research use only

Phospho-c-Kit (Tyr703) Antibody [K16C2]

Cat.No.: F0654

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:50
    Application
    WB, IP
    Reactivity
    Human
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    145 kDa
    Positive Control H526 cells (SCF-treated)
    Negative Control H526 cells

    Datasheet & SDS

    Biological Description

    Specificity
    Phospho-c-Kit (Tyr703) (D12E12) Rabbit mAb detects endogenous levels of total c-Kit protein only when it is phosphorylated at Tyr703.
    Clone
    K16C2
    Synonym(s)
    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
    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
    • https://pubmed.ncbi.nlm.nih.gov/10377264/
    • https://pubmed.ncbi.nlm.nih.gov/22437942/

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