Ignet

Gene Information

Gene symbol: KIT

Gene name: v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog

HGNC ID: 6342

Synonyms: CD117, SCFR, C-Kit

Related Genes

#	Gene Symbol	Number of hits
1	ABL1	1 hits
2	AHR	1 hits
3	AKT1	1 hits
4	CASP3	1 hits
5	CD44	1 hits
6	CSF1	1 hits
7	CSF1R	1 hits
8	CSF2	1 hits
9	FLT3	1 hits
10	IL2RA	1 hits
11	IL6	1 hits
12	INDO	1 hits
13	JUP	1 hits
14	KITLG	1 hits
15	MAPK1	1 hits
16	MAPK10	1 hits
17	PDGFRB	1 hits
18	PIK3CA	1 hits
19	PTK2B	1 hits
20	SNRPE	1 hits
21	SRC	1 hits
22	STAT3	1 hits
23	TEC	1 hits

Related Sentences

#	PMID	Sentence
1	9627131	CD4-CD8-C.B-17 SCID thymocytes enter the CD4+CD8+ stage in the presence of neonatally grafted T cells.
2	9627131	In these mice, the thymus size was correlated to the CD4-CD8- (double negative; DN) to CD4+CD8+ (double positive; DP) cell ratio, where at 2 months p.i., 8 out of 16 treated SCID mice contained 5 x 10(6) cells or more and also possessed the highest frequencies of endogenous DP cells (25-95%).
3	9627131	Furthermore, these thymocytes were developmentally blocked at the DP stage, occasionally in combination with the expression of CD25, CD44 and CD117 but in the absence of T-cell receptor (TCR) expression.
4	11495816	Produced from the 2-phenylaminopyrimidine class, a novel synthetic inhibitor, identified as CGP57148 (STI571), inhibits tyrosine kinase activity of c-ABL, BCR-ABL, PDGF-R and c-kit at micromolar concentrations.
5	12134042	Consistent with increased c-Kit expression, KHSV-infected DMVEC displayed enhanced proliferation in response to the c-Kit ligand, stem cell factor (SCF).
6	12134042	Inhibition of c-Kit activity with either a pharmacological inhibitor of c-Kit (STI 571) or a dominant-negative c-Kit protein reversed SCF-dependent proliferation.
7	12134042	Consistent with increased c-Kit expression, KHSV-infected DMVEC displayed enhanced proliferation in response to the c-Kit ligand, stem cell factor (SCF).
8	12134042	Inhibition of c-Kit activity with either a pharmacological inhibitor of c-Kit (STI 571) or a dominant-negative c-Kit protein reversed SCF-dependent proliferation.
9	12483109	These include chromosomal translocations affecting RUNX1-CBFbeta, RARalpha, and MLL.
10	12483109	There are known activating mutations in the genes for the receptor tyrosine kinases FLT3, KIT, and FMS.
11	12483109	Targeted therapies include targeted antibody therapy; inhibitors of FLT3, KIT, and farnesyltransferase; diphtheria toxin conjugated to the granulocyte-macrophage colony-stimulating factor; and antisense oligonucleotides.
12	12483109	These include chromosomal translocations affecting RUNX1-CBFbeta, RARalpha, and MLL.
13	12483109	There are known activating mutations in the genes for the receptor tyrosine kinases FLT3, KIT, and FMS.
14	12483109	Targeted therapies include targeted antibody therapy; inhibitors of FLT3, KIT, and farnesyltransferase; diphtheria toxin conjugated to the granulocyte-macrophage colony-stimulating factor; and antisense oligonucleotides.
15	14976038	In the current study, we tested whether higher numbers of hematopoietic stem cells correlate with the speed of immune reconstitution in a congenic transplantation model (C57BL/Ka, CD45.1, Thy1.1-->C57BL/6, CD45.2, Thy1.2) using purified hematopoietic stem cells (c-Kit(+)Thy1.1(low)Lin(-/low)Sca-1(+)).
16	14976038	Phenotypic analyses in peripheral blood and spleen demonstrated that higher numbers of infused stem cells are associated with more rapid regeneration of T cells (CD4(+), CD8(+), naive CD4(+), naive CD8(+)) and B cells at early time points.
17	19501868	Despite this upregulation of c-Kit, receptor activation and phosphorylation of downstream effectors such as MAP Kinase Erk 1/2 and GSK-3 still requires the addition of exogenous c-Kit ligand, stem cell factor (SCF).
18	19501868	These data indicate that KSHV does not induce constitutive c-Kit signaling, but instead upregulates c-Kit receptor levels, thus allowing infected ECs to respond to endogenous and exogenous SCF.
19	19501868	Despite this upregulation of c-Kit, receptor activation and phosphorylation of downstream effectors such as MAP Kinase Erk 1/2 and GSK-3 still requires the addition of exogenous c-Kit ligand, stem cell factor (SCF).
20	19501868	These data indicate that KSHV does not induce constitutive c-Kit signaling, but instead upregulates c-Kit receptor levels, thus allowing infected ECs to respond to endogenous and exogenous SCF.
21	21421113	Activating mutations in B-Raf and c-kit are associated with clinical response to the specific kinase inhibitors PLX4032 and imatinib, respectively.
22	22661045	In addition to the Bcr-Abl1 oncoprotein, TKIs also inhibit off-target kinases (e.g. c-kit, Src, Tec), some of them having physiological functions in immune responses.
23	24144734	A functional c-Kit/Kit ligand (KitL) signalling network is required for tumour angiogenesis and growth, and therefore the c-Kit/KitL system might well be a suitable target for the cancer immunotherapy approach.
24	24734217	Dasatinib (DAS) is a potent inhibitor of the BCR-ABL, SRC, c-KIT, PDGFR, and ephrin tyrosine kinases that has demonstrated only modest clinical efficacy in melanoma patients.
25	24734217	The superior efficacy of the combinatorial treatment regimen included a reduction in hypoxic-signaling associated with reduced levels of immunosuppressive CD11b⁺Gr1⁺ myeloid-derived suppressor cells (MDSC) and CD4⁺Foxp3⁺ regulatory T (Treg) populations in the melanoma microenvironment.
26	25822986	Imatinib mesylate (Gleevec) inhibits Abl1, c-Kit, and related protein tyrosine kinases (PTKs) and serves as a therapeutic for chronic myelogenous leukemia and gastrointestinal stromal tumors.
27	25822986	Whereas progenitor differentiation relies on partial inhibition of c-Kit by imatinib, lineage commitment depends upon inhibition of other PTKs.
28	25822986	Imatinib mesylate (Gleevec) inhibits Abl1, c-Kit, and related protein tyrosine kinases (PTKs) and serves as a therapeutic for chronic myelogenous leukemia and gastrointestinal stromal tumors.
29	25822986	Whereas progenitor differentiation relies on partial inhibition of c-Kit by imatinib, lineage commitment depends upon inhibition of other PTKs.
30	26343197	This review provides an appraisal of some of the key signaling pathways that may contribute to immune suppression in ovarian cancer, with a particular focus on the potential involvement of the c-KIT/PI3K/AKT, wnt/β-catenin, IL-6/STAT3 and AhR signaling pathways in regulation of indoleamine 2,3-dioxygenase expression in tumor-associated macrophages.