ライフサイエンスコーパス: c-Kit

1 as well as stem cell factor receptor CD117 (c-kit).

2 g, by targeting the receptor tyrosine kinase c-KIT.

3 high levels of the stem cell factor receptor c-Kit.

4 ted by ACK2, a neutralizing antibody against c-kit.

5 duct 9.5 (PGP 9.5), and the mast cell marker c-kit.

6 egulation of the IL3-Ralpha receptor but not c-Kit.

7 functions via the MC growth factor receptor c-Kit.

8 mouse basal cells selected for expression of c-KIT.

9 ple-immunofluorescence staining, we detected c-kit (a marker of cell transdifferentiation) positive d

10 ere we show that progenitor cells expressing c-Kit, a receptor tyrosine kinase marking stem cells in

11 nt and previously unrecognized site of adult c-Kit activity.

12 into functionally distinct subsets based on c-Kit activity.

13 otocol describes the isolation of endogenous c-Kit (also known as CD117)-positive (c-Kit(+)), CD45-ne

14 The receptor tyrosine kinase c-Kit, also known as the stem cell factor receptor, play

15 zyme B and CD107A), resistance to apoptosis (c-KIT and Bcl2), and enhanced stemness (beta-catenin and

16 Furthermore, in addition to increased c-Kit and CD133, Scf and EpCam expression were also incr

17 ignaling resulted in increased expression of c-Kit and CD133.

18 Inhibition of c-KIT and FLT3 expression significantly inhibited JAK/ST

19 AML LSCs, including receptor tyrosine kinase c-KIT and FMS-related tyrosine kinase 3 (FLT3).

20 rrelate with increased surface expression of c-Kit and IL-7 receptors on the IL-18-treated cells.

21 lopment, presumably via interaction with the c-Kit and IL-7 signaling axis.

22 d Cd25(+)-expressing cells and downregulated c-Kit and IL-7Ralpha intensities.

23 +) NK cells do not express the early markers c-kit and IL-7Ralpha, nor killer cell Ig-like receptors

24 ed treatment time points suggested increased c-Kit and PI3K/AKT pathway activation in resistant tumor

25 Activation of the c-kit and platelet-derived growth factor (PDGF) receptor

26 row transplantation could quickly knock down c-kit and PU.1 genes in hematopoietic stem and progenito

27 is platform simultaneously knocked down both c-Kit and PU.1 genes in the same primary cell population

28 Although the expression of c-Kit and PW1 showed little overlap in normal hearts, a

29 +) transgenic mice and were shown to express c-kit and Sca-1 as well as 8 paracrine factors involved

30 10(-)CD161(+) cells that transiently express c-Kit and stably express P-glycoprotein (P-gp)/multi-dru

31 progenitor cell regulation (stem cell factor/c-Kit), and c-Kit rescued Samd14 loss-of-function phenot

32 rrow HSPCs, operationally defined as the Lin-c-Kit+ and Lin-Sca-1+c-Kit+ populations, express negligi

33 observed among the inflammatory infiltrate, c-kit, and tryptase in individuals both with and without

34 gand (KitL) and its tyrosine kinase receptor c-kit are critical for germ cells, melanocytes, mastocyt

35 r receptors, VEGF receptors, PDGFR-beta, and c-KIT, as second-line therapy both in patients with FGFR

36 While c-kit blocking antibodies prevented spreading, imatinib

37 le complexes, which resisted dissociation by c-kit blocking mAbs and provided cell anchorage under ph

38 rived hematopoietic stem cells reconstituted c-kit but not MAT in Kit(W/W-v) mice.

39 Kinase inhibition of c-kit by imatinib reduced cluster coalescence, but allow

40 Juvenile mice with mutated c-Kit (c-Kit(Wv/+)) showed impaired islet vasculature an

41 Here we analyzed whether c-kit can function both as an adhesion and signaling rec

42 Autologous c-kit(+) cardiac progenitor cells (CPCs) are currently u

43 he repair of ischemic myocardium and whether c-kit(+) cardiac progenitor cells (CPCs) function can be

44 ABSTRACT: Therapeutic use of c-kit(+) cardiac progenitor cells (CPCs) is being evalua

45 unction of aged stem cells and in particular c-kit(+) cardiac progenitor cells (CPCs).

