ライフサイエンスコーパス: c-Crk

1 terminal SH3 domain from the proto-oncogene, c-Crk.

2 DGF receptor and tyrosine phosphorylation of c-Crk.

3 of which associate with the adapter protein c-Crk.

4 tyrosine phosphorylated and associates with c-Crk.

5 tion at tyrosine 207, a residue conserved in c-Crk, abrogates all in vivo tyrosine phosphorylation of

6 Src homology 3 (SH3) domain from the murine c-Crk adapter protein.

7 port we demonstrate that Arg associates with c-Crk, an adaptor protein composed of an SH2 domain and

8 We have studied the involvement of murine c-Crk, an SH2/SH3 containing adaptor protein, in signali

9 The complex between c-Crk and c-Cbl is also seen upon T-cell receptor cross-

10 ntaining motifs found on Sin correlated with c-Crk and cellular phosphoprotein binding to Sin as well

11 irectly to p120CBL, while the SH3 domains of c-CRK and CRKL bound to BCR/ABL and c-ABL.

12 -Cbl specifically associates with endogenous c-Crk and Fyn.

13 ng downstream signaling effectors, including c-Crk and Nck.

14 s indicated that the SH2 domains of CRKL and c-CRK bound directly to p120CBL, while the SH3 domains o

15 Overexpression of c-Crk enhanced insulin- but not PDGF-induced activation

16 However IRS-1 is also co-precipitated with c-Crk from quiescent L6 cells.

17 The C-CRK gene, cellular homolog of the avian v-crk oncogene

18 The Src homology 3 (SH3) domain from the c-Crk-I adaptor protein has been labeled with a Trp anal

19 igation of the 7AW-labeled SH3 domain to the c-Crk-I Src homology 2 (SH2) domain, via EPL, generated

20 Transient expression of v-Crk, c-Crk-I, or c-Crk-II activated JNK1 in human embryo kidn

21 via EPL, generated the multidomain protein, c-Crk-I, with a domain-specific label.

22 Deletion analysis of c-Crk II also revealed the presence of a C-terminal segm

23 data show that the phosphorylation cycle of c-Crk II determines its dynamic interaction with paxilli

24 d by a transient initial dissociation of the c-Crk II paxillin complex.

25 e c-Abl is an intermediary for NGF-inducible c-Crk II phosphorylation on the negative regulatory Tyr(

26 ll as c-Crk Y222F and c-Abl, suggesting that c-Crk II Tyr(222) phosphorylation induces both the disso

27 of NGF stimulation in PC12 cells showed that c-Crk II Tyr(222) phosphorylation preceded paxillin Tyr(

28 Transient expression of a c-Crk II Tyr(222) point mutant (c-Crk Y222F) in 293T cel

29 demonstrating the biological significance of c-Crk II tyrosine phosphorylation in NGF-dependent morph

30 kinase-inactive form of c-Abl (Abl) promotes c-Crk II/p130(CAS) (Crk-CAS) coupling, enhancing cell mi

31 o SH3 domains and is structurally related to c-CRK-II (CRK) and the v-Crk oncoprotein.

32 Transient expression of v-Crk, c-Crk-I, or c-Crk-II activated JNK1 in human embryo kidney cells, 29

33 ent results in the de-association of p130CAS/c-Crk-II complex in the absence of an apparent change in

34 2a, the state of tyrosine phosphorylation of c-Crk-II did not appear to change with NGF treatment.

35 hat NGF induces the association of TrkA with c-Crk-II in a multimeric complex that also includes SHC

36 These results clearly implicate c-Crk-II in the NGF signaling pathway and support the co

37 Furthermore, we show that c-Crk-II is associated with tyrosine phosphorylated p130

38 studies demonstrated that the interaction of c-Crk-II with TrkA not only occurs indirectly through th

39 The interaction of Arg with c-Crk in living cells was confirmed by the detection of

40 The association of IRS-1 with c-Crk in quiescent cells is probably not direct since Fa

41 We show here that c-Crk is associated with components of insulin- and PDGF

42 at CRKL, but not the related adapter protein c-CRK, is tyrosine phosphorylated in cell lines transfor

43 C-CRK mRNA expression was increased in more advanced (st

44 naling proteins which include p120CBL, PI3K, c-CRK or CRKL, c-ABL and BCR/ABL itself.

45 The site of c-Crk phosphorylation by Arg was identified as tyrosine

46 The proto-oncogene molecule c-Crk plays a role in growth factor-induced activation o

47 n lung tumors and provides evidence that the C-CRK proto-oncogene may foment a more aggressive phenot

48 cular dynamics simulations of a model of the c-Crk SH3 domain over a broad range of temperatures, and

49 on temperature-the temperature for which the c-Crk SH3 domain undergoes a rapid folding transition wi

50 nd thought to make key interactions with the c-Crk SH3 domain.

51 SH2 domain nor amino-terminal SH3 domain of c-Crk to IRS-1 from unstimulated cells.

52 In addition, increased phosphorylation of c-Crk was observed in cotransfected COS cells, indicatin

53 Interestingly, the adaptor proteins CRKL and c-CRK were also found in these complexes.

54 he formation of stable complex of endogenous c-Crk with insulin receptor substrate-1 (IRS-1) mediated

55 The ligand dependent physical association of c-Crk with IRS-1 is direct.

56 murine myoblast cells induces association of c-Crk with the PDGF receptor and tyrosine phosphorylatio

57 between c-Crk Y222F and paxillin as well as c-Crk Y222F and c-Abl, suggesting that c-Crk II Tyr(222)

58 r(31) and enhances complex formation between c-Crk Y222F and paxillin as well as c-Crk Y222F and c-Ab

59 PC12 cells overexpressing c-Crk Y222F manifested a defect in cellular adhesion and

60 ression of a c-Crk II Tyr(222) point mutant (c-Crk Y222F) in 293T cells induces hyperphosphorylation