Aliases for SMAD3 Gene
External Ids for SMAD3 Gene
Previous HGNC Symbols for SMAD3 Gene
Previous GeneCards Identifiers for SMAD3 Gene
The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein functions as a transcriptional modulator activated by transforming growth factor-beta and is thought to play a role in the regulation of carcinogenesis. [provided by RefSeq, Apr 2009]
GeneCards Summary for SMAD3 Gene
SMAD3 (SMAD Family Member 3) is a Protein Coding gene. Diseases associated with SMAD3 include loeys-dietz syndrome 3 and smad3-related loeys-dietz syndrome. Among its related pathways are Gene Expression and Signaling by GPCR. GO annotations related to this gene include transcription factor activity, sequence-specific DNA binding and sequence-specific DNA binding. An important paralog of this gene is SMAD1.
UniProtKB/Swiss-Prot for SMAD3 Gene
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.