Anti-Smad4 Rabbit Monoclonal Antibody

Mothers against decapentaplegic homolog 4; MAD homolog 4; Mothers against DPP homolog 4; Deletion target in pancreatic carcinoma 4; SMAD family member 4; SMAD 4; Smad4; hSMAD4; SMAD4; DPC4, MADH4

Apoptosis, Cancer, Cancer Metabolism, Cardiogenesis, Cardiovascular, Cytoplasmic, Epigenetics and Nuclear Signaling, Hypertrophy, Metabolism, Metabolism Processes, Nuclear Signaling, Nuclear Signaling Pathways, Oncoproteins/Suppressors, Pathways and Processes, Response To Hypoxia, Signal Transduction, Signaling Pathway, Stem Cells, TGF Beta, Transcription Factors, Transcription Factors/Regulators, Tumor Suppressors, Vasculature

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. Acts synergistically with SMAD1 and YY1 in bone morphogenetic protein (BMP) -mediated cardiac-specific gene expression. Binds to SMAD binding elements (SBEs) (5'-GTCT/AGAC-3') within BMP response element (BMPRE) of cardiac activating regions (By similarity) . 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. .

Cytoplasm. Nucleus. Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R- SMAD. PDPK1 prevents its nuclear translocation in response to TGF- beta.