ライフサイエンスコーパス: c-Kit receptor

1 ed by SCLC, but over 70% of SCLC contain the c-Kit receptor.

2 es alpha6-integrin, alphav-integrin, and the c-kit receptor.

3 by FRET, and tyrosine phosphorylation of the c-kit receptor.

4 report, a similar approach is applied to the c-kit receptor.

5 tor of Ras, via wild-type and mutant (W(41)) c-kit receptors.

6 ine, CTS, which expresses both the CXCR4 and c-kit receptors.

7 y and immunoreactivity to antibodies against c-Kit receptors.

8 ent with the expression of a single class of c-kit receptors.

9 in c-kit or stem cell factor, the ligand for c-Kit receptors.

10 We used an antibody against the murine c-Kit receptor (ACK2) to deplete fetal host hematopoieti

11 hanistically, these effects were mediated by c-Kit receptor activation, STAT5 phosphorylation, and re

12 ata suggest that interaction of SCF with the c-kit receptor affects the homing behavior of hematopoie

13 disruption leads to a destabilization of the c-Kit receptor and decreased survival of cells.

14 By targeting the mast cell c-Kit receptor and inhibiting mast cell activation and d

15 The c-kit receptor and its ligand, steel factor (SLF), are c

16 known about the biological properties of the c-kit receptor and its ligand, stem cell factor (SCF), l

17 uggest that exposure to Epo can activate the c-kit receptor and provide further evidence for cross-ta

18 ontrast to other tumor cells, CSCs expressed c-kit receptors and produced SCF.

19 and NCI-H249) SCLC cell lines had detectable c-Kit receptors and were inhibited in growth and viabili

20 involved in LC development, including GATA4, c-kit receptor, and leukemia inhibitory factor receptor.

21 ral tyrosine kinases, including BCR-ABL, the C-KIT receptor, and the platelet-derived growth factor r

22 c-Kit receptors are expressed in proliferating adult CE

23 ells with further recruitment of JAK2 to the c-kit receptor complex after SCF stimulation.

24 The mutant c-Kit receptor confers cytokine independence and induces

25 The mutant c-Kit receptor confers cytokine-independent survival of

26 e as they home and engraft in irradiated and c-Kit-receptor-deficient recipient mice.

27 ed cytokine thrombopoietin (Tpo), stimulated c-kit receptor dimerization detectable by FRET, and tyro

28 Prior biochemical studies of c-kit receptor dimerization have mainly used affinity cr

29 echnique is sufficiently sensitive to detect c-kit receptor dimerization on normal human hematopoieti

30 SCF induced a dose-dependent increase in c-kit receptor dimerization that correlated well with th

31 The ability of SCF to induce c-kit receptor dimerization was assessed by flow cytomet

32 of SCF and other hematopoietic cytokines on c-kit receptor dimerization.

33 the white spotting locus that causes reduced c-Kit receptor expression and an inability of mast cells

34 The up-regulation of c-kit receptor expression in diseased livers suggests an

35 skin, these results suggest that the loss of c-KIT receptor expression may allow malignant melanoma c

36 xtent of mediator release induced by SCF and c-kit receptor expression.

37 ocal microscopy showed redistribution of the c-kit receptor (from a diffuse distribution on the cell

38 These results suggest that c-kit receptor function may be required for optimal resp

39 poietic cells to the spleen was dependent on c-kit receptor function.

40 he platelet-derived growth factor (PDGF) and c-kit receptors has been proposed as important in mediat

41 rosine-phosphorylated upon activation of the c-Kit receptor, implicating it as a component of a signa

42 b is strictly required for expression of the c-Kit receptor in erythroid cells.

43 ular conjugate adenovirus vector through the c-kit receptor in hematopoietic progenitor cell lines.

44 PTP-RO was found to be associated with the c-Kit receptor in these transfected cells and the SCF/Ki

45 The extensive expression of the Erb and c-kit receptors in adult taste buds and in and around de

46 evidence for cross-talk between the Epo and c-kit receptors in human hematopoietic cell lines.

