Anti-Smad4(DPC4) Antibody (Monoclonal, DCS-46)

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

Boster Bio Anti-Smad4 (DPC4) Antibody (Monoclonal, DCS-46) catalog # MA1089. Tested in ICC, WB applications. This antibody reacts with Human, Mouse, Rat.

SMAD4

Other applications have not been tested. Optimal dilutions should be determined by end users.

Monoclonal

Mouse ascites fluid, 1.2% sodium acetate, 2mg BSA, with 0.01mg NaN3 as preservative.

Ascites

Store at -20˚C for one year from date of receipt. After reconstitution, at 4˚C for one month. It can also be aliquotted and stored frozen at -20˚C for six months. Avoid repeated freeze-thaw cycles.

Mothers against decapentaplegic homolog 4

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. 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. 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. 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 (By similarity)..

Mothers against decapentaplegic homolog 4