SMAD3-EPAS1
Information SMAD3-EPAS1
- Description
Fusion of SMAD3 and EPAS1. Mothers against decapentaplegic homolog 3: 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. (Source UniProtKB). Hypoxia-inducible factor 1-alpha : Functions as a master transcriptional regulator of the adaptive response to hypoxia. Heterodimerizes with ARNT; heterodimer binds to core DNA sequence 5'-TACGTG-3' within the hypoxia response element (HRE) of target gene promoters. (Source UniProtKB)
- Full Name
Fusion of SMAD3 and EPAS1
Source NCBI
- Species
Homo sapiens [tax_id: 9606]
- Genome
hg38
ReMap Statistics
- Datasets
- 1
- Biotypes
- 1
- Peaks
- 5,448
- Non-redundant peaks
- 5,448
TF Classification
- Super Class
- NA
- Class
- NA
- Familly
- NA
- Sub Familly
- NA
Source TFClass