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

9 ling, matrix metalloproteinase-9 and 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 globulin (B2M) that elicits the release of c-KIT ligand and interleukin-7 that greatly accelerate pos

21 nt through adulthood, we demonstrate that PC Kit Ligand and MLI Kit are required for, and capable of

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

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

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

25 -3 to the combination of steel factor (SF, c-kit ligand) and IL-11 abrogated the B-lymphoid potential

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

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

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

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

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

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

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

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

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

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

36 ne kinase Kit and the trans-membrane protein Kit Ligand by discrete populations of neurons in the mam

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 Conversely, misexpression of c-Kit ligand in the skin in larval zebrafish induced incre

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

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

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

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

71 stellate and basket cells), while cerebellar Kit Ligand is selectively expressed by a target of their

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

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

74 ly, these works in mice demonstrate that the Kit Ligand/Kit receptor dyad sustains mammalian central

75 ecline in signaling mediated by adiponectin, kit ligand (KITL) and insulin-like growth factor 1 (IGF1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 Kit ligand (KL) stimulation resulted in transient tyrosi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 , P-cadherin signaling, neuromediators, HGF, KIT ligand secretion, and autophagic flux.

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

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

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

146 ivation by its ligand stem cell factor (SCF, kit ligand, steel factor) alter prostate cancer aggressi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 nd localization to anatomical niches rich in KIT ligand, the major mast cell growth and survival fact

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

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

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

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

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

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

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

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

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