|Reactivity||Human, Mouse, Rat|
|Calculated MW||60439 Da|
|Application & Usage||Western blotting (0.5-4 µg/ml). However, the optimal concentrations should be determined individually. The antibody recognizes ~68 kDa Smad4 from samples of of human, mouse, and rat origins. Reactivity to other species has not been tested.|
|Other Names||DPC4, JIP, MADH4|
|Formulation||100 µg (0.5 mg/ml) antigen affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 0.5% BSA, and 0.01% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||Smad4 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Cellular Location||Cytoplasm. Nucleus. Note=Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R-SMAD (PubMed:15799969). PDPK1 prevents its nuclear translocation in response to TGF-beta (PubMed:17327236)|
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Provided below are standard protocols that you may find useful for product applications.
Smad proteins, the mammalian homologs of the Drosophila Mothers against dpp (Mad), have been implicated as downstream effectors of TGFβ/BMP signaling. Smad1, Smad5, and Smad8 are effectors of BMP2 and BMP4 function while Smad2 and Smad3 are involved in TGF-β and activin-mediated growth modulation. Smad4 has been shown to mediate all of the above activities thro µgh interaction with various Smad family members. Smad6 and Smad7 regulate the response to activin/TGFβ signaling by interfering with TGFβ-mediated phosphorylation of other Smad family members.
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