Synthesized peptide derived from human Smad7 (Acetyl Lys70)

This antibody detects endogenous levels of Human,Mouse,Rat Smad7 (Acetyl Lys70).The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):GAkGH

SMAD7 MADH7 MADH8

Smad7 (Acetyl Lys70)

Mothers against decapentaplegic homolog 7 ;
MAD homolog 7 ;
Mothers against DPP homolog 7 ;
Mothers against decapentaplegic homolog 8 ;
MAD homolog 8 ;
Mothers against DPP homolog 8 ;
SMAD family member 7 ;
SMAD 7 ;
Smad7 ;
hSMAD7 ;

The protein encoded by this gene is a nuclear protein that binds the E3 ubiquitin ligase SMURF2. Upon binding, this complex translocates to the cytoplasm, where it interacts with TGF-beta receptor type-1 (TGFBR1), leading to the degradation of both the encoded protein and TGFBR1. Expression of this gene is induced by TGFBR1. Variations in this gene are a cause of susceptibility to colorectal cancer type 3 (CRCS3). Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jun 2010],

Disease:Genetic variations in SMAD7 influence susceptibility to colorectal cancer type 3 (CRCS3) [MIM:612229]. Colorectal cancer consists of tumors or cancer of either the colon or rectum or both. Cancers of the large intestine are the second most common form of cancer found in males and females. Symptoms include rectal bleeding, occult blood in stools, bowel obstruction and weight loss. Treatment is based largely on the extent of cancer penetration into the intestinal wall. Surgical cures are possible if the malignancy is confined to the intestine. Risk can be reduced when following a diet which is low in fat and high in fiber.,Function:Antagonist of signaling by TGF-beta (transforming growth factor) type 1 receptor superfamily members; has been shown to inhibit TGF-beta (Transforming growth factor) and activin signaling by associating with their receptors thus preventing SMAD2 access. Functions as an adapter to recruit SMURF2 to the TGF-beta receptor complex. Also acts by recruiting the PPP1R15A-PP1 complex to TGFBR1, which promotes its dephosphorylation.,induction:By TGF-beta.,PTM:Acetylation prevents ubiquitination and degradation mediated by SMURF1.,PTM:Phosphorylation on Ser-249 does not affect its stability, nuclear localization or inhibitory function in TGFB signaling; however it affects its ability to regulate transcription.,PTM:Polyubiquitinated by RNF111, which is enhanced by AXIN1 and promotes proteasomal degradation. In response to TGF-beta, ubiquitinated by SMURF1; which promotes its degradation.,similarity:Belongs to the dwarfin/SMAD family.,similarity:Contains 1 MH1 (MAD homology 1) domain.,similarity:Contains 1 MH2 (MAD homology 2) domain.,subcellular location:Interaction with NEDD4L or RNF111 induces translocation from the nucleus to the cytoplasm.,subunit:Interacts with TGF-beta type I receptor. Interacts with COPS5. Interacts with NEDD4L. Interacts with STAMBP. Interacts with RNF111, AXIN1 and AXIN2. Interacts with PPP1R15A. Interacts (via MH2 domain) with EP300. Interacts with SMURF2.,tissue specificity:Ubiquitous with higher expression in the lung and vascular endothelium.,

Nucleus . Cytoplasm . Interaction with NEDD4L or RNF111 induces translocation from the nucleus to the cytoplasm (PubMed:16601693). TGF-beta stimulates its translocation from the nucleus to the cytoplasm. PDPK1 inhibits its translocation from the nucleus to the cytoplasm in response to TGF-beta (PubMed:17327236). .

Ubiquitous with higher expression in the lung and vascular endothelium.

>>TGF-beta signaling pathway ;
>>Hippo signaling pathway