46 LE: Autologous stem cell therapy using human c-Kit(+) cardiac progenitor cells (hCPCs) is a promising

47 ow-derived mesenchymal stem cells (MSCs) and c-kit(+) cardiac stem cells (CSCs) improve left ventricu

48 topics of recent debates-the contribution of c-Kit(+) cardiac stem cells to cardiomyocytes in the hea

49 aging associated with cellular senescence in c-kit+ cardiac progenitor cells (CPCs).

50 e activity, and enhanced expression of CD90, c-Kit (CD117), integrin alpha6 (CD49f), and CXCR4 (CD184

51 ly controls expression of Pecam-1 (CD31) and c-kit (CD117).

52 nd contained a proliferative (Ki67(+)) Lin(-)c-Kit(+)CD135(-)CD115(+)CX3CR1(+)Ly6C(+)CD11b(-) subpopu

53 on myeloid progenitors (CMPs) (Lin(-)Sca-1(+)c-Kit(+)CD34(+)CD41(hi)) establish an early branch point

54 ti-potent progenitors (LMPPs) (Lin(-)Sca-1(+)c-Kit(+)CD34(+)Flt3(hi)) and common myeloid progenitors

55 bilized increased number of lineage-negative c-Kit+, CD34+, and CD133+ stem cells.

56 acrophage progenitor (pre-GM) (Lin(-)Sca-1(-)c-Kit(+)CD41(-)FcgammaRII/III(-)CD150(-)CD105(-)).

57 whereas the P/-8-kb enhancer targeted TIE2+/c-KIT+/CD41- endothelial cells that were enriched for he

58 The c-Kit(+)CD45(-) eCSC population is isolated by magnetic-

59 The c-Kit(+)CD45(-) eCSCs exhibit the defining characteristi

60 We also describe how to characterize c-Kit(+)CD45(-) eCSCs.

61 genous c-Kit (also known as CD117)-positive (c-Kit(+)), CD45-negative (CD45(-)) cardiac stem cells (e

62 e Kit (c-Kit) expression that enriches for 2 c-Kit(+) cell populations yielding a mixture of cardiac

63 an induced pluripotent stem cells stimulated c-kit(+) cell recruitment to BZ and the rate of bromodeo

64 icantly promoted BM-derived stem cell (GFP(+)c-kit(+) cell) recruitment into the infarcted heart and

65 ytes, endothelial cells, myofibroblasts, and c-Kit + cells present in the border zone of the remodeli

66 By contrast, c-kit(+) cells amply generated cardiac endothelial cells

67 e of bromodeoxyuridine incorporation in both c-kit(+) cells and cardiomyocytes (P<0.05).

68 us to image thousands of alpha-catulin-GFP(+)c-kit(+) cells and to digitally reconstruct large segmen

69 Although cardiac c-kit(+) cells are being tested in clinical trials, the

70 ed mice, indicating that alpha-catulin-GFP(+)c-kit(+) cells are comparable in HSC purity to cells obt

71 ogical analyses confirmed the recruitment of c-kit(+) cells as well as a reduced degree of apoptosis

72 on of SCF post-MI induces the recruitment of c-kit(+) cells at the infarct border area acutely.

73 Here we test the lineage potential of c-kit(+) cells by inducible genetic lineage tracing.

74 Thus, endogenous c-kit(+) cells can generate cardiomyocytes within the he

75 oaches in mice to examine whether endogenous c-kit(+) cells contribute differentiated cardiomyocytes

76 Endogenous c-kit(+) cells did produce new cardiomyocytes within the

77 We find that c-kit(+) cells do not contribute to lung epithelium duri

78 Furthermore, Asxl1(-/-) Lin(-)c-Kit(+) cells exhibited decreased global levels of H3K2

79 nges at multiple time points in Lin(-)Sca1(+)c-kit(+) cells from mice transplanted with bone marrow c

80 We isolated c-kit(+) cells from young (3 months) and aged (24 months

81 hat approximately 30% of alpha-catulin-GFP(+)c-kit(+) cells give long-term multilineage reconstitutio

82 a significant decrease in lineage(-) Sca(+) c-Kit(+) cells in bone marrow.

