JAK / STAT Signaling Antibody Sampler Pack

JAK / STAT Signaling Antibody Sampler Pack

The JAK / STAT Signaling Antibody Sampler Pack from Assay Genie brings together 8 rigorously validated antibodies spanning the key nodes of this pathway, supplied in a convenient 20µL trial size. It lets researchers screen an entire signalling axis in a single, cost-effective pack — validated for applications including ChIP-seq, ELISA, IF/ICC, IHC-P, IP, WB — before committing to full-size vials. Each antibody is also available individually in a full 100µL size.

The Janus kinase and signal transducer and activator of transcription (JAK-STAT) pathway is a rapid, direct conduit linking cytokine and growth factor receptors to changes in gene expression, and it is indispensable for hematopoiesis, immune cell differentiation, and inflammatory responses. Cytokine binding induces receptor dimerization and brings receptor-associated JAKs into apposition, enabling their trans-autophosphorylation. JAK1 and JAK2 are key family members that, once activated, phosphorylate tyrosine residues on the receptor cytoplasmic tail, creating docking sites for STAT proteins. Recruited STATs are themselves tyrosine-phosphorylated, dimerize through reciprocal SH2-phosphotyrosine interactions, and translocate to the nucleus to bind specific response elements. STAT1, and its phosphorylated active form Phospho-STAT1, principally drives interferon-stimulated, antiviral, and proinflammatory transcription. STAT3 and Phospho-STAT3 integrate signals from IL-6 family and other cytokines to promote acute-phase responses, cell survival, and, when constitutively active, tumorigenesis. STAT5 transmits signals from IL-2, growth hormone, and erythropoietin to regulate lymphocyte proliferation and survival. Signal duration is constrained by negative regulators, most notably suppressor of cytokine signaling 3 (SOCS3), a feedback-induced protein that binds activated receptors and JAKs to inhibit further phosphorylation and target them for degradation. Aberrant JAK-STAT activity, whether through activating JAK mutations, persistent STAT3 signaling, or loss of SOCS feedback, contributes to myeloproliferative neoplasms, leukemias, solid tumors, and autoimmune and inflammatory disorders, which is why JAK inhibitors have become important clinical agents. Dissecting this pathway requires the ability to track both total and phosphorylated kinase and transcription factor pools simultaneously. This sampler pack brings together validated antibodies against JAK1, JAK2, STAT1, Phospho-STAT1, STAT3, Phospho-STAT3, STAT5, and SOCS3 for studying cytokine-driven JAK-STAT signaling and its negative regulation.