ライフサイエンスコーパス: c-Kit

1 ibodies (mAbs) that bind cell-surface CD117 (c-Kit).

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

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

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

5 y quantitative real-time PCR for chymase and c-kit.

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

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

8 utations with KI and KO, or imprecise KI, of c-kit.

9 inhibitor against unactivated and activated c-KIT.

10 n activating mutations in a single oncogene, c-Kit.

11 ting further cooperation between miR-155 and c-Kit.

12 ydrolase), ERalpha (a nuclear receptor), and c-KIT (a kinase).

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

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

15 n complete tumor regression, indicating that c-Kit activity is crucial in the oncogenic process.

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

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

18 c-Kit and CCR6 define this ILC2 subpopulation that exhib

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

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

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

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

23 Two receptor tyrosine kinases, c-KIT and fms-tyrosine kinase (FLT3), are frequently mut

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

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

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

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

28 revealed the unique binding mode of 15a with c-KIT and may elucidate its high potency in inhibiting c

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

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

31 SPRED1 binds directly to both c-KIT and to the RasGAP, neurofibromin, whose function i

32 inase (RTK)-dependent signaling event, m-SCF/c-Kit and VEGF-A/vascular endothelial growth factor rece

33 xamine the translatome in LSK (Lin(-)Sca-1(+)c-Kit(+)) and myeloid progenitor (MP; Lin(-)Sca-1(-)c-Ki

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

35 oma cells, we showed activation of EPH RTKs, c-KIT, and SFK members independent of mTORC1/2 activatio

36 ated that 15a inhibited the proliferation of c-KIT- and FLT3-driven AML cells in vitro and in vivo.

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

38 the activation loop to switch the activated c-KIT back to its structurally inactive state.

39 mprise an N-terminal EVH-1 domain, a central c-Kit-binding domain, and C-terminal SROUTY domain.

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

41 ing how a compound can inhibit the activated c-KIT by switching back to its inactive state through a

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

43 protein, SAMD14, promotes SCF/proto-oncogene c-Kit (c-Kit) signaling, erythroid progenitor function,

44 Cs), endothelial progenitor cells (EPCs) and c-Kit(+) cardiac interstitial cells (cCICs) when culture

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

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

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

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

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

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

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

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

53 Inactivation of either Foxf1 or c-Kit caused alveolar simplification.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Most c-Kit(+) cells in the renal pelvis are mast cells.

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

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

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

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

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

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

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

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

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

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

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

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

85 The majority of c-Kit(+) cells were mast cells.

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

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

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

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

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

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

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

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

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

95 )) and myeloid progenitor (MP; Lin(-)Sca-1(-)c-Kit(+)) cells.

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

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

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

99 Here, we employ a c-Kit-CreER-driven model that specifically targets McSCs

100 c-KIT proteins (c-KIT(WT), c-KIT(D816V), and c-KIT(D816H)) to select aptamers from a random RNA pool

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

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

103 hibit the in vitro kinase activity of mutant c-KIT(D816V) with an IC(50) value that is 9-fold more po

104 ain of a group of c-KIT proteins (c-KIT(WT), c-KIT(D816V), and c-KIT(D816H)) to select aptamers from

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

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

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

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

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

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

111 bition against single or double mutations of c-KIT developed in GISTs.

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

113 are prototypes of stem cell factor receptor (c-KIT)-driven cancer.

114 yperoxia.Conclusions: Cell therapy involving c-KIT(+) EC progenitors can be beneficial for the treatm

115 ung.Measurements and Main Results: Pulmonary c-KIT(+) EC progenitors expressing PECAM-1, CD34, VE-Cad

116 survival, proliferation, and engraftment of c-KIT(+) EC progenitors in the neonatal lung.Measurement

117 ain unknown.Objectives: To determine whether c-KIT(+) EC progenitors stimulate alveologenesis in the

118 , neonatal hyperoxia decreased the number of c-KIT(+) EC progenitors.

119 networks shared by human and mouse pulmonary c-KIT(+) EC progenitors.

120 Adoptive transfer of c-KIT(+) ECs into the neonatal circulation increased lun

121 The transcriptomic signature of c-KIT(+) ECs was conserved in mouse and human lungs and

122 sed apoptosis and decreased proliferation of c-KIT(+) ECs.

123 Although c-KIT(+) endothelial cell (EC) progenitors are abundant

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

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

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

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

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

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

130 Interestingly, c-Kit expression is high when miR-155 is overexpressed,

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

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

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

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

135 In one MS-RO+ LCH patient, CD34+c-Kit+Flt3+ cell frequency in blood and its BRAF-mutated

136 CD34+c-Kit+Flt3+ cells from BM of MS-RO+ LCH patients produce

137 We have examined the CD34+c-Kit+Flt3+ myeloid progenitor population as potential m

138 n both high- and low-risk LCH patients, CD34+c-Kit+Flt3+ progenitor frequency in blood was higher tha

139 CD34+c-Kit+Flt3+ progenitors from blood of both high- and low

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

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

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

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

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

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

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

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

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

149 t reduced the proliferation of Lin(-)Sca-1(+)c-Kit(+) hematopoietic stem and progenitor cells in the

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

151 induced gene activation include c-MYC, KRAS, c-KIT, HIF-1alpha, PDGF-A and hTERT.

