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Phospho-STAT3 (Y705) Mouse anti-Human, Mouse, FITC, Clone: LUVNKLA, eBioscience™

Mouse Monoclonal Antibody

$187.05 - $448.05

Specifications

Antigen Phospho-STAT3 (Y705)
Clone LUVNKLA
Host Species Mouse
Gene Alias Signal transducer and activator of transcription 3
Species Reactivity Human, Mouse
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 Disclaimers

For Research Use Only.

Products
Catalog Number Mfr. No. Quantity Price Quantity    

501122168

 
affymetrix
11903341
25 tests Each for $187.05

501122169

 
affymetrix
11903342
100 tests Each for $448.05
Description & Specifications

Specifications

Antigen Phospho-STAT3 (Y705)
Clone LUVNKLA
Host Species Mouse
Gene Alias Signal transducer and activator of transcription 3
Species Reactivity Human, Mouse
Applications Flow Cytometry (Intracellular Staining)
Regulatory Status RUO
Conjugate FITC
Format Conjugated
Storage Requirements Store at 2-8°C. Do not freeze. Light-sensitive material.
Primary or Secondary Primary
Monoclonal or Polyclonal Monoclonal
Formulation aqueous buffer, 0.09% sodium azide, may contain carrier protein/stabilizer
Concentration 5μL (0.125μg)/test

This LUVNKLA monoclonal antibody recognizes human and mouse signal transducer and activator of transcription 3 (STAT3) when phosphorylated on tyrosine 705 (Y705). The STAT family represents seven transcription factors (STATs 1, 2, 3, 4, 5A, 5B, and 6) that are involved in many cellular processes including apoptosis, cell differentiation, and proliferation in a cell type- and cytokine-specific manner. STAT proteins are activated by ligand binding to cytokine receptors that associate with Janus kinase (JAK) family members.

Following their phosphorylation by JAKs, STAT proteins translocate to the nucleus where they bind to DNA and regulate transcription of specific genes in a cell type- and cytokine-specific manner. STAT3 is activated downstream of numerous cytokines including interferons, IL-5, IL-6, IL-10, and LIF. STAT3 is important for the differentiation of Th17 cells and mediates a variety of cellular processes including cell growth and survival. The importance of STAT3 is highlighted by both loss-of-function and gain-of-function mutations. Deletion of STAT3 in T cells results in decreased IL-6- and IL-2-mediated proliferation, while deletion of STAT3 in neutrophils and macrophages results in increased susceptibility to LPS-induced endotoxic shock and increased production of the pro-inflammatory cytokines IL-6 and TNF alpha. Hyper STAT3 activity is associated with poor prognosis of many different cancers.