Tyrosine-protein kinase JAK2 (EC 2.7.10.2; UniProt Q62120; also known as JAK-2, Janus kinase 2) is encoded by the Jak2 (also known as Fd17) gene (Gene ID 16452) in murine species. JAK2 belongs to the family of non-receptor Janus tyrosine kinases that regulate a spectrum of cellular functions downstream of activated cytokine receptors in the lympho-hematopoietic system. Immunological stimuli, such as interferons and cytokines cause the recruitment of Stat transcription factors to cytokine receptor. Subsequent phosphorylation by receptor-associated JAK2 causes Stat dimerization, nuclear translocation, and Stat-mediated target genes transcription. The canonical JAK/Stat pathway is integral to maintaining a normal immune system by stimulating proliferation, differentiation, survival, and host resistance to pathogens. Altering JAK/Stat signaling to reduce immune cells cytokine responses represents an attractive target for anti-inflammatory therapies. Within the JAK2 kinase domain, there is a region that has considerable sequence homology to the regulatory region of the insulin receptor.
Immunogen
Epitope: Residues 758-776
KLH-conjugated linear peptide corresponding to residues 758-776 of mouse JAK2.
Application
Research Category Signaling
Research Sub Category Developmental Signaling
Quality
Evaluated by Western Blotting in RAW264.7 cell lysate.
Western Blotting Analysis: 0.5 µg/mL of this antibody detected JAK2 in 10 µg of RAW264.7 cell lysate.
Target description
~130 kDa observed. Uncharacterized band(s) may appear in some lysates.
Physical form
Format: Purified
Protein A purified
Purified rabbit polyclonal antibody in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Storage and Stability
Stable for 1 year at 2-8°C from date of receipt.
Other Notes
Concentration: Please refer to lot specific datasheet.
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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JAK2-V617F plays a key role in the pathogenesis of myeloproliferative neoplasm. However, its inhibitor ruxolitinib has shown limited clinical efficacies because of the ruxolitinib-persistent proliferation of JAK2-V617F-positive cells. We here demonstrate that the USP9X inhibitor WP1130 or EOAI3402143 (G9) inhibited
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