Anti-Smad3 Antibody Picoband® Fluoro488 Conjugated

Mothers against decapentaplegic homolog 3 also known as SMAD family member 3 or SMAD3 is a protein that in humans is encoded by the SMAD3 gene. SMAD3 is a member of the SMAD family of proteins. It is located in 15q22.33. And it mediates the signals from the transforming growth factor beta (TGF-β) super family ligands that regulate cell proliferation, differentiation and death. Based on its essential role in TGF beta signaling pathway, SMAD3 has been related with tumor growth in cancer development.

Mothers against decapentaplegic homolog 3; MAD homolog 3; Mad3; Mothers against DPP homolog 3; hMAD-3; JV15-2; SMAD family member 3; SMAD 3; Smad3; hSMAD3; SMAD3; MADH3

Cancer, Cancer Metabolism, Cytoplasmic, Epigenetics and Nuclear Signaling, Metabolism, Metabolism Processes, Nuclear Signaling, Nuclear Signaling Pathways, Pathways and Processes, Response To Hypoxia, Signal Transduction, Signaling Pathway, Stem Cells, TGF Beta

Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF- mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator. .

1. Entrez Gene: SMAD3 SMAD family member 3. 2. Moustakas A, Souchelnytskyi S, Heldin CH (2001) . Smad regulation in TGF-beta signal transduction. J. Cell. Sci. 114 (Pt 24) : 4359–69. 3. Zhang Y, Feng X, We R, Derynck R (September 1996) . Receptor-associated Mad homologues synergize as effectors of the TGF-beta response. Nature 383 (6596) : 168–72.

Cytoplasm. Nucleus. Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4. Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1. Co-localizes with LEMD3 at the nucleus inner membrane. MAPK-mediated phosphorylation appears to have no effect on nuclear import. PDPK1 prevents its nuclear translocation in response to TGF-beta.