JAK2 is a tyrosine kinase involved in signaling through cytokine receptors (e.g., erythropoietin, thrombopoietin). Mutations such as JAK2 V617F drive myeloproliferative neoplasms (MPNs) like myelofibrosis and polycythemia vera . Monoclonal antibodies are engineered to bind specific epitopes of JAK2, enabling precise detection or neutralization.
Specificity: Engineered to avoid cross-reactivity with JAK1, JAK3, or Tyk2 .
Applications: Western blot (WB), immunofluorescence (IF), immunoprecipitation (IP), and immunohistochemistry (IHC) .
Therapeutic Potential: Targeting mutant JAK2 (e.g., JAK2 V617F) in MPNs .
JAK2 monoclonal antibodies are widely used to study JAK2 expression, phosphorylation, and signaling pathways.
Rheumatoid Arthritis: JAK2 expression is elevated in inflammatory cells (macrophages, neutrophils) and mast cells in rat adjuvant-induced arthritis models .
Cancer Biology: JAK2 antibodies confirm JAK2 overexpression in myeloid malignancies and its role in STAT5 activation .
Several antibodies are validated for research, each with distinct characteristics.
While JAK2 inhibitors (e.g., ruxolitinib) dominate MPN treatment, monoclonal antibodies offer complementary mechanisms:
Targeted Depletion: Antibodies bind mutant JAK2 (e.g., JAK2 V617F), inducing apoptosis in neoplastic cells .
Immune Modulation: Enhance anti-tumor immunity by blocking PD-L1 expression on MPN cells .
Myelofibrosis: A novel monoclonal antibody (preclinical) reduces CALR-mutant cells and improves splenomegaly .
MPNs: Deleting JAK2 V617F via dual-recombinase systems depletes mutant hematopoietic stem cells, prolonging survival .
Cross-Reactivity: Early antibodies risk binding non-JAK2 kinases (e.g., JAK1) .
Delivery Challenges: Systemic administration required for hematologic malignancies.
Specificity: Avoiding off-target effects on JAK1/3 or other kinases .
Resistance: Chronic JAK inhibitor use may select for persistent clones .