JAK/STAT Signaling Pathway Research Reagents

The JAK/STAT pathway is the principal signaling mechanism downstream of cytokine and interferon receptors, governing immune cell development, hematopoiesis, inflammation, and host defense. Ligand binding induces receptor dimerization and activation of receptor-associated Janus kinases (JAK1, JAK2, JAK3, TYK2), which trans-phosphorylate each other and create docking sites on the receptor intracellular domain. STAT (Signal Transducer and Activator of Transcription) proteins are then recruited, phosphorylated on a conserved tyrosine residue, dimerize via reciprocal SH2–phosphotyrosine interactions, and translocate to the nucleus to drive target gene transcription. Negative regulation is mediated by SOCS (Suppressors of Cytokine Signaling) proteins, protein tyrosine phosphatases (SHP-1/2), and PIAS (Protein Inhibitors of Activated STATs). Constitutive JAK/STAT activation — through gain-of-function JAK2 V617F mutations, autocrine cytokine loops, or SOCS silencing — is a driver of myeloproliferative neoplasms, lymphomas, and solid tumor immune evasion.

Research Use Only (RUO)Not intended for diagnostic or therapeutic procedures.

abinScience provides recombinant proteins and antibodies for key JAK/STAT signaling targets — cytokine ligands, receptor chains, JAK kinases, STAT transcription factors, and pathway regulators. Available in His-tag, Fc-tag, and biotin-conjugated formats. All products are manufactured by our parent company AtaGenix Laboratories under ISO quality systems. Browse products below or contact us for custom development.

Cytokine Ligands & Receptors

IL-6 — A pleiotropic cytokine that signals through the IL-6Rα/gp130 complex to activate JAK1/2 and STAT3. IL-6 is a central mediator of acute-phase responses, B cell differentiation, and inflammatory cascades. Chronic IL-6/STAT3 signaling promotes tumor cell survival, angiogenesis, and immune evasion. IL-6 pathway blockade (tocilizumab, siltuximab) is used in rheumatoid arthritis, Castleman disease, and cytokine release syndrome management.
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IFN-γ — The sole type II interferon, signaling through the IFNGR1/IFNGR2 complex to activate JAK1/JAK2 and predominantly STAT1 homodimers. IFN-γ is the principal macrophage-activating cytokine, drives MHC class I/II upregulation, and is critical for anti-tumor and anti-viral immunity. Recombinant IFN-γ is used in macrophage polarization, antigen presentation, and immune checkpoint studies.
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EPO (Erythropoietin) — A glycoprotein hormone that signals through the homodimeric EPO receptor to activate JAK2 and STAT5, driving erythroid progenitor survival, proliferation, and terminal differentiation. EPO/EPOR/JAK2 signaling is the physiological axis disrupted in polycythemia vera (JAK2 V617F) and the pharmacological target of recombinant EPO therapies for anemia.
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IL-2 — A key T cell growth factor that signals through the IL-2Rα/β/γ_c complex to activate JAK1/JAK3 and STAT5. IL-2 drives effector T cell expansion and is required for regulatory T cell (T_reg) homeostasis. The shared γ_c (common gamma chain, IL2RG) is also used by IL-4, IL-7, IL-9, IL-15, and IL-21, making it a hub for JAK3-dependent lymphocyte signaling. Recombinant IL-2 is a standard supplement in T cell, NK cell, and TIL expansion protocols.
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Janus Kinases (JAKs)

JAK1 — The most broadly utilized JAK family member, paired with JAK2, JAK3, or TYK2 across type I/II cytokine receptor complexes. JAK1 is essential for signaling downstream of IFN-α/β, IFN-γ, IL-6 family, and γ_c-chain cytokines. JAK1 gain-of-function mutations occur in a subset of T-ALL and B-ALL. Selective JAK1 inhibitors are in clinical development for autoimmune and inflammatory diseases.
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JAK2 — A non-receptor tyrosine kinase essential for signaling by EPO, TPO, G-CSF, GM-CSF, and the IL-3/IL-5 family. The JAK2 V617F somatic mutation constitutively activates the kinase and is found in approximately 95% of polycythemia vera and 50–60% of essential thrombocythemia and primary myelofibrosis cases. Ruxolitinib, a JAK1/JAK2 inhibitor, is approved for myelofibrosis and polycythemia vera.
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JAK3 — Exclusively associated with the common gamma chain (γ_c, IL2RG), making JAK3 selectively required for lymphocyte development and function. Loss-of-function mutations in JAK3 cause autosomal recessive severe combined immunodeficiency (SCID). JAK3-selective inhibitors are being pursued as immunosuppressants with a narrower target profile than pan-JAK inhibitors.
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TYK2 — A JAK family member that pairs with JAK1 or JAK2 downstream of type I interferons (IFN-α/β), IL-12, and IL-23 receptors. TYK2 is required for Th1 and Th17 differentiation and plays a role in psoriasis, inflammatory bowel disease, and systemic lupus erythematosus. The selective TYK2 inhibitor deucravacitinib is approved for moderate-to-severe plaque psoriasis.
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STAT Transcription Factors & Negative Regulators

STAT3 — A transcription factor persistently activated in a wide range of cancers, where it drives expression of genes promoting survival (BCL-XL, MCL-1), proliferation (Cyclin D1, MYC), angiogenesis (VEGF), and immune evasion (IL-10, PD-L1). Unlike most STATs, STAT3 is considered oncogenic and is constitutively phosphorylated in many solid and hematological malignancies via autocrine IL-6/IL-10 loops or upstream kinase activation. Phospho-STAT3 (Tyr705) is a standard biomarker for pathway activation.
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STAT1 — The primary mediator of IFN-γ (STAT1 homodimer / GAF) and IFN-α/β (STAT1–STAT2 heterodimer / ISGF3) signaling. STAT1 drives expression of interferon-stimulated genes (ISGs) involved in anti-viral defense and anti-tumor immunity. STAT1 and STAT3 frequently exert opposing effects in the tumor microenvironment — STAT1 promoting immune surveillance while STAT3 suppresses it.
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STAT5A/5B — Critical mediators of cytokine signaling in hematopoiesis and lymphocyte development, activated downstream of IL-2, IL-7, EPO, TPO, and prolactin receptors. Constitutive STAT5 activation is associated with BCR-ABL+ chronic myeloid leukemia, FLT3-ITD+ acute myeloid leukemia, and JAK2 V617F-driven myeloproliferative neoplasms.
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SOCS1/SOCS3 — Suppressors of cytokine signaling that provide critical negative feedback. SOCS proteins are transcriptionally induced by STAT activation and inhibit JAK/STAT signaling through direct JAK kinase inhibition (SOCS1) or competition for receptor phosphotyrosine docking sites (SOCS3), and by targeting signaling components for proteasomal degradation via a C-terminal SOCS box. Epigenetic silencing of SOCS1 by promoter hypermethylation is observed in hepatocellular carcinoma, lymphoma, and other malignancies and contributes to constitutive JAK/STAT activation.
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References

1. O’Shea JJ, et al. The JAK-STAT pathway: impact on human disease and therapeutic intervention. Annu Rev Med. 2015;66:311-328. DOI

2. Baxter EJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet. 2005;365(9464):1054-1061. DOI

3. Yu H, Pardoll D, Bhatt DK, Jove R. STATs in cancer inflammation and immunity: a leading role for STAT3. Nat Rev Cancer. 2009;9(11):798-809. DOI

4. Yoshimura A, Naka T, Kubo M. SOCS proteins, cytokine signalling and immune regulation. Nat Rev Immunol. 2007;7(6):454-465. DOI