ライフサイエンスコーパス: IGFR

1 The Di-diabody binds to both EGFR and IGFR and effectively blocked both EGF- and IGF-stimulate

2 antibodies (BsAb) that target both EGFR and IGFR, using two neutralizing human antibodies originally

3 nsformation of RIE cells by oncogenic IR and IGFR versus Src and the pattern of requirements is diffe

4 ons at this edge discriminate between IR and IGFR.

5 s substrates such as TGF-beta, MT-MMP's, and IGFR-1 have been identified.

6 lity of Vav3 to induce membrane ruffles, but IGFR activation specifically promoted Vav3-mediated micr

7 Cotargeting IGFR-I with EGFR greatly enhanced both spontaneous and r

8 y several interrelated mechanisms: decreased IGFR processing, reduced IGFR cell-surface expression, a

9 in the absence of mesoderm formation and DN-IGFR inhibited neural induction by the BMP antagonist Ch

10 ed dominant-negative type I IGF receptor (DN-IGFR) had the opposite effect.

11 and Akt phosphorylation via an integrin/FAK/IGFR-dependent process.

12 vated in cells transformed by gag-IR and gag-IGFR but is activated in v-Src transformed cells.

13 he colony forming ability of gag-IR- and gag-IGFR-, but is partially required for v-Src-transformed c

14 athways of an oncogenic variant of IGFR, Gag-IGFR, called NM1.

15 n insulin-like growth factor I receptor (gag-IGFR) were systematically mutated to phenylalanines to i

16 , insulin-like growth factor-1 receptor (gag-IGFR), and v-Src.

17 in mediating the interaction between the gag-IGFR and insulin receptor substrate 1.

18 which is strongly phosphorylated by the gag-IGFR but not by the Phe-1136 mutant.

19 The transforming potential of the gag-IGFR correlates well with its ability to phosphorylate o

20 The Gag-IGFR fusion protein dimerizes, whereas Gag-Ros does not.

21 enzymatic and biological function of the gag-IGFR.

22 on of insulin-like growth factor receptor I (IGFR-I) levels on AG1478 administration.

23 Mevalonic acid depletion impaired IGFR processing, decreased the expression of mature IGFR

24 Intervention in IGFR/PI3k/Akt loop further depreciated Akt phosphorylati

25 ch also harbors Y950F and F951S mutations in IGFR, exhibits dramatic reductions in both activities.

26 the PI3K-Akt pathway, also inhibited gag-IR/IGFR-induced, but not v-Src-induced, focus and colony fo

27 ly slightly affected whereas those of gag-IR/IGFR-RIE cells were greatly inhibited.

28 pression on day 0 (e.g., TGFB1, TGFBIIR, M6P/IGFR-2), and no genes decreased on both days 3 and 7, co

29 ocessing, decreased the expression of mature IGFRs at the cell surface, and inhibited the downstream

30 f SirT1 in chondrocytes led to activation of IGFR and the downstream kinases phosphatidylinositol 3-k

31 Activation of IGFR occurs at least in part via SirT1-mediated repressi

32 he IGF receptor (IGFR) and the importance of IGFR glycosylation in the maintenance of the VSMC phenot

33 sion kinase-mediated adhesomes, induction of IGFR/IR-dependent PI3K activation, and Akt phosphorylati

34 ntal cells likely because of the presence of IGFR /InsR hybrid receptors.

35 has identified several tyrosine residues of IGFR important for its PTK activity and substrate intera

36 peared to be important downstream targets of IGFR-I-mediated resistance to anti-EGFR targeting.

37 ignaling pathways of an oncogenic variant of IGFR, Gag-IGFR, called NM1.

38 ll growth, which is prevented with mTOR plus IGFR inhibitors, supporting this combination as a therap

39 teracts with insulin growth factor receptor (IGFR) and is essential for activating the IGF receptor-m

40 and the insulin-like growth factor receptor (IGFR) have been implicated in the tumorigenesis of a var

41 and the insulin-like growth factor receptor (IGFR) have been implicated in the tumorigenesis of a var

42 ing the insulin-like growth factor receptor (IGFR).

43 of the insulin-like growth factor receptor (IGFR)/Akt pathway was assessed using immunoblotting.

44 d Gag-insulin-like growth factor I receptor (IGFR) fusion proteins, respectively.

45 Insulin-like growth factor I receptor (IGFR) plays an important role in cell growth and transfo

46 R) or insulin-like growth factor-I receptor (IGFR).

47 y, we examined the role of the IGF receptor (IGFR) and the importance of IGFR glycosylation in the ma

48 1 insulin-like growth factor (IGF) receptor (IGFR).

49 , and insulin-like growth factor I receptor [IGFR]) led to tyrosine phosphorylation of Vav3 and its a

50 chondrocytes increased apoptosis and reduced IGFR phosphorylation, while down-regulation of PTP1B by

51 chanisms: decreased IGFR processing, reduced IGFR cell-surface expression, and reduced downstream sig

52 ntibodies; it triggers rapid and significant IGFR internalization and degradation and mediates effect

53 ment of clinical analogs lacking significant IGFR cross-binding may enhance the safety of insulin rep

54 These findings suggest that IGFR-I signaling through phosphoinositide 3-kinase may r

55 dly, the engagement of beta-arrestins by the IGFR but not by the V2R was needed to promote the vasopr

56 ynthesis of survivin protein mediated by the IGFR/EGFR heterodimer counteracts the antitumor action o

57 nity for the IR but reduced affinity for the IGFR.

58 that alterations in the glycosylation of the IGFR disrupt the ability of IGF-I to protect against the

59 rrestins were found to act downstream of the IGFR transactivation.

60 ation and be required for the release of the IGFR-activating factor, beta-arrestins were found to act

61 of mTOR led to the activation of Akt through IGFR/PI3k/Akt feedback loop.

62 antibodies: IMC-11F8 to EGFR and IMC-A12 to IGFR.

63 in those with squamous cell carcinoma, where IGFR expression is typically high.