ライフサイエンスコーパス: IGFR

1 cruitment is blunted in the absence of DAF-2/IGFR and modulated by the competitive action of insulin

2 r 1 receptor (IGF1R) in BECs, and activating IGFR signaling increased BEC numbers but suppressed BEC

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

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

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

6 ons at this edge discriminate between IR and IGFR.

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

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

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

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

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

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

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

14 key step in conveying IGF-1 stimulation from IGFR to IRS-1.

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

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

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

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

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

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

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

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

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

24 enzymatic and biological function of the gag-IGFR.

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

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

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

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

29 eceptors and oncogenic regulators, including IGFR and RAS signaling, that significantly contribute to

30 verexpression of TRAF4 enhances IGF1-induced IGFR-IRS-1 interaction, IRS-1 tyrosine phosphorylation,

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

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

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

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

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

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

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

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

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

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

41 ression (PCR) analysis of the EEM spectra of IGFR samples correlates to GCMS data with R(2) = 0.988 f

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

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

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

45 ar diffusion inverted gravity flame reactor (IGFR) operated on ethylene and ethane.

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

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

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

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

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

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

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

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

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

55 ent mitogen that activates the IGF receptor (IGFR)/insulin receptor substrate (IRS) axis, thus stimul

56 1 insulin-like growth factor (IGF) receptor (IGFR).

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

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

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

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

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

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

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

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

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

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

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

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

69 PCR-EEM analysis trained on the IGFR samples was applied to PM samples from woodsmoke an

70 dictions using live-cell imaging data on the IGFR/FoxO pathway.

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

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

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