Background:

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.

Clonality:

polyclonal

Classification:

Primary antibody

Alternative names:

DPC4, MADH4

Specificity:

Human, Mouse, Rat

Host:

Rabbit

Isotype:

IgG

Immunogen:

SMAD family member 4

Purification:

Immunogen affinity purified

Purity:

≥95% as determined by SDS-PAGE

Calculated molecular weight:

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Form:

liquid

Applications:

ELISA, WB, IHC

Recommended dilution:

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Storage:

PBS with 0.02% sodium azide and 50% glycerol pH 7.3,-20℃ for 12 months(Avoid repeated freeze / thaw cycles.)

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