83 ng endothelial progenitor cells-like CD31(+)/c-Kit(+) cells in mice following hindlimb ischaemia.

84 of the existence of vascular and mesenchymal c-kit(+) cells in normal hearts.

85 Thus, our work strongly suggests that c-kit(+) cells in the murine heart are endothelial cells

86 es that determine lineage differentiation of c-kit(+) cells in vivo are unknown.

87 gical stimuli induce different cell fates of c-kit(+) cells in vivo.

88 The distribution of alpha-catulin-GFP(+)c-kit(+) cells indicated that HSCs were more common in c

89 overall rate of cardiomyocyte formation from c-kit(+) cells is still below clinically relevant levels

90 ent findings suggest that endogenous cardiac c-kit(+) cells rarely contribute cardiomyocytes to the a

91 istically, doxorubicin-induced DNA damage in c-kit(+) cells resulted in expression of p53.

92 After acute cardiac injury, c-kit(+) cells retain their endothelial identity and do

93 Single-cell sequencing of cardiac CD45(-)c-kit(+) cells showed innate heterogeneity, indicative o

94 Moreover, RNA sequencing of c-Kit(+) cells showed that CHD7 functions mostly through

95 f wild-type and premalignant Tet2(-/-) Lin(-)c-Kit(+) cells shows higher mutation frequencies in Tet2

96 e show that p53 is central to the ability of c-kit(+) cells to adopt cardiomyocyte fates, which could

97 ll sequencing and genetic lineage tracing of c-kit(+) cells to determine whether various pathological

98 Previously, cardiac c-kit(+) cells were reported to be CSCs with a potential

99 atopoietic stem and progenitor cells (Sca1(+)c-Kit(+) cells).

100 condary assays following knockdown in murine c-Kit(+) cells, and Cxcl4(-/-) mice showed a decrease in

101 mice had significantly fewer lineage-Sca1(+)c-Kit(+) cells, short-term hematopoietic stem cells (HSC

102 further insights into the nature of cardiac c-kit(+) cells.

103 he cell cycle and increases in the number of c-Kit(+) cells.

104 erentially affect the eventual cell fates of c-kit(+) cells.

105 l stimuli would result in different fates of c-kit(+) cells.

106 preferentially generate cardiomyocytes from c-kit(+) cells.

107 row hypocellularity and the disappearance of c-kit(+) cells.

108 sis and mitosis in Lineage(-)c-Kit(+) (Lin(-)c-Kit(+)) cells, consistent with human MDS.

109 d circulatory ST6Gal-1 have marrow Lin-Sca-1+c-Kit+ cells with reduced S. nigra agglutinin reactivity

110 -kit demonstrated kinase-independent mb-KitL/c-kit clustering, anchorage, F-actin polymerization, and

111 e of crenolanib is its reduced inhibition of c-Kit compared with quizartinib.

112 d-type RhoA into the RhoA(-/-) Lin(-)Sca-1(+)c-Kit(+) compartment.

113 W/W-v) mice indicated that interleukin-3 and c-Kit contribute to expulsion of the intestinal nematode

114 cardiac commitment concurrent with increased c-kit(+) CPCs in vivo 8 weeks after in vivo transfer alo

115 y different between c-kit D816V-positive and c-kit D816V-negative patients, while 11beta-prostaglandi

116 nary NMH was significantly different between c-kit D816V-positive and c-kit D816V-negative patients,

117 ence the distribution of melanocyte markers (C-KIT, DCT, PAX3, and TYR) coupled with markers of proli

118 Mutational analysis of c-kit demonstrated kinase-independent mb-KitL/c-kit clus

119 MC precursors to the corneal limbus and that c-Kit-dependent MCs appeared to be involved in the forma

120 bilization of p53 was sufficient to increase c-kit-derived cardiomyocyte differentiation.

121 re overload resulted in a modest increase in c-kit-derived cardiomyocytes, with significant increases

122 nduced acute cardiotoxicity did not increase c-kit-derived endothelial cell fates but instead induced

123 nism-based SCF partial agonist that impaired c-Kit dimerization, truncating downstream signaling ampl

124 o-B cells showed decreased activation of the c-Kit downstream protein Src upon Sox4 deletion.

