ライフサイエンスコーパス: Kit ligand

1 iferate rapidly in response to steel factor (Kit ligand).

2 mbers of this family include M-CSF and the c-kit ligand.

3 n cells can be increased by stimulation with Kit ligand.

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

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

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

7 ild-type mast cells via the secretion of the Kit ligand.

8 ling, matrix metalloproteinase-9 and soluble Kit ligand.

9 oteinase-9, mediating the release of soluble Kit ligand.

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

11 e in their proliferative response to the SCF/Kit ligand.

12 referred to as osteoprotegerin ligand), and kit ligand-1 (KL-1) in vitro.

13 d from beta-amyloid precursor protein (APP), Kit-ligand-1 (KL-1), tumor necrosis factor-related activ

14 ubstrates, including heparin-binding EGF and Kit ligand 2 in this context.

15 Activation of heparin-binding EGF or Kit ligand 2 shedding by ADAM17 in iRhom2(-/-) mEFs can

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

17 ymphopoiesis is preceded by the actions of c-Kit ligand (also called stem cell factor; SCF) and fetal

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

19 /ERK) mitogenic signaling pathway, including KIT ligand and caveolins 1 and 2.

20 alloproteinase-9 mediated release of soluble kit-ligand and recruit these proangiogenic cells to area

21 nsion of hematopoietic progenitor cells with kit-ligand and thrombopoietin for 10 days and further pu

22 ely, by stem cell factor (SCF; also known as Kit ligand) and by allergen in complex with allergen-spe

23 -3 to the combination of steel factor (SF, c-kit ligand) and IL-11 abrogated the B-lymphoid potential

24 s, during pre-expansion by thrombopoietin, c-kit ligand, and FLT-3 ligand, on recombinant fibronectin

25 SCF), also known as mast cell growth factor, kit ligand, and steel factor, is the ligand for the tyro

26 ding the expression of angiopoietin 1, the c-Kit ligand, and VCAM-1.

27 ow report that glucocorticoids inhibit the c-kit ligand- and IL-3-induced proliferation of mBMMC, the

28 Furthermore, we pinpoint KIT-ligand as a dermal papilla signal promoting melanocy

29 conclude that chronic stimulation of the KIT-kit ligand axis does not irrevocably commit mast cells t

30 The in vivo influence of the KIT-kit ligand axis on the phenotype of human mast cells has

31 t cell growth factor, which is also known as kit ligand because its obligate receptor is KIT, the pro

32 sm can result from missense mutations in the Kit ligand-binding domain, although the resulting phenot

33 ation of the second Ig-like (D2) loop of the Kit ligand-binding domain.

34 ssary to prevent apoptosis in HSCs, and that Kit ligand by itself provides a strong proliferative sti

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

36 ls are indirect and include mediation by the kit ligand/c-Kit pathway, rather than being an autocrine

37 liferation in response to erythropoietin and Kit ligand compared with control cells.

38 lls developed with interleukin (IL) 10 and c-kit ligand contain mMCP-9 transcript, whereas those deve

39 yte/macrophage colony-stimulating factor and kit ligand cotreatment did not overcome this inhibition.

40 PD173955 inhibited kit ligand-dependent c-kit autophosphorylation (IC(50) =

41 orylation (IC(50) = approximately 25 nM) and kit ligand-dependent proliferation of M07e cells (IC(50)

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

43 ein kinase C, and Ca2+, respectively, in the kit ligand effect.

44 rogram in which p53 stabilization stimulates Kit ligand expression, and, consequently, epidermal mela

45 depletion, decreased caveolin, and increased KIT ligand expression, are all independently associated

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

47 ne (FSH) receptor expression, and stimulates kit ligand expression.

48 is of stem cell factor (SCF, or steel factor/kit ligand) expression in Sertoli cells of rat testis, 1

49 ctivated by down-regulation of Steel factor (kit ligand) expression in the midline between E9.5 and E

50 n in serum-deprived medium supplemented with kit ligand, flk2/flt3 ligand, GM-CSF, c-mpl ligand, eryt

51 arrow cells in suspension in the presence of KIT ligand, FLK2/FLT3 ligand, interleukin-6 (IL-6), and

52 tokines (interleukin-2 [IL-2], IL-3, IL-7, c-kit ligand), FLT-3 ligand (FL), and stroma-derived facto

53 ogenitor cells to the early-acting cytokines kit ligand, flt3 ligand, and thrombopoietin.

