|Other Accession||Q13485, NP_005350, NM_005359|
|Reactivity||Human, Mouse, Rat, Rabbit, Goat, Dog, Guinea Pig, Horse, Sheep, Bovine|
|Predicted||Human, Mouse, Rat, Pig, Goat, Guinea Pig, Horse, Bovine|
|Calculated MW||60 kDa|
|Alias Symbol||JIP, DPC4, MADH4, MYHRS|
|Other Names||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|
|Target/Specificity||SMAD4 is one of the Smad family members, which are essential intracellular signalling components of the transforming growth factor-beta (TGF-beta) superfamily. Smad2 and Smad3 are structurally highly similar and mediate TGF-beta signals. Smad4 is distantly related to Smads 2 and 3, and forms a heteromeric complex with Smad2 after TGF-beta or activin stimulation. TGF-beta induces heteromeric complexes of Smads 2, 3 and 4, and their concomitant translocation to the nucleus, which is required for efficient TGF-beta signal transduction|
|Format||Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.|
|Reconstitution & Storage||Add 100 ul of distilled water. Final anti-SMAD4 antibody concentration is 1 mg/ml in PBS buffer with 2% sucrose. For longer periods of storage, store at -20°C. Avoid repeat freeze-thaw cycles.|
|Precautions||SMAD4 antibody - middle region 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. PDPK1 prevents its nuclear translocation in response to TGF- beta|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
firstname.lastname@example.org, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
This is a rabbit polyclonal antibody against SMAD4. It was validated on Western Blot using a cell lysate as a positive control. Abgent strives to provide antibodies covering each member of a whole protein family of your interest. We also use our best efforts to provide you antibodies recognize various epitopes of a target protein. For availability of antibody needed for your experiment, please inquire (email@example.com).
If you have used an Abgent product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at firstname.lastname@example.org.