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

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.

60469 MW

Immunocytochemistry , 1?g/ml, Human, -
Western blot, 0.5-1?g/ml, Human, Mouse, Rat

Cyclin-dependent kinase 1

SMAD4 plays a pivotal role in signal transduction of the transforming growth factor beta superfamily cytokines by mediating transcriptional activation of target genes. Smad4 signalling in T cells is required for suppression of gastrointestinal cancer. Mutational inactivation of SMAD4 causes TGF-beta unresponsiveness and gave a basis for understanding the physiologic role of this gene in tumorigenesis. Mutations in DPC4 (SMAD4) cause juvenile polyposis syndrome, but only account for a minority of cases.

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

Add 1 ml of PBS buffer will yield a concentration of 100 ug/ml.

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

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).

Although predominant among the water-soluble brain proteins, S100 is also found in a variety of other tissues..