54 and minimal concentrations of thrombopoietin/Kit-ligand/Flt3-ligand resulted in a 400-fold expansion

55 on in 85 healthy individuals, a locus in the Kit ligand gene (KITLG; cg27512205) showed the strongest

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

57 cursors when cultured for 12 to 14 days in c-kit ligand, granulocyte-macrophage colony-stimulating fa

58 produced by nonosteoblastic stromal cells (c-Kit ligand, IL-6, and IL-3) shifted the cultures toward

59 by examining the expression of both KIT and KIT ligand in fetal and neonatal ovaries.

60 udy describes the role of mTOR signaling and KIT ligand in granulosa cells of primordial follicles fo

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

62 Moreover, suppressing production of KIT-ligand in Sca1(+) progenitors inhibits their ability

63 eptor in these transfected cells and the SCF/Kit ligand induced a rapid tyrosine phosphorylation of P

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

65 nsion in the presence of multiple cytokines (kit ligand, interleukin-3, interleukin-6, and granulocyt

66 In fact, soluble KIT ligand is sufficient to induce tyrosinase expression

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

68 Kit ligand (KitL) and its tyrosine kinase receptor c-kit

69 pts and Sld is an intragenic deletion of the kit ligand (Kitl) from which only the soluble protein is

70 ulators matrix metallopeptidase-9 (MMP9) and kit ligand (KITL) were decreased with heterozygous level

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

72 d a decrease in proliferation in response to kit ligand (kitL), a growth factor important for control

73 ger the awakening of dormant oocytes through KIT ligand (KITL), and we present an essential communica

74 Kit ligand (Kitl), encoded by the Steel (Sl) locus, play

75 us Nf1 mutant (Nf1-/-) Schwann cells secrete Kit ligand (KitL), which stimulates mast cell migration,

76 gand for the Kit receptor tyrosine kinase is Kit ligand (Kitl; also known as mast cell growth factor,

77 rived CD34(+) progenitors in the presence of kit ligand (KITLG) and the cytokines IL-3, IL-9, and IL-

78 map to a divergent regulatory allele of the Kit ligand (Kitlg) gene.

79 Although IL-10 also enhanced kit ligand (KL) + IL-7-induced proliferation of Lin-Sca-

80 Combinations of cytokines, such as kit ligand (KL) + interleukin-3 or KL + granulocyte-macr

81 In contrast, KIT ligand (KL) and granulocyte-macrophage colony-stimul

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

83 KIT ligand (KL) and its receptor, c-kit, are coexpressed

84 type Kit to lipid rafts after stimulation by Kit ligand (KL) and the constitutive localization of onc

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

86 (+) peripheral blood cells, we observed that Kit ligand (KL) failed to induce degranulation but acted

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

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

89 timulation of Mo7 hematopoietic cells with c-Kit ligand (KL) induces phosphatidylinositol (PI) 3-kina

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

91 The effects of FLT3/FLK-2 ligand (FL) and KIT ligand (KL) on in vitro expansion of hematopoietic s

92 Kit ligand (KL) stimulation resulted in transient tyrosi

93 Kit ligand (KL), a product of granulosa cells in ovarian

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

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

96 e expression patterns of Flt3 ligand (FL), c-Kit ligand (KL), and macrophage colony-stimulating facto

97 protein-15 (BMP-15) and a GC-derived factor, kit ligand (KL), both of which have been shown to be cru

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

99 th interleukin-7 (IL-7), flt3 ligand (FL), c-kit ligand (KL), IL-3, IL-2, and AFT024, a murine fetal

100 cells were exposed to thrombopoietin (TPO), kit ligand (KL), interleukin-1alpha (IL-1alpha), and IL-

101 ed that the Rac1/JNK pathway is critical for Kit ligand (KL)-induced proliferation of mast cells but

102 alone, and increased in response to FL plus kit ligand (KL).

103 r hematopoietic growth factors such as the c-kit ligand (KL).

104 e markedly hyper-proliferated in response to Kit ligand (KL). stimulation.

