ライフサイエンスコーパス: CDK3

1 e CIP/KIP family and activates both CDK2 and CDK3.

2 LXCXE motif in cyclin D, but not by Cdk2 or Cdk3.

3 ts ER activity and cell growth via targeting CDK3.

4 In contrast, little is known about CDK3, a homolog of CDK2 and cell division cycle kinase 2

5 EGF-induced Cdk3 activation caused c-Jun phosphorylation at Ser63 an

6 closely related to human Cdk1/Cdc2, Cdk2 and Cdk3 and yeast CDC28/cdc2(+).

7 noblastoma gene product (pRb), activation by cdk3, and S-phase-dependent down-regulation of DNA-bindi

8 The cyclin-dependent kinases cdk2 and cdk3 are required for the G1-S transition in mammalian c

9 e assays revealed cyclin-dependent kinase 3 (CDK3) as a direct target of miR-873.

10 These results clearly showed that the cdk3-ATF1 signaling axis is critical for cell proliferat

11 Cl41 cells and si-cdk3 suppresses Ras(G12V)/cdk3/ATF1-induced foci formation in NIH3T3 cells.

12 Cdk3 bound specifically to E2F-1/DP-1 complexes in vivo,

13 These results showed that the Cdk3/c-Jun signaling axis plays an important role in EGF

14 wn G1 cyclin dependent kinases (CDKs), Cdk2, Cdk3, Cdk4, and Cdk6, in primary cultured rat superior c

15 Knockouts of Cdk2, Cdk3, Cdk4, or Cdk6 have resulted in viable mice, but th

16 with Cdk4 and Cdk6, but not with Cdc2, Cdk2, Cdk3, Cdk5 and any of a number of cyclins tested.

17 B, cyclin D, cyclin A and E2F-4 but not with cdk3, cdk5, cdk6, E2F-1, E2F-2, E2F-3, E2F-5 and cyclin

18 Purified cyclin E/CDK2 or cyclin E/CDK3 complex, but not other cdks, partially complemented

19 in quiescent cells and identify new cyclin C/Cdk3 complexes as key regulators of cell cycle reentry i

20 assay showed that cyclin-dependent kinase 3 (CDK3) directly interacted with NFAT3 and phosphorylated

21 Dominant negative mutants of CDC2, CDK2, and CDK3 each suppressed apoptosis induced by both staurospo

22 Importantly, we showed that cdk3 enhances epidermal growth factor-induced transforma

23 In stark contrast, CDK3 from two wild-mice species (Mus spretus and Mus mus

24 Thus, cdk3 function contributes to the activation of E2F-1, E2

25 e presence of a single point mutation in the CDK3 gene from several Mus musculus strains commonly use

26 However, the role of cdk3 in cell proliferation, as well as cell transformati

27 contrast, phosphorylation of pRb by Cdk2 or Cdk3 in complexes with A- or E-type cyclins is not suffi

28 d suggest that any functional role played by CDK3 in the G(1)/S-phase transition is likely to be redu

29 Dominant-negative cdk3 inhibited E2F-1, E2F-2, and, less significantly, E2

30 Moreover, overexpression of cyclin C and CDK3 inhibits induction of endogenous Tyms expression at

31 report that the protein expression level of cdk3 is higher in human cancer cell lines and human glio

32 These data indicate that CDK3 is not required for M. musculus development and sug

33 tamoxifen-resistant MCF-7/TamR cells, while CDK3 is overexpressed in these cells.

34 ogenic potential of NFAT3 and suggested that CDK3-mediated phosphorylation of NFAT3 has an important

35 nt increased Cdc25A protein levels; Cdk1 and Cdk3 mutants had no effect.

36 Importantly, we showed that CDK3, NFAT3 and phosphorylated NFAT3-Ser259 were highly

37 Overexpression of wild type CDC2, CDK2, CDK3, or cyclin A (but not cyclin B) markedly elevated t

38 Furthermore, we found that cdk3 phosphorylates activating transcription factor 1 (A

39 kinase 2 (CDK2), cyclin C/CDK2, and cyclin C/CDK3, predominantly on S309.

40 ative forms of Cdk4 or Cdk6, but not Cdk2 or Cdk3, protects NGF-deprived sympathetic neurons from dea

41 Ectopic expression of Cdk3 resulted in anchorage-independent cell transformati

42 s also indicated that siRNA directed against cdk3 (si-cdk3) suppresses ATF1 activity, resulting in in

43 us studies using ectopic expression of human CDK3 suggest a role for this kinase in the G(1)/S-phase

44 uced transformation of JB6 Cl41 cells and si-cdk3 suppresses Ras(G12V)/cdk3/ATF1-induced foci formati

45 dicated that siRNA directed against cdk3 (si-cdk3) suppresses ATF1 activity, resulting in inhibition

46 Although mouse fibroblasts lack functional CDK3 (the partner of cyclin C in early G(1) in human cel

47 ated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during

48 ecreased during explant cultivation, whereas cdk3 was detected in the same small percentage of neuron

49 CDK3 was shown to be overexpressed in breast cancer and

50 Like CDC2 and CDK2, CDK3 was shown to form a complex with cyclin A in vivo.

51 Cdk3 was shown to phosphorylate c-Jun at Ser63 and Ser73