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Cat.No.: F0654
| Dilution |
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|
| Application |
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| WB, IP |
| Reactivity |
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| Human |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 145 kDa |
| Positive Control | H526 cells (SCF-treated) |
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| Negative Control | H526 cells |
| Specificity |
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| Phospho-c-Kit (Tyr703) (D12E12) Rabbit mAb detects endogenous levels of total c-Kit protein only when it is phosphorylated at Tyr703. |
| Clone |
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| K16C2 |
| Synonym(s) |
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| Mast/stem cell growth factor receptor Kit; SCFR; Piebald trait protein (PBT); Proto-oncogene c-Kit; Tyrosine-protein kinase Kit; p145 c-kit; v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog; CD117 |
| Background |
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| Phospho-c-Kit (Tyr703) marks the activated state of c-Kit, a type III receptor tyrosine kinase (RTK) essential for the survival, proliferation, and differentiation of hematopoietic stem cells, mast cells, melanocytes, and germ cells. c-Kit comprises five immunoglobulin-like extracellular domains for stem cell factor (SCF) binding, a transmembrane domain, a juxtamembrane (JM) domain, and a split kinase domain containing a kinase insert (KI) with Tyr703. Upon SCF engagement, the receptor dimerizes and undergoes sequential autophosphorylation, starting at JM residues (Tyr568/570) to relieve auto-inhibition, followed by phosphorylation of KI sites, including Tyr703. Specifically, phosphorylation at Tyr703 creates a crucial docking site for the adaptor protein Grb2, which initiates the Ras-ERK MAPK pathway to promote cellular proliferation and survival. While normal signaling regulates essential processes like hematopoiesis and melanogenesis, dysregulation through gain-of-function mutations or overexpression leads to constitutive Tyr703 phosphorylation, driving oncogenesis in gastrointestinal stromal tumors (GIST), mastocytosis, acute myeloid leukemia (AML), and melanoma. |
| References |
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