HCK Rabbit Polyclonal Antibody
CNY 1,999.00
CNY 2,700.00
CNY 300.00
CNY 1,430.00
CNY 2,900.00
CNY 6,650.00
CNY 3,080.00
CNY 3,080.00
Specifications
Product Data | |
Applications | ICC/IF, WB |
Recommend Dilution | WB 1:500 - 1:2000;IF 1:10 - 1:100 |
Reactivity | Human |
Host | Rabbit |
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 Condition | Store at -20°C as received. |
Predicted Protein Size | 57 kDa |
Gene Name | HCK proto-oncogene, Src family tyrosine kinase |
Database Link | |
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 |
Documents
Product Manuals |
FAQs |
SDS |
Resources
抗体相关资料 |