|Application ||WB, IHC, IF|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||60439 Da|
|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||A synthetic peptide corresponding to residues in the C-term of human Smad 4 was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Smad4 Antibody (C-term) 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 4 is a member of the Mothers Against Dpp (MAD)-related family of proteins. So far, eight Smads have been identified and can be divided in 3 subgroups based on their structure and functions; pathway-restricted, common mediator and inhibitory Smad. Smad 4 is the common Smad (co-Smad) (1-2). Previously identified as the tumor suppressor DPC4 (deleted in pancreatic carcinoma, locus 4), Smad 4 is functionally distinct among the Smad family, and is required for the assembly and transcriptional activation of diverse, Smad-DNA complexes (3). In contrast to the R-Smads, Smad 4 is not regulated by phosphorylation, but acts as a common mediator of TGF-β, activin, and bone morphogenetic protein signaling responses (4). Smad 4 is frequently inactivated in pancreatic, biliary and colorectal tumors (5-6).
1. Eppert et al. Cell 86: 543-552, 1996
2. Derynck et al.1996.Curr. Biol. 6: 1226-1229
3. Hudson er al. (1998) Development 125, 1407-1420
4. Lagna et al. (1996) Nature 383, 832-836
5. Hahn,et al. (1996) Science 271, 350-353
6. Goggins et al. (1998) Cancer Res. 58, 5329-5332
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