47 ptor shares several characteristics with the c-kit receptor including dimerization and rapid internal

48 ic microenvironment is more dependent on SCF/c-kit receptor interaction than is erythropoiesis in the

49 trong evidence that, during development, the c-kit receptor is expressed in different pools of cardia

50 d new protein synthesis, suggesting that the c-kit receptor is not recycled to the cell surface after

51 The c-Kit receptor is regarded as one of the CSC markers in

52 Stem cell factor (SCF), a ligand of the c-kit receptor, is a critical cytokine, which contribute

53 with PKC412 (an inhibitor of PDGF, VEGF, and c-kit receptor kinases and several isoforms of PKC), PTK

54 KC), PTK787 (an inhibitor of PDGF, VEGF, and c-kit receptor kinases), SU1498 (an inhibitor of VEGF re

55 n contrast to the pleiotropic effects of the c-kit receptor ligand, stem cell factor.

56 brane targeted fusion protein containing the c-kit receptor linked to one or more copies of FKBP12 al

57 The nonneutralizing anti-c-kit receptor monoclonal antibody 104D2 was directly co

58 Mutations in the c-KIT receptor occur somatically in many sporadic Gastro

59 Reappearance of the c-kit receptor on the cell surface required new protein

60 topoietic cells that universally express the c-Kit receptor on their cell surface.

61 al involvement in the stem cell factor (SCF)/c-Kit receptor pathway, COS-7 and 293 cells were cotrans

62 75 (CT53518), inhibits Flt-3, betaPDGFR, and c-Kit receptor phosphorylation with IC(50) values of 50-

63 5 d, surviving hair bulb melanocytes express c-kit receptor, proliferate, and appear to migrate up th

64 ity of only two of these genes is known: the c-kit receptor protein tyrosine kinase and the c-kit lig

65 The activity of the c-Kit receptor protein-tyrosine kinase is tightly regula

66 ly kinase (SFK) binding sites in the mutated c-Kit receptor restored cellular survival and migration

67 tutively activated STAT3 restores the mutant c-Kit receptor's transforming ability in 293 cells.

68 Although c-Kit receptor signaling promotes angiogenesis in multip

69 ibes the hitherto-unknown role of SWAP-70 in c-kit receptor signaling, a key proliferation and differ

70 n CRTh2(+)ILC2 differentially express CD117 (c-kit receptor), some ILC2 surface phenotypes are unstab

71 addition of the biotinylated ligand for the c-Kit receptor, stem cell factor (SCF), through an avidi

72 a subset of which also coexpressed Thy-1 and c-kit receptors, suggesting that the CD34(+) population

73 rated a functionally and biochemically inert c-Kit receptor that lacked the binding sites for seven e

74 p85(PI3K) is known to bind to the activated c-Kit receptor, the possibility that CRKL interacted wit

75 termolecular tyrosine phosphorylation of the c-kit receptor, thus initiating signal transduction.

76 Stem cell factor (SCF) binding to the c-kit receptor triggers homodimerization and intermolecu

77 oid hematopoietic cells in vitro through the c-kit receptor tyrosine kinase (dominant white spotting,

78 members may negatively modulate function of c-kit receptor tyrosine kinase and thus regulate recepto

79 D63, and CD81 are physically associated with c-kit receptor tyrosine kinase in the human factor-depen

80 The c-KIT receptor tyrosine kinase is constitutively activat

81 Signaling from the c-Kit receptor tyrosine kinase is essential for primordi

82 ent samples, differing classes of activating c-KIT receptor tyrosine kinase mutations have been obser

83 CF) is a growth factor that acts through the c-Kit receptor tyrosine kinase to elicit hematopoietic p

84 n naturally occurring point mutations in the c-kit receptor tyrosine kinase, which suppresses the fun

85 re potent inhibitors of both the Bcr-Abl and c-kit receptor tyrosine kinases and deserve further stud

86 l antibody ACK2, which recognizes the murine c-kit receptor, was used to selectively block the hemato