125 study, we demonstrate that signaling through c-Kit exerts distinct effects on EAE susceptibility in m

126 hematopoietic stem cells (lineage(-)Sca-1(+)c-Kit(+)) expressed high levels of IL-15, suggesting tha

127 c-kit-expressing cardiac progenitor cells have been repo

128 C-Kit-expressing pro-B cells showed decreased activation

129 ntification of the requirement for olfactory c-Kit-expressing progenitors in olfactory maintenance pr

130 studies show HSCs with low levels of surface c-Kit expression (c-Kit(lo)) and signaling exhibit enhan

131 t HCV core protein significantly upregulates c-Kit expression at the transcriptional level.

132 f-renewal potential can be isolated based on c-Kit expression during both steady state and stress hem

133 e and beta-cell dysfunction, while restoring c-Kit expression in beta-cells of c-Kit(Wv/+) mice rescu

134 Reconstituting c-Kit expression in L1-transfected cells blocked the bio

135 The concept that c-kit expression in the adult heart identifies epicardiu

136 Capsaicin did not alter c-KIT expression or nasal epithelial morphology in patie

137 ultiple reporter genes in mice, we find that c-kit expression rarely co-localizes with the expression

138 sed in both osteoclasts and osteoblasts, and c-Kit expression was decreased in W(sh)/W(sh)osteoclasts

139 ing is based on tyrosine-protein kinase Kit (c-Kit) expression that enriches for 2 c-Kit(+) cell popu

140 The tumor cells were positive for CD117 (c-kit) (Fig 1B) and DOG-1(Fig 1C).

141 ibroblasts and MC/9 mast cells, mb-KitL, and c-kit formed ligand/receptor clusters that formed stable

142 lex sequence from the promoter region of the c-KIT gene forms a stable quadruplex, as characterized b

143 e transcriptional regulatory elements of the c-Kit gene, are fertile.

144 ting with a newly identified silencer in the c-kit gene.

145 However, c-Kit(+)/Gr-1(-) cells remained viable in Runx1/Cbfb-del

146 ective mast/stem cell growth factor receptor c-Kit have suggested key roles for mast cells (MCs) in p

147 c-Kit(+) hCPCs were isolated from cardiac biopsies of mu

148 METHODS AND c-Kit(+) hCPCs were isolated from cardiac tissue of pati

149 of mast cell-deficient mice that have normal c-kit ("Hello Kitty" and MasTRECK mice) confirmed prior

150 ly expressed by HSCs, and at lower levels by c-kit(+) hematopoietic progenitors, megakaryocytes, and

151 s show that the transition from c-Kit(lo) to c-Kit(hi) HSC is negatively regulated by c-Cbl.

152 Furthermore, c-Kit(lo) and c-Kit(hi) HSCs are hierarchically organized, with c-Kit(

153 (hi) HSCs are hierarchically organized, with c-Kit(hi) HSCs arising from c-Kit(lo) HSCs.

154 In addition, whereas c-Kit(hi) HSCs give rise to long-term lymphomyeloid graf

155 functional differences between c-Kit(lo) and c-Kit(hi) HSCs persist even under conditions of stress h

156 -term reconstitution potential compared with c-Kit(hi) HSCs.

157 tissues as non-T, non-B (lineage-negative), c-Kit(+)IL-7Ralpha(+) (CD117(+)CD127(+)) cells.

158 stem and progenitor cells (lineage(-)Sca-1(+)c-Kit(+) immunophenotype) normalized.

159 MCs on cardiac function after MI, using the c-Kit-independent MC-deficient (Cpa3(Cre/+)) mice.

160 Cediranib, an inhibitor of VEGFR1-3 and c-kit, inhibited in vivo metastasis of VEGFC-overexpress

161 Treatment of mice with the c-KIT inhibitor imatinib mesylate limited effusion preci

162 The use of imatinib or dasatinib as a c-Kit inhibitor reduced the level of sphere-forming cell

163 th c-kit ligand to establish further a FIH-1/c-kit interaction via Western analysis.

