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Mouse Anti-STAT5A Monoclonal Antibody (1B12) (CBMAB-1559-YC)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
1B12
Antibody Isotype
IgG1, κ
Application
ELISA, WB

Basic Information

Immunogen
Partial recombinant protein STAT5A (AAH27036, aa 1-104) with GST tag.
Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
STAT5A
Introduction
STAT5A is a member of the STAT family of transcription factors. This protein is activated by, and mediates the responses of many cell ligands, such as IL2, IL3, IL7 GM-CSF, erythropoietin, thrombopoietin, and different growth hormones. Activation of this protein in myeloma and lymphoma associated with a TEL/JAK2 gene fusion is independent of cell stimulus and has been shown to be essential for tumorigenesis. The mouse counterpart of this gene is found to induce the expression of BCL2L1/BCL-X(L), which suggests the antiapoptotic function of this gene in cells.
Entrez Gene ID
6776
UniProt ID
P42229
Alternative Names
MGF; STAT5
Function
Carries out a dual function: signal transduction and activation of transcription. Mediates cellular responses to the cytokine KITLG/SCF and other growth factors. Mediates cellular responses to ERBB4. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4. Binds to the GAS element and activates PRL-induced transcription. Regulates the expression of milk proteins during lactation.
Biological Process
Biological Process cytokine-mediated signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central
Biological Process defense responseManual Assertion Based On ExperimentIBA:GO_Central
Biological Process growth hormone receptor signaling pathway via JAK-STATManual Assertion Based On ExperimentIBA:GO_Central
Biological Process lactationIEA:UniProtKB-KW
Biological Process positive regulation of blood vessel endothelial cell migrationManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process positive regulation of endothelial cell proliferationManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process positive regulation of transcription by RNA polymerase II1 PublicationIC:ComplexPortal
Biological Process receptor signaling pathway via JAK-STATManual Assertion Based On ExperimentIBA:GO_Central
Biological Process reelin-mediated signaling pathwayManual Assertion Based On ExperimentIDA:MGI
Biological Process regulation of cell population proliferationManual Assertion Based On ExperimentIBA:GO_Central
Biological Process regulation of multicellular organism growthISS:BHF-UCL
Biological Process regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Biological Process response to peptide hormoneManual Assertion Based On ExperimentIBA:GO_Central
Biological Process taurine metabolic processISS:BHF-UCL
Cellular Location
Cytoplasm
Nucleus
Translocated into the nucleus in response to phosphorylation.
PTM
Tyrosine phosphorylated in response to KITLG/SCF, IL2, IL3, IL7, IL15, CSF2/GMCSF, GH1, PRL, EPO and THPO (By similarity).
Activated KIT promotes phosphorylation on tyrosine residues and subsequent translocation to the nucleus (PubMed:21135090).
Tyrosine phosphorylated in response to constitutively activated FGFR1, FGFR2, FGFR3 and FGFR4 (By similarity).
Tyrosine phosphorylation is required for DNA-binding activity and dimerization. Serine phosphorylation is also required for maximal transcriptional activity (By similarity).
Tyrosine phosphorylated in response to signaling via activated FLT3; wild-type FLT3 results in much weaker phosphorylation than constitutively activated mutant FLT3 (PubMed:14504097).
Alternatively, can be phosphorylated by JAK2 at Tyr-694 (PubMed:12529425).
ISGylated.
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For research use only. Not intended for any clinical use.

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