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1                     Since its discovery as a CDKI (cyclin-dependent kinase inhibitor) in 1993, the tu
2                 Its mechanism of action as a CDKI has been elegantly elucidated and involves binding
3                 In addition to its role as a CDKI, p27 is a putative tumor suppressor gene, regulator
4 ed consistent benefit from the addition of a CDKI to hormonal therapy.
5  1320 received an aromatase inhibitor plus a CDKI, 932 received placebo plus an aromatase inhibitor,
6  inhibitor, 1296 received fulvestrant plus a CDKI, and 652 received fulvestrant plus placebo.
7  survival results in patients treated with a CDKI and fulvestrant.
8 e aimed to investigate the benefit of adding CDKIs to endocrine therapy in patients whose tumours mig
9 ors only in combination with loss of another CDKI, p18(Ink4c).
10                  Here we report that another CDKI, p27(kip1) (p27), does not affect stem cell number,
11 tion factor 1 (Pbx1) gene, down-regulated by CDKI treatment.
12 and silibinin modulate G1 phase cyclins-CDKs-CDKIs for G1 arrest, and the Chk2-Cdc25C-Cdc2/cyclin B1
13 ns also raise the possibility that combining CDKIs and differentiation-inducing agents may represent
14                          Therefore, distinct CDKIs govern the highly divergent stem and progenitor ce
15 , pharmacological interventions that elevate CDKI in the vessel wall and target cyclin-dependent kina
16 n overall survival was 7.0 months, favouring CDKIs.
17 n overall survival was 7.1 months, favouring CDKIs.
18 served effect of silymarin on an increase in CDKI protein levels is mediated via inhibition of erbB1
19 universal cyclin-dependent kinase inhibitor (CDKI) family.
20 tween the cyclin-dependent kinase inhibitor (CDKI) flavopiridol (FP) and phorbol 12-myristate 13-acet
21 ls of the cyclin-dependent kinase inhibitor (CDKI) p15 as compared to the levels in untreated cells.
22 clude the cyclin-dependent kinase inhibitor (CDKI) p18INK4c, the master transcriptional regulator of
23 on of the cyclin-dependent kinase inhibitor (CDKI) p27(Kip1) is present in thyroid tumors, and recent
24           Cyclin-dependent kinase inhibitor (CDKI) p27(kip1) protein levels and pRb phosphorylation w
25 levels of cyclin-dependent kinase inhibitor (CDKI) proteins p21(Cip1) and p27(Kip1).
26 tein is a cyclin-dependent kinase inhibitor (CDKI) that binds to cyclin/cyclin-dependent kinase (CDK)
27       The cyclin-dependent kinase inhibitor (CDKI), p21(cip1/waf1) (p21) dominates stem cell kinetics
28 P1/p21, a cyclin-dependent kinase inhibitor (CDKI), which is important in blocking the cell cycle, wa
29 rget, the cyclin-dependent kinase inhibitor (CDKI)-p27.
30 spase1 induces the levels of CDK inhibitors (CDKI: p16, p21, and p27) and reduces the level of antiap
31 (CDK) by cyclin dependent kinase inhibitors (CDKI) blocks cell cycle progression and inhibits cellula
32 wed that cyclin-dependent kinase inhibitors (CDKI) induce autophagy.
33      Cyclin-dependent kinase 4/6 inhibitors (CDKIs) are indicated with endocrine therapy as first-lin
34      Cyclin-dependent kinase 4/6 inhibitors (CDKIs) are oral targeted agents approved for use in comb
35 dependent kinases (CDKs) and CDK inhibitors (CDKIs) could be tightly regulated during differentiation
36 together with an increase in CDK inhibitors (CDKIs) Kip1/p27 and Cip1/p21.
37 ively by naturally occurring CDK inhibitors (CDKIs).
38 ouse embryos that lack Rb or CDK inhibitors (CDKIs).
39 of cyclin-dependent kinase (CDK) inhibitors (CDKIs), including p16(INK4a), p21(CIP1), and p15(INK4b),
40 ction of cyclin-dependent kinase inhibitors (CDKIs) Cip1/p21 and Kip1/p27, concomitant with a signifi
41 ened all cyclin-dependent kinase inhibitors (CDKIs) for their ability to induce HbF using CRISPR acti
42          Cyclin-dependent kinase inhibitors (CDKIs) have been shown to block human immunodeficiency v
43 s of the cyclin-dependent kinase inhibitors (CDKIs) p15INK4B and p27KIP1.
44 n of the cyclin-dependent kinase inhibitors (CDKIs) p21 and p27.
45 elevated cyclin-dependent kinase inhibitors (CDKIs) p21/Cip and p27/Kip, as a consequence of impaired
46 h as the cyclin-dependent kinase inhibitors (CDKIs) p27 and p21.
