ライフサイエンスコーパス: v-Crk

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1 containing protein in cells transformed with v-Crk.

2 alling and on transformation by the oncogene v-crk.

3 nsformation by the oncoproteins v-SRC and/or v-CRK.

4 as, that forms a stable complex in vivo with v-Crk.

5 Our results indicate that v-Crk activates the Rho-signaling pathway and serves as

6 ly, we have shown that ectopic expression of v-Crk, an SH2/SH3 domain-containing adapter proteins, in

7 ially found to be tyrosine-phosphorylated in v-Crk and v-Src transformed cells.

8 formation by certain oncoproteins, including v-Crk and v-Src, and to tumor growth and metastasis.

9 f tyrosine kinases, the transforming protein v-crk, and the cytoskeletal proteins vinculin and the ty

10 ssociated coiled-coil-containing kinase) and v-Crk, but not SH2 or SH3 mutants of v-Crk, results in h

11 Transient expression of v-Crk, c-Crk-I, or c-Crk-II activated JNK1 in human embr

12 When wild-type PTP1B is expressed in 3Y1-v-crk cells, p130(Cas) shows substantial dephosphorylati

13 Currently comprising four members, v-Crk, CrkI, CrkII and Crk-like protein, we have introdu

14 cellular counterparts of the viral oncogene v-Crk Elevated levels of Crk and CrkL have been observed

15 kPC12 cells compared to the levels in mutant v-Crk-expressing cells or wild-type cells, consistent wi

16 idic acid-containing medium, the majority of v-Crk-expressing PC12 cells (v-CrkPC12 cells) display a

17 al adhesion kinase pp125FAK (FAK), v-SRC and v-CRK have been mapped to distinct regions of CAS.

18 Jun kinase (JNK) is moderately activated by v-Crk in both NIH 3T3 cells and chicken embryo fibroblas

19 Expression of v-Crk in PC12 cells does not result in activation of Rac

20 The requirement for JNK activation in v-Crk induced transformation was demonstrated by the sup

21 PI3K/AKT pathway plays an essential role in v-Crk-induced transformation of CEF.

22 t a PI3K inhibitor, LY294002, suppresses the v-Crk-induced transformation.

23 We studied the molecular mechanism of the v-Crk-induced transformation.

24 v-Crk induces cellular tyrosine phosphorylation and tran

25 v-Crk-mediated cell flattening is inhibited by treatment

26 he suppression of colony forming activity of v-Crk NIH 3T3 cells when a dominant-negative form of JNK

27 activity and the colony forming potential of v-Crk NIH 3T3 cells.

28 wth rate and anchorage-independent growth of v-Crk NIH 3T3 cells.

29 The cellular homologs of the v-Crk oncogene product are composed exclusively of Src h

30 The cellular homologs of the v-Crk oncogene product consist primarily of Src homology

31 The v-Crk oncogene product consists of two protein interacti

32 he C-CRK gene, cellular homolog of the avian v-crk oncogene, encodes two alternatively spliced adapto

33 tyrosine kinase receptors, and the v-src and v-crk oncogenes.

34 ructurally related to c-CRK-II (CRK) and the v-Crk oncoprotein.

35 n protein that associated with the v-Src and v-Crk-oncoproteins, considerable effort has been made to

36 v-Crk overexpression causes cell transformation and elev

37 v-Crk overexpression in fibroblasts causes cell transfor

38 se) and v-Crk, but not SH2 or SH3 mutants of v-Crk, results in hyperactivation of p160ROCK.

39 NleH1 kinase substrates and identified CRKL (v-Crk sarcoma virus CT10 oncogene-like protein), a subst

40 its transformation of rat 3Y1 fibroblasts by v-crk, -src, and -ras, but not by v-raf.

41 guanine nucleotide exchange factor, mediates v-crk transformation are not well understood.

42 activation of MAPK, one of the hallmarks of v-crk transformation previously thought to be mediated t

43 ane binding of C3G, which also occurs during v-crk transformation, results in cell fate changes and o

44 K/AKT pathway is constitutively activated in v-Crk-transformed CEF.

45 hosphorylated on tyrosine in both v-src- and v-crk-transformed cells.

46 In 3Y1 and 3Y1 v-crk-transformed fibroblasts, almost all of the total P

47 rexpression of CrkI, the cellular homolog of v-Crk, transforms mouse fibroblasts, and elevated CrkI e

48 gnaling cascade involving an adaptor protein v-Crk, which transmits signals through C3G toward JNK ac

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