ライフサイエンスコーパス: CDKI

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 ors only in combination with loss of another CDKI, p18(Ink4c).

5 Here we report that another CDKI, p27(kip1) (p27), does not affect stem cell number,

6 tion factor 1 (Pbx1) gene, down-regulated by CDKI treatment.

7 and silibinin modulate G1 phase cyclins-CDKs-CDKIs for G1 arrest, and the Chk2-Cdc25C-Cdc2/cyclin B1

8 ns also raise the possibility that combining CDKIs and differentiation-inducing agents may represent

9 Therefore, distinct CDKIs govern the highly divergent stem and progenitor ce

10 , pharmacological interventions that elevate CDKI in the vessel wall and target cyclin-dependent kina

11 served effect of silymarin on an increase in CDKI protein levels is mediated via inhibition of erbB1

12 universal cyclin-dependent kinase inhibitor (CDKI) family.

13 tween the cyclin-dependent kinase inhibitor (CDKI) flavopiridol (FP) and phorbol 12-myristate 13-acet

14 ls of the cyclin-dependent kinase inhibitor (CDKI) p15 as compared to the levels in untreated cells.

15 clude the cyclin-dependent kinase inhibitor (CDKI) p18INK4c, the master transcriptional regulator of

16 on of the cyclin-dependent kinase inhibitor (CDKI) p27(Kip1) is present in thyroid tumors, and recent

17 Cyclin-dependent kinase inhibitor (CDKI) p27(kip1) protein levels and pRb phosphorylation w

18 levels of cyclin-dependent kinase inhibitor (CDKI) proteins p21(Cip1) and p27(Kip1).

19 tein is a cyclin-dependent kinase inhibitor (CDKI) that binds to cyclin/cyclin-dependent kinase (CDK)

20 The cyclin-dependent kinase inhibitor (CDKI), p21(cip1/waf1) (p21) dominates stem cell kinetics

21 P1/p21, a cyclin-dependent kinase inhibitor (CDKI), which is important in blocking the cell cycle, wa

22 spase1 induces the levels of CDK inhibitors (CDKI: p16, p21, and p27) and reduces the level of antiap

23 (CDK) by cyclin dependent kinase inhibitors (CDKI) blocks cell cycle progression and inhibits cellula

24 wed that cyclin-dependent kinase inhibitors (CDKI) induce autophagy.

25 dependent kinases (CDKs) and CDK inhibitors (CDKIs) could be tightly regulated during differentiation

26 together with an increase in CDK inhibitors (CDKIs) Kip1/p27 and Cip1/p21.

27 ively by naturally occurring CDK inhibitors (CDKIs).

28 ouse embryos that lack Rb or CDK inhibitors (CDKIs).

29 of cyclin-dependent kinase (CDK) inhibitors (CDKIs), including p16(INK4a), p21(CIP1), and p15(INK4b),

30 ction of cyclin-dependent kinase inhibitors (CDKIs) Cip1/p21 and Kip1/p27, concomitant with a signifi

31 Cyclin-dependent kinase inhibitors (CDKIs) have been shown to block human immunodeficiency v

32 s of the cyclin-dependent kinase inhibitors (CDKIs) p15INK4B and p27KIP1.

33 n of the cyclin-dependent kinase inhibitors (CDKIs) p21 and p27.

34 elevated cyclin-dependent kinase inhibitors (CDKIs) p21/Cip and p27/Kip, as a consequence of impaired

35 h as the cyclin-dependent kinase inhibitors (CDKIs) p27 and p21.

36 amily of cyclin-dependent kinase inhibitors (CDKIs) which cause arrest at the G1 phase of the cell cy

37 ssion of cyclin dependent kinase inhibitors (CDKIs), p21 and p27.

38 The archetypical member of the INK4 CDKI family, p16INK4A (also called CDKN2), is a tumor su

39 ilymarin also showed an increased binding of CDKIs with CDKs, together with a marked decrease in the

40 hnology to examine the inhibitory effects of CDKIs, we observed a cellular gene, the pre-B-cell leuke

41 function analysis, two distinct families of CDKIs, the INK4 and the Cip/Kip family have been identif

42 The sequences of the Ink4 family of CDKIs are highly conserved

43 SHC-mediated signaling pathway, induction of CDKIs, and a resultant G1 arrest.

44 a critical role for FAK in the regulation of CDKIs through two independent mechanisms: Skp2 dependent

45 ey tumor suppressor and downstream target of CDKIs, induces autophagy is not clear.

46 may be dependent on the expression of ICE or CDKIs.

47 e increasingly important roles of p27, other CDKIs, and cyclins in endocrine cell hyperplasia and tum

48 Cells without pRb or the p16 CDKI were more resistant to the inhibitory effects of th

49 d miR-221 transcription, which inhibited p27 CDKI translation and, consequently, promoted cell prolif

50 ng cells is mediated by induction of several CDKIs, thereby leading to inhibition of CDK2 and CDK4.

51 7 and p21 during differentiation, suggesting CDKIs may regulate establishment of adipocyte number in

52 ssion of Skp2, an F-box protein that targets CDKIs, by inhibiting mitogen-induced mRNA.

53 It is hypothesized that CDKIs block viral replication by inhibiting transcriptio

54 site in the Bcl-2 promoter by activating the CDKI-RB axis.

55 clin D1, its catalytic subunit Cdk4, and the CDKI p16Ink4a, which alter the protein or its level of e

56 uced expression and reporter activity of the CDKI p21WAF/CIP1 and triggered caspase-mediated cleavage

57 CA in the pig by increasing the level of the CDKI p27(kip1) and inhibition of the pRb phosphorylation

58 d triggered caspase-mediated cleavage of the CDKI p27KIP1.

59 ciency causes elevated nuclear levels of the CDKI proteins p21(Cip1) and p27(Kip1).

60 at overexpress cyclins or do not express the CDKIs continue to undergo unregulated cell growth.

61 ubiquitin ligase complex that targets these CDKI proteins for degradation during the G(1)/S transiti

62 To study the role of these CDKIs in adipogenesis, we analyzed adult p27 knockout (p

63 nhibitor p21CIP1, antisense ablation of this CDKI increased, rather than decreased, SAHA-related leth

64 Here we find that three CDKIs, flavopiridol, purvalanol A, and methoxy-roscoviti