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Phospho-Jak1 (Tyr1034/1035) Recombinant Rabbit mAb (S-4908)

Phospho-Jak1 (Tyr1034/1035) Recombinant Rabbit mAb (S-4908)

Catalog Number: S0B6872 Application: WB Reactivity: Hu, Ms Conjugation: Unconjugated Brand: Starter
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Regular price $100 USD
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Product Details

Product Specification


Host Rabbit
Antigen Phospho-Jak1 (Tyr1034/1035)
Synonyms Tyrosine-protein kinase JAK1; Janus kinase 1 (JAK-1); JAK1A; JAK1B; JAK1
Location Membrane
Accession P23458
Clone Number S-4908
Antibody Type Recombinant mAb
Isotype IgG
Application WB
Reactivity Hu, Ms
Purification Protein A
Concentration 0.5 mg/ml
Conjugation Unconjugated
Physical Appearance Liquid
Storage Buffer

PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300

Stability & Storage

12 months from date of receipt / reconstitution, -20 °C as supplied

Dilution


application dilution species
WB 1:1000 Hu, Ms

Background

Phospho-Jak1 (Tyr1034/1035) refers to the specific phosphorylated state of tyrosine residues 1034 and 1035 within the activation loop of Janus kinase 1 (JAK1), serving as a critical molecular switch that initiates the JAK-STAT signaling pathway. Under physiological conditions, following cytokine binding to its receptor, JAK1 undergoes trans-phosphorylation with adjacent kinases (such as TYK2 or JAK3); phosphorylation of these two residues induces the kinase domain to transition from a self-inhibited, closed conformation to an open, active conformation, thereby significantly enhancing its catalytic activity. This modification not only serves as a hallmark event of JAK1 activation but is also a prerequisite for its ability to catalyze the phosphorylation of downstream STAT signaling molecules — mutations at these sites completely abolish JAK1 kinase activity. In research settings, antibodies specifically recognizing this modification are essential tools for studying immune regulation, inflammatory responses, and cancer signaling. They are used to evaluate the efficacy of JAK inhibitors (such as ruxolitinib, used to treat myelofibrosis) or to detect the molecular mechanisms underlying diseases driven by aberrant JAK1 activation, such as acute lymphoblastic leukemia.