HCK Rabbit Polyclonal Antibody

CAT#: TA327260

HCK Rabbit Polyclonal Antibody

Product Images

Western blot analysis of extracts of HL-60 cell lines, using HCK antibody.

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  Immunofluorescence analysis of A549 cell using HCK antibody. Blue: DAPI for nuclear staining.

Specifications

Product Data

• Applications: ICC/IF, WB
• Recommended Dilution: WB 1:500 - 1:2000;IF 1:10 - 1:100
• Reactivities: Human
• Host: Rabbit
• Isotype: IgG
• Clonality: Polyclonal
• Immunogen: Recombinant protein of human HCK
• Formulation: Store at -20C or -80C. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3
• Concentration: lot specific
• Purification: Affinity purification
• Conjugation: Unconjugated
• Storage: Store at -20°C as received.
• Stability: Stable for 12 months from date of receipt.
• Predicted Protein Size: 57 kDa
• Gene Name: HCK proto-oncogene, Src family tyrosine kinase
• Database Link:
  NP_002101
  Entrez Gene 3055 Human
  UniProt ID P08631
• Background: Hck (hemopoietic cell kinase) is a protein tyrosine kinase of the Src family prominently expressed in the lymphoid and myeloid lineages of hemopoiesis. It participates in transducing a variety of extracellular signals, which ultimately affect cellular processes including proliferation, differentiation and migration.The well-defined modular structure of Hck comprises a relatively divergent, NH2-terminal "unique" domain, which is subject to post-translational lipid modifications thereby targeting Hck to the plasma membrane. Src homology 3 (SH3) and 2 (SH2) domains, and a tyrosine kinase catalytic domain follow the "unique" domain. The catalytic activity of Hck is regulated, both positively and negatively, by tyrosine phosphorylation of highly conserved tyrosine (Y) residues. Phosphorylation of a single conserved Tyr499 residue in the COOH terminus of Hck by the protein kinase Csk renders Hck inactive as a result of an intramolecular interaction between the phosphorylated tyrosine (pY) residue and its own SH2 domain. Disruption of this interaction, either as a result of dephosphorylation, or substitution of the COOH-terminal regulatory Y residue with phenylalanine (F; e.g., HckY499F), or COOH-terminal truncation mutations as observed in the virally transduced v-Src oncoprotein, results in constitutive activation of Hck. In contrast to phosphorylation of the COOH-terminal regulatory tyrosine residue, autophosphorylation of a tyrosine residue (Tyr388) within the kinase domain of Hck acts to positively regulate its catalytic activity. Thus, activation of Hck requires both disruption of the COOH-terminal regulatory tyrosine-SH2 domain interaction and autophosphorylation of the regulatory tyrosine residue within the kinase domain. The dysfunction or dysregulation of Hck may contribute to the pathogenesis of some human leukemias.
• Synonyms: JTK9

Reference Data

• Protein Families: Druggable Genome, Protein Kinase
• Protein Pathways: Chemokine signaling pathway, Fc gamma R-mediated phagocytosis