Anti-Smad4 Antibody Picoband® Fluoro488 Conjugated

SMAD4 (Mothers Against Decapentaplegic Drosophila Homolog of 4), also known as MADH4 or DPC4, is a protein that in humans is encoded by the SMAD4 gene. It belongs to the Darfwin family of proteins that modulate members of the TGFβ protein superfamily. Hahn et al. (1996) identified the SMAD4 gene on chromosome 18q21.1. Howe et al. (1998) identified the SMAD4 gene within a region on 18q21.1 defined by linkage analysis in kindred with juvenile polyposis syndrome. To test ly the hypothesis that the SMAD4 gene is a tumor suppressor that is critical for transmitting signals from transforming growth factor-beta and related ligands. SMAD4 plays a pivotal role in signal transduction of the transforming growth factor beta superfamily cytokines by mediating transcriptional activation of target genes.

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

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

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. .

1. Hein, L.; Altman, J. D.; Kobilka, B. K. :Two functionally distinct alpha-2-adrenergic receptors regulate sympathetic neurotransmission. Nature 402: 181-184, 1999. 2. Hoehe, M. R.; Berrettini, W. H.; Lentes, K.-U.:Dra I identifies a two allele DNA polymorphism in the human alpha-2-adrenergic receptor gene (ADRAR), using a 5.5 kb probe (p ADRAR) . Nucleic Acids Res. 16: 9070 only, 1988. 3. Yang-Feng, T. L.; Kobilka, B. K.; Caron, M. G.; Lefkowitz, R. J.; Francke, U.:Chromosomal assignment of genes for an alpha-adrenergic receptor (ADRAR) and for another member of this receptor family coupled to guanine nucleotide regulatory proteins (RG21) . (Abstract) Cytogenet. Cell Genet. 46: 722-723, 1987.

Cytoplasm. Nucleus. 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.