152 c-Kit(+) ICs are a minor population of ICs in murine ren

153 PDGFRalpha(+) ICs were distinct from c-Kit(+) ICs in the renal pelvis.

154 ontaneous Ca(2+) transients were observed in c-Kit(+) ICs, smMHC(+) PDGFRalpha cells and smMHC(-) PDG

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

156 h factor-beta in promoting the conversion of c-Kit(-) ILC2s into RORgammat-expressing cells by induci

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

158 iferation and induced apoptosis by targeting c-KIT in c-KIT-mutant GIST cell lines.

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

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

161 CC-PDX xenograft tumor-bearing mice with the c-Kit inhibitor imatinib significantly reduced tumor gro

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

163 3beta inhibitor) and Dasatinib (Abl, Src and c-Kit inhibitor) were found to confer miPSCs with the CS

164 s and pelvis-kidney junction regions whereas c-Kit(+) interstitial cells (CD117(+) /CD45(-) ) are fou

165 ontaneous Ca(2+) transients were observed in c-Kit(+) interstitial cells, smMHC(+) PDGFRalpha cells a

166 PDGFRalpha(+) cells are distinct from c-Kit(+) interstitial cells.

167 uired mutations that constitutively activate c-KIT is a significant challenge in the treatment of pat

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

169 may elucidate its high potency in inhibiting c-KIT kinase activity.

170 40-fold selectivity toward FLT3 relative to c-Kit kinase, which might reduce myelosuppression toxici

171 wed the potential to distinguish between the c-KIT kinases by modulating the phosphorylation activity

172 in BCR-ABL1+ CD150+ lineage-negative Sca-1+ c-Kit+ leukemic cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 p12KO) We found that NOD/SCID/gamma(C) (-/-) c-kit(+) mice engrafted with human tissues 1 day after b

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 ly higher level of receptor tyrosine kinase (c-Kit) mRNA.

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

196 and induced apoptosis by targeting c-KIT in c-KIT-mutant GIST cell lines.

197 oreover, 10a can effectively inhibit various c-KIT mutants and the proliferation of several GIST cell

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

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

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

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

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

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

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

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

206 70% (P 5 .12) for patients with and without c-KIT mutations, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 he age-dependent reparative effects of human c-kit+ progenitor cells (hCPCs) in a rat model of juveni

239 at we may be able to identify patients whose c-kit+ progenitor cells exceed or underperform expectati

240 We performed RNA sequencing from c-kit+ progenitor cells isolated from 32 patients, inclu

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

242 lied against the kinase domain of a group of c-KIT proteins (c-KIT(WT), c-KIT(D816V), and c-KIT(D816H

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

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

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

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

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

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

249 rine production of SCF activates a transient c-kit receptor in keratinocytes.

250 Transient activation of the c-kit receptor induces the expression of growth factors

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

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

253 The c-KIT receptor represents an attractive target for cance

254 Although c-Kit receptor signaling promotes angiogenesis in multip

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

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

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

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

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

260 (+) cells is also necessary to maintain many c-kit(+)-restricted hematopoietic progenitors.

261 ice with dasatinib or imatinib, which target c-Kit, resulted in complete tumor regression, indicating

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

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

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

268 Samd14-Enh deletion reduces anemia-dependent c-Kit signaling by lowering SAMD14 levels, we developed

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

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

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

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

273 SAMD14 to increase colony-forming activity, c-Kit signaling, and progenitor survival.

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

275 MD14 expression at endogenous levels rescued c-Kit signaling.

276 , SAMD14, promotes SCF/proto-oncogene c-Kit (c-Kit) signaling, erythroid progenitor function, and ery

277 uggesting there is no role for cardiomyocyte c-Kit signalling in pathological LV remodelling followin

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

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

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

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

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

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

290 tor-like protein (PDGFR) alpha and beta, and c-KIT tyrosine kinases.

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 Expression of FOXF1 and c-KIT was decreased in the lungs of infants with BPD.

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

296 The expression of stem cell factor receptor, c-Kit, was low basally in cardiomyocytes and did not cha

297 tive warhead is employed to target Cys788 in c-KIT, where acrylamide has previously failed to form co

298 kinase domain of a group of c-KIT proteins (c-KIT(WT), c-KIT(D816V), and c-KIT(D816H)) to select apt

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-