164 We also found c-Kit is highly expressed in transformed human hepatocyt

165 Although c-Kit is required for HSC function, gain and loss-of-fun

166 ependent of kinase function and resistant to c-kit kinase inhibitors.-

167 Activating mutations in c-Kit lead to alteration of these cellular processes and

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

169 We reported previously that c-kit ligation by membrane-bound stem cell factor (mSCF)

170 increased apoptosis and mitosis in Lineage(-)c-Kit(+) (Lin(-)c-Kit(+)) cells, consistent with human M

171 The Lin(-)Sca1(-)c-Kit(+) (LK) population was significantly lower in Chd7

172 Furthermore, c-Kit(lo) and c-Kit(hi) HSCs are hierarchically organize

173 These functional differences between c-Kit(lo) and c-Kit(hi) HSCs persist even under conditio

174 organized, with c-Kit(hi) HSCs arising from c-Kit(lo) HSCs.

175 y, our studies show that the transition from c-Kit(lo) to c-Kit(hi) HSC is negatively regulated by c-

176 with low levels of surface c-Kit expression (c-Kit(lo)) and signaling exhibit enhanced self-renewal a

177 By targeting the c-kit locus with multiple reporter genes in mice, we fin

178 The c-Kit loss-of-function mutations in WBB6F1/J-Kit(W/W-v)

179 d in a decreased number of Lineage(-)Sca-1(+)c-Kit(+) (LSK) cells in the circulation, which was norma

180 tic progenitors, including lineage(-)Sca-1(+)c-kit(+) (LSK), common myeloid progenitor, and granulocy

181 Lineage(-)Sca-1(+)c-Kit(-) (LSK(-)) cells are a lymphoid progenitor popula

182 en of C57BL/6 mice, with a lineage(-)Sca-1(+)c-Kit(-) (LSK(-)) phenotype that proliferates in respons

183 matopoietic stem/progenitor cells (Lin-/Sca+/c-Kit+; LSK phenotype) in the AT (AT-LSK) has been repor

184 Synergies between integrin and c-kit-mediated spreading and adhesion of MC/9 cells were

185 This study examines the effects of c-Kit-mediated vascular endothelial growth factor isofor

186 These results suggest that c-Kit-mediated VEGF-A action in beta-cells plays a pivot

187 ssible secondary melanocyte germ composed of C-KIT+ melanocytes was found in the infundibulum and int

188 Flowthrough c-Kit(-) mesenchymal stem cells are positively selected

189 Among 609 differentially expressed genes, c-Kit, Met and EphA3 cytokine/tyrosine-kinase (TK) recep

190 ivated mast cell MPs (CD137(+) FcepsilonRI(+)c-kit(+)MPs) were significantly increased in NLFs of con

191 (high-affinity IgE receptor [FcepsilonRI](+)c-kit(+)MPs), and basophil MPs (CD203c(+)c-kit(-)MPs).

192 ](+)c-kit(+)MPs), and basophil MPs (CD203c(+)c-kit(-)MPs).

193 Analysis of c-Kit mRNA displayed a significant increase in the liver

194 Collectively, these results show that the c-kit/mSCF/MMP-9 axis regulates IL-23 gene expression in

195 Previous work in Il3-deficient and c-kit mutant Kit(W/W-v) mice indicated that interleukin-

196 for HSC function, gain and loss-of-function c-Kit mutants suggest that even small changes in c-Kit s

197 Cs, we used recipient embryos that carried a c-Kit mutation (W(sh)/W(sh)), which leads to a loss of m

198 umber of MC, spindle shape, CD25 expression, c-Kit mutation and sBT values >20 mug/l.

199 be analysed for their number, clonality and c-Kit mutation.

200 mast cells, the presence of aggregates, and c-kit mutation.

201 Because c-Kit mutations affect multiple cell types of both immun

202 Exome sequencing identified cooperating c-Kit mutations found only in the leukemic samples.

203 One of the two exon 11 c-kit mutations in synchronous adenocarcinomas with GIST

204 equencing analysis demonstrated that exon 11 c-kit mutations were present in two of six synchronous t

205 70% (P 5 .12) for patients with and without c-KIT mutations, respectively.

206 t the first 3 months after HSCT, rather than c-KIT mutations,was an independent factor for CIR (P5.00

207 isk for relapse, together with the impact of c-KIT mutations.

208 and was more predictive of relapse risk than c-KIT mutations.

