ライフサイエンスコーパス: c-Kit ligand

1 ls, such as those triggered by alpha-MSH and c-Kit ligand.

2 g HCEKs could be restored by the addition of c-kit ligand.

3 members of this family include M-CSF and the c-kit ligand.

4 /Fas-L-dependent signals that are blocked by c-kit ligand.

5 an be regulated in vitro by IL-3, IL-10, and c-kit ligand.

6 us different doses of stem cell factor (SCF; c-kit ligand) after chemotherapy or G-CSF alone after ch

7 lymphopoiesis is preceded by the actions of c-Kit ligand (also called stem cell factor; SCF) and fet

8 Culture of CD34(+) HPCs in the presence of c-Kit ligand and Axl-Fc resulted in a significant decrea

9 roglobulin (B2M) that elicits the release of c-KIT ligand and interleukin-7 that greatly accelerate p

10 IL-3 to the combination of steel factor (SF, c-kit ligand) and IL-11 abrogated the B-lymphoid potenti

11 lls, during pre-expansion by thrombopoietin, c-kit ligand, and FLT-3 ligand, on recombinant fibronect

12 luding the expression of angiopoietin 1, the c-Kit ligand, and VCAM-1.

13 now report that glucocorticoids inhibit the c-kit ligand- and IL-3-induced proliferation of mBMMC, t

14 reated with either GM-CSF, GM-CSF plus IL-4, c-kit ligand (c-kitL), or G-CSF, class II+ CD11c+ cells

15 cells developed with interleukin (IL) 10 and c-kit ligand contain mMCP-9 transcript, whereas those de

16 it, with diminished apoptosis in response to c-Kit ligand deprivation.

17 d to real-time quantitative PCR to determine c-kit ligand expression.

18 cytokines (interleukin-2 [IL-2], IL-3, IL-7, c-kit ligand), FLT-3 ligand (FL), and stroma-derived fac

19 bipotential intermediate in the presence of c-kit ligand, GM-CSF, and TNF-alpha.

20 recursors when cultured for 12 to 14 days in c-kit ligand, granulocyte-macrophage colony-stimulating

21 sing stem cell factor (SCF), also known as a c-Kit ligand, had great promise for treating ischemia fo

22 s produced by nonosteoblastic stromal cells (c-Kit ligand, IL-6, and IL-3) shifted the cultures towar

23 lentiviral vectors were used to express the c-kit ligand in Sl/Sl(d) Sertoli cells.

24 Conversely, misexpression of c-Kit ligand in the skin in larval zebrafish induced inc

25 , IDO, fms-related tyrosine kinase 3 ligand, c-kit ligand, inducible NO synthase, arginase-1, TNF-alp

26 d enhances mast cell survival in response to c-kit ligand (kit-L).

27 The mRNA levels of IGF-1 and c-Kit ligand (KITL) were induced by 10 mg/kg DEHP.

28 th BM niche cells that produce growth factor c-Kit ligand (Kitl/SCF) and chemokine CXCL12, and were t

29 The addition of c-kit ligand (KL) and IL-10 to IL-3-derived mouse bone m

30 We have previously demonstrated that c-kit ligand (KL) can enhance IL-2-induced proliferation

31 PO and interleukin-3 (IL-3), or with TPO and c-kit ligand (KL) in the presence of a murine stromal ce

32 with interleukin (IL)-3 can be stimulated by c-kit ligand (KL) in the presence of IL-10 and IL-1beta

33 stimulation of Mo7 hematopoietic cells with c-Kit ligand (KL) induces phosphatidylinositol (PI) 3-ki

34 The native form of soluble c-kit ligand (KL) is a noncovalent dimer.

35 day 6 when cultured in thrombopoietin (TPO), c-kit ligand (KL), and flk2/flt3 ligand (FL).

36 in the presence of interleukin (IL)-3, IL-6, c-kit ligand (KL), and leukemia inhibitory factor (LIF).

37 the expression patterns of Flt3 ligand (FL), c-Kit ligand (KL), and macrophage colony-stimulating fac

38 d limited clonal growth, but synergized with c-kit ligand (KL), flt3 ligand (FL), or IL-3 to potently

39 with interleukin-7 (IL-7), flt3 ligand (FL), c-kit ligand (KL), IL-3, IL-2, and AFT024, a murine feta

40 her hematopoietic growth factors such as the c-kit ligand (KL).

41 l system in which lack of transmembrane type c-kit ligand (KL2) expression on the somatic Sertoli cel

42 ease in glycogen levels as well as increased c-kit ligand mRNA compared with wild-type controls.

43 ation, and activation has been identified as c-kit ligand or stem cell factor (SCF).

44 nd that seven markers at 12p22 within KITLG (c-KIT ligand) reached genome-wide significance (P < 5.0

45 rough analysis of the stem cell factor (SCF)/c-kit ligand receptor pair, we describe an additional di

46 The stem cell factor (SCF)/c-kit ligand/receptor system has been implicated in stem

47 f HPC at proportions similar to or less than c-kit ligand (steel factor, SF).

48 ells, and specifically blocks binding of the c-kit ligand stem cell factor (SCF).

49 Inhibition was prevented, however, if c-kit ligand (stem cell factor (SCF)) was added to cultu

50 ockout (-/-) mice after stimulation with the c-Kit ligand, stem cell factor (SCF), an important regul

51 ported that repetitive administration of the c-kit ligand, stem cell factor (SCF), can increase mast

52 ed enhanced proliferation in response to the c-Kit ligand, stem cell factor (SCF).

53 munohistochemistry, expression levels of the c-kit ligand, stem cell factor, in skin and epidermis ar

54 s with VRP alone and in combination with the c-kit ligand/stem cell factor increased cell growth.

55 kit receptor protein tyrosine kinase and the c-kit ligand (the steel factor).

56 se to vascular endothelial growth factor and c-kit ligand these precursors give rise to colonies cont

57 EKs) transduced with FIH-1 were treated with c-kit ligand to establish further a FIH-1/c-kit interact

58 of specific cytokines in response to IgE or c-Kit ligand was markedly reduced in MEKK2(-/-) ESMC rel

59 edium with thrombopoietin, flk-2 ligand, and c-kit ligand, with or without IL-3 and found that CAFCs