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findings that the CD56 (show NCAM1 Proteins) and CD117 expression levels are lower in advanced stages than earlier stages and that LDH level and CD117 expression have an inverse relationship in patients with newly diagnosed multiple myeloma (MM) suggest that CD56 (show NCAM1 Proteins) and CD117 expressions may be prognostic markers for MM.
activation of KIT by a gain-of-function, somatic mutation is a novel mechanism of resistance to crizotinib in ROS1 rearranged non-small cell lung cancer
Mutational activation of Kit-, Ras/Raf (show RAF1 Proteins)/Erk (show EPHB2 Proteins)- and Akt (show AKT1 Proteins)- pathways indicate the biological importance of these pathways and their components as potential targets for therapy.
KIT exon 11 codons 557-558 deletion enhanced CXCL12 (show CXCL12 Proteins)-mediated GIST cell migration.
Data show the kinetic behavior of a G-rich sequence located within the c-KIT proximal promoter (kit2) in the presence of monovalent cations K+ and Na+.
Long-term follow-up of patients with metastatic GIST treated with regorafenib suggests particular benefit among patients with primary KIT exon 11 mutations and those with SDH-deficient GIST. Dose modifications are frequently required to manage treatment-related toxicities
c-kit-positive cells derived from right atrium tissue were associated with serum BNP
For hot spots in KIT and PDGFRA (show PDGFRA Proteins) genes, 23 out of 146 KIT/PDGFRA (show PDGFRA Proteins) wild-type cases carried mutations according to next-generation sequencing (NGS).
KIT and DNMT1 (show DNMT1 Proteins) co-expression promotes, whereas dual inactivation of them suppresses, lung cancer cell proliferation and metastatic growth in vitro and in vivo, in a synergistic manner.
Data indicate that BRAF, NRAS and C-KIT melanomas constitute distinct clinico-pathological entities.
exposure of HSPCs to SCF and diminished number of c-Kit receptors in their cell membranes do not compromise the capacity of HSPCs to reconstitute damaged hematopoietic tissue.
the stem cell gene Kit is regulated inversely from Krt5 (show KRT5 Proteins)/Krt14 (show KRT14 Proteins) by RA signaling
TPO (show THPO Proteins) and its receptor Mpl (show MPL Proteins) are dispensable for platelet survival in adult mice
Artificially applied c-kit(+) cells interact with the target organ endothelium following ischemia reperfusion injury. This interaction seems to depend on TLR-MyD88 (show MYD88 Proteins) signaling.
a critical role for PRL2 phosphatase in mediating Notch and c-Kit signals in early T cell progenitors, is reported.
These results suggest that CD44 (show CD44 Proteins)(+)CD117(+) T cells are stem cells and a specific T-cell phenotype that initially develops in the thymus, but they do not progress through DN3 and DN4 stages, lack a DP stage, and potently suppress T-cell proliferation and modulate the CTLA-4 (show CTLA4 Proteins) pathway.
we studied the efficacy of ACK2, an antibody that blocks KIT, followed by low-dose irradiation as a preconditioning regimen for hematopoietic cell transplantation using a murine model of Mucopolysaccharidosis type II.
C-kit-positive hematopoietic stem/progenitor cells expressed significantly higher of Nox1 (show NOX1 Proteins) and catalase (show CAT Proteins), but less of lactoperoxidase (show LPO Proteins) than in matured mononuclear cells.
c-KIT signaling regulates self-renewal capacity and prevents neurodifferentiation in culture.
These findings identify functional redundancy among Kit-dependent hematopoietic lineages and establish an unanticipated capacity of megakaryocytes to mediate IL-1 (show IL1A Proteins)-driven systemic inflammatory disease.
FGF7 (show FGF7 Proteins) may be an important regulator for oocyte growth and its action is mediated via the KIT/KITLG (show KITLG Proteins) signaling pathway.
mRNA expression of c-kit and SCF was decreased in gallbladder tissues in the HCD group. Consistent with the findings of RT-PCR, a lower expression level of c-kit and SCF protein was also observed in HCD animals.
Delayed enrichment for c-kit and inducing cardiac differentiation attenuated protective effects of BMSCs' transplantation in pig model of acute myocardial infarction.
Pravastatin improves function in hibernating myocardium by mobilizing CD133+ and cKit+ bone marrow progenitor cells and promoting myocytes to reenter the growth phase of the cardiac cell cycle.
c-kit is primarily expressed in the spermatogonia and spermatocytes of goat testes.
This gene encodes the human homolog of the proto-oncogene c-kit. C-kit was first identified as the cellular homolog of the feline sarcoma viral oncogene v-kit. This protein is a type 3 transmembrane receptor for MGF (mast cell growth factor, also known as stem cell factor). Mutations in this gene are associated with gastrointestinal stromal tumors, mast cell disease, acute myelogenous lukemia, and piebaldism. Multiple transcript variants encoding different isoforms have been found for this gene.
mast/stem cell growth factor receptor Kit
, p145 c-kit
, piebald trait protein
, proto-oncogene c-Kit
, proto-oncogene tyrosine-protein kinase Kit
, soluble KIT variant 1
, tyrosine-protein kinase Kit
, v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene-like protein
, Dominant white spotting
, Steel Factor Receptor
, c-kit proto-oncogene protein
, dominant spotting
, spotted sterile male
, c-kit receptor tyrosine kinase
, mast/stem cell growth factor receptor
, protein kinase
, c-kit receptor
, mast cell growth factor receptor
, c-KIT gene1
, receptor tyrosine kinase c-kit
, Mast/stem cell growth factor receptor
, Proto-oncogene c-Kit
, Tyrosine-protein kinase Kit
, caprine c-kit protein