47 amily of cyclin-dependent kinase inhibitors (CDKIs) which cause arrest at the G1 phase of the cell cy
48 ssion of cyclin dependent kinase inhibitors (CDKIs), p21 and p27.
49          The archetypical member of the INK4 CDKI family, p16INK4A (also called CDKN2), is a tumor su
50                        Since the addition of CDKI to endocrine therapy seemed to benefit all clinicop
51 st cancer, and received at least one dose of CDKI or placebo in combination with fulvestrant.
52 ese trials who received at least one dose of CDKI or placebo with endocrine therapy (an aromatase inh
53 on-free survival was 8.8 months in favour of CDKI plus endocrine therapy over placebo plus endocrine
54 data from three phase 3 randomised trials of CDKI or placebo in combination with fulvestrant in patie
55                              The addition of CDKIs to fulvestrant resulted in a consistent overall su
56 ilymarin also showed an increased binding of CDKIs with CDKs, together with a marked decrease in the
57 ngs support the existing standard of care of CDKIs plus fulvestrant for the treatment of patients wit
58 hnology to examine the inhibitory effects of CDKIs, we observed a cellular gene, the pre-B-cell leuke
59  function analysis, two distinct families of CDKIs, the INK4 and the Cip/Kip family have been identif
60          The sequences of the Ink4 family of CDKIs are highly conserved
61 SHC-mediated signaling pathway, induction of CDKIs, and a resultant G1 arrest.
62 a critical role for FAK in the regulation of CDKIs through two independent mechanisms: Skp2 dependent
63 ey tumor suppressor and downstream target of CDKIs, induces autophagy is not clear.
64 l phase 3 randomised breast cancer trials of CDKIs plus endocrine therapy submitted to the US Food an
65 may be dependent on the expression of ICE or CDKIs.
66 des p27Kip1 (but not overexpression of other CDKIs), induces gamma-globin expression at the transcrip
67 e increasingly important roles of p27, other CDKIs, and cyclins in endocrine cell hyperplasia and tum
68                 Cells without pRb or the p16 CDKI were more resistant to the inhibitory effects of th
69 d miR-221 transcription, which inhibited p27 CDKI translation and, consequently, promoted cell prolif
70                     In patients who received CDKIs or placebo in combination with fulvestrant as firs
71                     In patients who received CDKIs or placebo in combination with fulvestrant as seco
72 ng cells is mediated by induction of several CDKIs, thereby leading to inhibition of CDK2 and CDK4.
73 7 and p21 during differentiation, suggesting CDKIs may regulate establishment of adipocyte number in
74 ssion of Skp2, an F-box protein that targets CDKIs, by inhibiting mitogen-induced mRNA.
75                      It is hypothesized that CDKIs block viral replication by inhibiting transcriptio
76 site in the Bcl-2 promoter by activating the CDKI-RB axis.
77 clin D1, its catalytic subunit Cdk4, and the CDKI p16Ink4a, which alter the protein or its level of e
78 median progression-free survival between the CDKI plus fulvestrant group and the placebo plus fulvest
79 ogression-free survival results favoured the CDKI group in all prespecified clinicopathological subgr
80 estimable (95% CI 50.9-not estimable) in the CDKI group and was 45.7 months (95% CI 41.7-not estimabl
81  the median progression-free survival in the CDKI plus aromatase inhibitor group was 28.0 months (95%
82 not estimable (22.4 to not estimable) in the CDKI plus fulvestrant group (difference not estimable; H
83 strant group was 6.9 months in favour of the CDKI group (range across the trials 5.5-7.3 months; HR 0
84 g as critical mechanistic events loss of the CDKI p21(CIP1) and gain of its regulator, the ubiquitin
85 uced expression and reporter activity of the CDKI p21WAF/CIP1 and triggered caspase-mediated cleavage
86 CA in the pig by increasing the level of the CDKI p27(kip1) and inhibition of the pRb phosphorylation
87 d triggered caspase-mediated cleavage of the CDKI p27KIP1.
88 ciency causes elevated nuclear levels of the CDKI proteins p21(Cip1) and p27(Kip1).
89 at overexpress cyclins or do not express the CDKIs continue to undergo unregulated cell growth.
90  ubiquitin ligase complex that targets these CDKI proteins for degradation during the G(1)/S transiti
91                   To study the role of these CDKIs in adipogenesis, we analyzed adult p27 knockout (p
92 nhibitor p21CIP1, antisense ablation of this CDKI increased, rather than decreased, SAHA-related leth
93                      Here we find that three CDKIs, flavopiridol, purvalanol A, and methoxy-roscoviti
94 296 [66%] patients were randomly assigned to CDKI and 652 [33%] to placebo).