209 We identified a novel population of c-kit-negative reparative cardiac cells (SA CMCs) that c

210 Our data suggest that c-Kit negatively regulates bone turnover, and disrupted

211 enic endothelial cell specification requires c-Kit, notch signaling, and p27-mediated cell-cycle cont

212 steoblasts, suggesting an indirect effect of c-Kit on bone formation.

213 able to suppress stem cell factor receptor (c-kit or CD117) gene expression by interacting with a ne

214 subtype 1 (TRPA1)-deficient mice but not in c-kit or proteinase-activated receptor 2 mice.

215 nts were immunohistochemically processed for c-Kit or stained with cuprolinic blue.

216 Furthermore, beta-cell-specific c-Kit overexpression (c-KitbetaTg) in aged mice showed s

217 g of migrating cells revealed a possible SCF/c-Kit paracrine mechanism contributing to migration via

218 us stimulation of the stem cell factor (SCF)/c-Kit pathway yielded high levels of gene editing in hae

219 In a pilot study, imatinib, a c-kit/PDGF-receptor inhibitor, induced partial regressio

220 Moreover, DAB2IP is able to inhibit c-kit-PI3K-Akt-mTOR signaling pathway that increases c-m

221 The receptor tyrosine kinase c-Kit plays an integral role in maintaining beta-cell ma

222 -mapping analyses show that embryonically, a c-Kit(+) population contributes to olfactory neurogenesi

223 After 1 week of culture, the c-Kit(+) population is further enriched by selection for

224 ally defined as the Lin-c-Kit+ and Lin-Sca-1+c-Kit+ populations, express negligible endogenous ST6Gal

225 sistently demonstrated salubrious effects of c-kit(pos) cardiac cells administered after myocardial i

226 this conceptual construct "string theory" of c-kit(pos) cardiac cells because it reconciles multifari

227 vantages, appearing to be more suitable than c-kit(POS) cardiac progenitor cells for widespread clini

228 Although c-kit(pos) cardiac stem cells (CSCs) preserve left ventr

229 e helps to explain the beneficial effects of c-kit(pos) cell administration to ischemically damaged h

230 s might be reconciled with recent results of c-kit(pos) cell lineage tracing studies.

231 C-kit(pos) cells derived from the first heart field exhi

232 The residual c-kit(pos) cells found in the adult heart are probably o

233 previously reported that the c-kit-positive (c-kit(POS)) cells isolated from slowly adhering (SA) but

234 more rarely cardiomyocytes, originated from c-kit positive progenitors in their murine model.

235 broblasts and adventitial cells derived from c-kit positive progenitors in their studies.

236 lls, and rare cardiomyocytes originated from c-kit positive progenitors.

237 The authors previously reported that the c-kit-positive (c-kit(POS)) cells isolated from slowly a

238 eage-negative, stem cell antigen-1-positive, c-Kit-positive) cells were quantified and proliferation

239 Accordingly, c-kit positivity, in itself, does not define the embryon

240 Instead, c-kit predominantly labels a cardiac endothelial cell po

241 normal turnover, there is relatively sparse c-Kit(+) progenitor cell (ckPC) activity.

242 It has been reported that c-kit(+) progenitor cells resident in the human lung reg

243 ere uniformly distributed in the BM, and all c-kit(+) progenitor cells were adjacent to Gr1(+) myeloi

244 The 22-mer c-kit promoter sequence folds into a parallel-stranded q

245 on of several cancer/testis antigens and the c-kit proto-oncogene throughout multiple recurrences.

246 Thus, "mechanical" activation of c-kit provides signaling, niche-anchorage, and synergies

247 vior of a G-rich sequence located within the c-KIT proximal promoter (kit2) in the presence of monova

248 (-) cells that showed cardiogenic potential, c-Kit(+)/PW1(+) cells were fibrogenic.

249 In contrast to the small proportion of c-Kit(+)/PW1(-) cells that showed cardiogenic potential,

250 he existing structures, demonstrate that the c-KIT quadruplex fold does not change with differing env

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

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

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

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

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

256 Although c-Kit receptor signaling promotes angiogenesis in multip

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

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

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

260 In cultured INS-1 cells and primary islets, c-Kit regulates VEGF-A expression via the Akt/mammalian

261 ell regulation (stem cell factor/c-Kit), and c-Kit rescued Samd14 loss-of-function phenotypes.