105 The Kit ligand (KL)/Kit receptor pair functions in hematopoi

106 Administration of kit-ligand (KL) before and after doses of 5-fluorouracil

107 The membrane growth factor Kit-ligand (KL), the ligand of the Kit receptor tyrosine

108 or phosphatidylinositide-3' (PI 3)-kinase in Kit-ligand (KL)-induced adhesion of BMMCs to fibronectin

109 ipts were found for numerous growth factors (kit ligand [KL], FLT3 ligand, fibroblast growth factor-2

110 system in which lack of transmembrane type c-kit ligand (KL2) expression on the somatic Sertoli cell

111 gelatinase B mRNA signal and also attenuates kit ligand-mediated induction of gelatinase B expression

112 Addition of the Kit ligand Mgf or endothelin 3 or a combination of these

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

114 othesis that oocytes regulate granulosa cell kit ligand mRNA levels in a way that is characteristic o

115 ion with thrombopoietin and stem cell factor/kit ligand on megakaryocyte production in vitro were not

116 a dosage effect of transmembrane-associated kit ligand on TGCT susceptibility and that the kit recep

117 examine the role of stem cell factor (SCF or Kit ligand) on the early- to mid-stages of oocyte growth

118 is is bolstered by several factors including KIT ligand, oncostatin-M, glucocorticoids, and erythropo

119 en combinations of cytokines, ie, G-CSF plus kit ligand or G-CSF plus Flt3-ligand were used with anti

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

121 in cultures treated with recombinant Tpo and Kit ligand or with Tpo and interleukin 3 and 11.

122 The product of the Sl locus is Kit ligand (or Kitl; also known as mast cell growth fact

123 interfollicular melanocytes are retained by Kit ligand overexpression and an immune response is init

124 ; and (3) migration mediated through the kit/kit ligand pathway may be a common contributor to differ

125 this cooperative signaling involves the kit/kit ligand pathway, and provides a novel example of inte

126 he ischemic hind limb, and increased soluble Kit ligand plasma levels.

127 ese findings suggest that factors other than kit ligand predominate in determining mast cell phenotyp

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

129 ugh analysis of the stem cell factor (SCF)/c-kit ligand receptor pair, we describe an additional dist

130 ing interaction mediated by the Steel factor/Kit ligand/receptor interaction.

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

132 Stem cell factor/kit ligand (SCF/KL), an early acting cytokine, has recen

133 MP-9), induced in BM cells, releases soluble Kit-ligand (sKitL), permitting the transfer of endotheli

134 Soluble Kit-ligand (sKitL), thrombopoietin (TPO, encoded by Thpo

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

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

137 CD24, on cDC1s upregulates expression of the Kit ligand stem cell factor on these cells.

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

139 nced by long-term treatment of mice with the kit ligand (stem cell factor) at least in part because o

140 ss-of-function mutations in Kit receptors or Kit ligand (stem cell factor), ICC failed to develop in

141 kout (-/-) mice after stimulation with the c-Kit ligand, stem cell factor (SCF), an important regulat

142 rted that repetitive administration of the c-kit ligand, stem cell factor (SCF), can increase mast ce

143 The KIT ligand, stem cell factor (SCF), is critical for mast

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

145 nohistochemistry, expression levels of the c-kit ligand, stem cell factor, in skin and epidermis are

146 of Kit after mast cells were exposed to the Kit ligand, stem cell factor.

147 nced by long-term treatment of mice with the kit ligand, stem cell factor.

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

149 f p85alpha gene products partially inhibited Kit ligand/stem cell factor-induced secretory granule ex

150 t-derived growth factor B, stem cell factor (kit ligand), stromal-derived factor 1, and vascular endo

151 egulatory region of the KITLG gene (encoding KIT ligand) that is significantly associated with common

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

153 themselves, but must be capable of providing KIT ligand, the cognate ligand for the tyrosine kinase r

154 to vascular endothelial growth factor and c-kit ligand these precursors give rise to colonies contai

155 s) transduced with FIH-1 were treated with c-kit ligand to establish further a FIH-1/c-kit interactio

156 ony-stimulating factor (G-CSF ) treatment or kit ligand treatment leads to significant enhancement of

157 sed levels of phosphorylated MAP Kinase when KIT ligand was added to culture.

158 f specific cytokines in response to IgE or c-Kit ligand was markedly reduced in MEKK2(-/-) ESMC relat

159 d only in oocytes during cyst breakdown, but KIT ligand was present in both oocytes and somatic cells

160 ced by the critical mast cell growth factor, kit ligand, which is produced by fibroblasts and other s

161 ium with thrombopoietin, flk-2 ligand, and c-kit ligand, with or without IL-3 and found that CAFCs cu

162 tivity of these progenitors to steel factor (KIT ligand) without affecting interleukin-3 response, wh