|Other Accession||NM_008540, NP_032566|
|Reactivity||Human, Mouse, Rat, Zebrafish, Goat, Sheep, Horse, Bovine, Dog|
|Predicted||Human, Mouse, Rat, Pig, Goat, Bovine, Guinea Pig|
|Alias Symbol||AW743858, D18Wsu70e, DPC4, Madh4|
|Other Names||Mothers against decapentaplegic homolog 4, MAD homolog 4, Mothers against DPP homolog 4, Deletion target in pancreatic carcinoma 4 homolog, SMAD family member 4, SMAD 4, Smad4, Smad4, Dpc4, Madh4|
|Format||Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.|
|Reconstitution & Storage||Add 50 ul of distilled water. Final anti-Smad4 antibody concentration is 1 mg/ml in PBS buffer with 2% sucrose. For longer periods of storage, store at 20°C. Avoid repeat freeze-thaw cycles.|
|Precautions||Smad4 antibody - middle region is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Common SMAD (co-SMAD) is the coactivator and mediator of signal transduction by TGF-beta (transforming growth factor). Component of the heterotrimeric SMAD2/SMAD3-SMAD4 complex that forms in the nucleus and is required for the TGF-mediated signaling. Promotes binding of the SMAD2/SMAD4/FAST-1 complex to DNA and provides an activation function required for SMAD1 or SMAD2 to stimulate transcription. Component of the multimeric SMAD3/SMAD4/JUN/FOS complex which forms at the AP1 promoter site; required for synergistic transcriptional activity in response to TGF-beta. May act as a tumor suppressor. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14- 3-3 protein YWHAQ which acts as a negative regulator (By similarity). Acts synergistically with SMAD1 and YY1 in bone morphogenetic protein (BMP)-mediated cardiac-specific gene expression (PubMed:15329343). Binds to SMAD binding elements (SBEs) (5'-GTCT/AGAC-3') within BMP response element (BMPRE) of cardiac activating regions (PubMed:15329343). In muscle physiology, plays a central role in the balance between atrophy and hypertrophy. When recruited by MSTN, promotes atrophy response via phosphorylated SMAD2/4. MSTN decrease causes SMAD4 release and subsequent recruitment by the BMP pathway to promote hypertrophy via phosphorylated SMAD1/5/8.|
|Cellular Location||Cytoplasm. Nucleus. Note=In the cytoplasm in the absence of ligand Migration to the nucleus when complexed with R-SMAD. PDPK1 prevents its nuclear translocation (By similarity).|
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