262 stration inhibited this activation of lin(-) c-kit(+) Sca-1(+) cells.

263 aused a remarkable increase in marrow lin(-) c-kit(+) Sca-1(+) cells.

264 tion supported the increase in marrow lin(-) c-kit(+) Sca-1(+) cells.

265 ulation of Sca-1 expression by marrow lin(-) c-kit(+) Sca-1(-) cells.

266 etic stem cells (CD150(+)/CD48(-)/Lineage(-)/c-kit(+)/Sca-1(+)) identified a large number of differen

267 FN-gamma treatment expanded bone marrow (BM) c-Kit(+)Sca1(+)Lin(-) (KSL) cell number but reduced BM K

268 actor (Gdnf) is highly expressed in Lin-CD24+c-Kit+Sca1+ stem cells.

269 ar gland, this specific population, Lin-CD24+c-Kit+Sca1+, possessed the highest capacity for prolifer

270 Purified (c-kit+/sca1+/lin-) HSCs were infused repeatedly into mic

271 ic T-cell response elicited by cryopreserved c-kit-selected hCPC.

272 ively regulates bone turnover, and disrupted c-Kit signaling couples increased bone resorption with b

273 the Akt/mTOR/VEGF-A pathway, indicating that c-Kit signaling in beta-cells is a required regulator fo

274 , when exposed to a long-term high-fat diet, c-Kit signaling in c-KitbetaTg mice induced substantial

275 t mutants suggest that even small changes in c-Kit signaling profoundly affect HSC function.

276 We show that c-KIT signaling regulates self-renewal capacity and prev

277 Samd14-Enh stimulated stem cell factor/c-Kit signaling, which promotes erythrocyte regeneration

278 ible wild-type females, indicating that both c-Kit signals and undefined male-specific factors are re

279 whether adherence to plastic alone, without c-kit sorting, was sufficient to isolate reparative CMCs

280 A-seq) in SSEA4(+) hSSCs and differentiating c-KIT(+) spermatogonia, and performed validation studies

281 T5 signaling axis and the composition of the c-Kit/STAT signalosome.

282 However, the Lin(-)Sca-1(+)c-Kit(+) stem cell compartment in E14.5 FL was not affec

283 all attention to the clinical application of c-kit(+) stem cells as lung epithelial progenitors for t

284 Inhibition of c-kit+ stem cell proliferation by inducing apoptosis exa

285 otic cell death of cardiac- and bone-derived c-kit+ stem cells in vitro and decreased the number of B

286 migrate into CCA tumor microenvironment via c-Kit/stem cell factor and increase tumor progression, a

287 tor cell-1 (HPC-1), HPC-2, and Lin(-)Sca-1(+)c-Kit(+) subpopulations.

288 d proepicardium) express different levels of c-kit, the cardiomyogenic potential of first heart field

289 onstrate a previously undescribed deficit in c-Kit(+) type 2 innate lymphoid cells (ILC2s) in W/W(v)

290 c-Kit tyrosine kinase receptor has been identified as a

291 Ectopic introduction of c-Kit variants into a Dnmt3a-deficient background produc

292 The c-Kit W(sh) mutation increased osteoclast differentiatio

293 WT, NK1R(-/-), and c-Kit(W-sh/W-sh) mice reconstituted with WT or NK1R(-/-)

294 c-Kit was expressed in both osteoclasts and osteoblasts,

295 Activating mutations in PDGF-R and c-kit were not found at baseline or at disease progressi

296 ogenitor cell percentages (Lineage(-)Sca-I(+)c-kit(+)) were also detected in the bone marrow.

297 ine differentiation; they did not develop in c-Kit(wsh/wsh) mice and were labeled with transplanted b

298 ase 1 (Tph1)-cyan fluorescent protein (CFP), c-Kit(wsh/wsh), and Neurog3Cre;ROSA(tdTom) mice by immun

299 restoring c-Kit expression in beta-cells of c-Kit(Wv/+) mice rescued islet vascular defects through

300 Juvenile mice with mutated c-Kit (c-Kit(Wv/+)) showed impaired islet vasculature and beta-