC formation through repression of cyclin-dependent kinase inhibitor CDKN1A (p21(Cip1)).
245 repressor, which leads to expression of the cyclin-dependent kinase inhibitor CDKN1A (p21(CIP1/WAF1)
248 the mRNA expression of osteoblast marker and cyclin-dependent kinase inhibitor genes were all reduced
251 We have found that the expression of p21, a cyclin-dependent kinase inhibitor involved in cell cycle
252 cyclin functions specifically to bypass the cyclin-dependent kinase inhibitor p18(INK4c), revealing
253 l cycle regulators cyclins D, A2, and B2 and cyclin-dependent kinase inhibitor p20 in brain tissue.
254 rrest accompanied by increased expression of cyclin-dependent kinase inhibitor p21 and decreased expr
256 rminus deficiency promotes expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1) (Cdkn1a
257 ntly increases transcription and activity of cyclin-dependent kinase inhibitor p21(WAF1/CIP1), leadin
258 53 response, accompanied by induction of the cyclin-dependent kinase inhibitor p21/CIP1, which can be
259 ng the receptors EGFR, ERBB3 (HER3), and the cyclin-dependent kinase inhibitor p27 (CDKN1B) was found
260 tating translation of mRNAs encoding for the cyclin-dependent kinase inhibitor p27(Kip1) and antiapop
261 s T-cell proliferation by the destruction of cyclin-dependent kinase inhibitor p27(kip1), and deletio
262 osol, which causes hyper-accumulation of the cyclin-dependent kinase inhibitor p27, leading to mitoti
264 differentiation by modulating expression of cyclin-dependent kinase inhibitor p27/p57 and E3 ubiquit
271 ase 4 and 6, and increased the expression of cyclin dependent kinase inhibitors (CDKIs), p21 and p27.
272 ar access of signaling cargos and sequesters cyclin-dependent kinase inhibitors (CKIs) involved in ET
273 w targets and associated therapeutic agents: cyclin-dependent kinase inhibitors and poly(adenosine di
274 its downstream targets, cJUN, ATF3, and the cyclin-dependent kinase inhibitors CDKN1A and CDKN2B.
275 reveals differential roles of two homologous cyclin-dependent kinase inhibitors in regulating cell-cy
276 liferation is due in part to derepression of cyclin-dependent kinase inhibitors Ink4a/b, while ineffe
277 ost inhibitors p27(Kip1) and p18(INK4c), two cyclin-dependent kinase inhibitors known to be important
278 ignificant increase in the expression of the cyclin-dependent kinase inhibitors p21 and p27, and a de
279 ore rearrangement and release of sequestered cyclin-dependent kinase inhibitors to elicit immunity an
280 ty, and resulting in accumulation of p53 and cyclin-dependent kinase inhibitors, cell cycle arrest, a
281 ggers a host senescence response mediated by cyclin-dependent kinase inhibitors: p21(CIP1/WAF1) (p21)
283 d learning and memory.SIGNIFICANCE STATEMENT Cyclin-dependent kinase-like 5 (CDKL5) deficiency is a s
286 le binding, which is negatively regulated by Cyclin-dependent kinase-mediated phosphorylation of segm
287 uggest that combined inhibition of RAF and d-cyclin-dependent kinases might provide an effective appr
288 ally, we investigated how phosphorylation by Cyclin-dependent kinase on distinct residues regulates p
289 se inhibitor genes were all reduced, that of cyclin-dependent kinase, osteocyte marker, and pro-apopt
290 In this study, we show that in yeast, the cyclin-dependent kinase Pho85/CDK5 provides protection a
293 he core MuvB complex simultaneously but that cyclin-dependent kinase phosphorylation of p130 weakens
296 Dbf4-dependent kinase (DDK) and S-phase cyclin-dependent kinase (S-CDK) are two S phase-specific
298 eport that Magnaporthe oryzae CKS1 encodes a cyclin-dependent kinase subunit, which plays a significa
300 e human cytomegalovirus (HCMV)-encoded viral cyclin-dependent kinase (v-CDK) UL97 phosphorylates the
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