Smad7 Protein

An inhibitory smad protein that associates with TRANSFORMING GROWTH FACTOR BETA RECEPTORS and BONE MORPHOGENETIC PROTEIN RECEPTORS. It negatively regulates SIGNAL TRANSDUCTION PATHWAYS by inhibiting PHOSPHORYLATION of RECEPTOR-REGULATED SMAD PROTEINS.

Also Known As:

Networked: 29 relevant articles (0 outcomes, 1 trials/studies)

Bio-Agent Context: Research Results

Experts

1.	ten Dijke, Peter: 2 articles (04/2013 - 02/2003)
2.	Li, Xiao-Zhao: 2 articles (01/2007 - 01/2006)
3.	Liu, Fu-You: 2 articles (01/2007 - 01/2006)
4.	Hirano, Taizou: 1 article (01/2022)
5.	Inoue, Chihiro: 1 article (01/2022)
6.	Irokawa, Toshiya: 1 article (01/2022)
7.	Kanehira, Masahiko: 1 article (01/2022)
8.	Kurosawa, Hajime: 1 article (01/2022)
9.	Notsuda, Hirotsugu: 1 article (01/2022)
10.	Numakura, Tadahisa: 1 article (01/2022)

Related Diseases

1.	Fibrosis (Cirrhosis) 01/01/2006 - "Studies indicate that the level of Smad7 protein expression is decreased in progression of tubulointerstitial fibrosis. " 09/01/2010 - "Trps1 haploinsufficiency promoted tubulointerstitial fibrosis via increased phosphorylation of Smad3 and decreased Smad7 protein. " 06/08/2004 - "Our results suggest that the reduction of Smad7 protein resulting from enhanced ubiquitin-dependent degradation plays a pathogenic role in progression of tubulointerstitial fibrosis." 01/01/2022 - "STC1 upregulates SMAD7 in an uncoupling protein 2-dependent manner, induces demethylation of the SMAD7 promoter region and acetylation of the SMAD7 protein in human alveolar epithelial and fibroblast cell lines and a bleomycin-treated mouse model, and subsequently attenuates fibrosis. " 09/03/2021 - "Mechanistically, circHNRNPH1 colocalized with and sponged microRNA (miR)-216-5p in the cytoplasm of cardiac fibroblasts to induce SMAD7 (protein family of signal transduction component of the canonical transforming growth factor-β signaling pathway) expression, accelerating the degradation of TGF-β receptor I. Thus, our results indicated that circHNRNPH1 negatively regulates the fibrogenesis of cardiac fibroblasts and may provide a new therapeutic strategy for postischemic myocardial fibrosis."
2.	Keloid 11/24/2021 - "In addition, inhibiting exosomal miR-21 up-regulated Smad7 protein expression and reduced Smad2 and Smad3 protein levels in target keloid fibroblasts. " 07/01/2013 - "The expression of TGF-beta1, phospho-smad2 and phospho-smad3 protein were significantly suppressed while the expression of smad7 protein increased in keloid fibroblasts with 5-aza-2-deoxycytidine. " 07/08/2016 - "?To explore if Smad7 protein can inhibit growth of keloids by observing the gene and protein expressions of Smad7, collagen type I, and collagen type Ⅲ and cell proliferation after over-expression vectors of Smad7 transfecting keloid fibroblasts (KFb). "
3.	Carcinogenesis 08/01/2011 - "Smad7 protein is a known inhibitor of TGF-β signalling pathway which has a prominent role in tumorigenesis. " 01/01/2014 - "SMAD7 protein is a known antagonist of the transforming growth factor beta (TGF-β) signaling pathway which is involved in tumorigenesis. "
4.	Airway Remodeling 01/01/2019 - "Inhibiting miR-21 expression upregulated the level of Smad7 protein, thus reducing the expression of airway remodeling-related proteins induced by TGFβ1 stimulation in HBFs. " 09/02/2016 - "Thus, positive effects of CMD against asthmatic airway remodeling may be due to its regulatory effect on TGF-β1, Smad3, and Smad7 protein levels and on cytokines such as IL-10 and IL-17."
5.	Neoplasms (Cancer) 01/01/2018 - "MiR-21-5p was highly expressed in the tumor tissues of NSCLC patients, and its expression was significantly correlated with the clinical classification of NSCLC patients (χ2=7.154, P=0.007), tumor size (χ2=4.372, P=0.037), differentiation (χ2=13.713, P=0.001), lymph node metastasis (χ2=5.101, P=0.024), distant metastasis (χ2=12.599, P=0.000), and TNM stage (χ2=6.344, P=0.012), whereas it was positively correlated with the expression of SMAD7 protein (r=0.669, P<0.05). " 01/01/2023 - "The bioassays revealed that the HA and FA-functionalized AF markedly hindered cancer cell growth and enhanced radiotherapy (RT) through inducing cell cycle arrest (pre-G1 and G2/M) and increasing apoptosis, as well as reducing the tumorigenicity of BCs by inhibiting Silent information regulation factor 1 (SIRT1) and restoring p53 expression, deactivating the Yes-associated protein (YAP)/ Transcriptional coactivator with PDZ-binding motif (TAZ) signaling axis, and interfering with the tumor growth factor- β(TGF- β)/SMAD3 and HIF-1α/VEGF signaling hub while up-regulating SMAD7 protein expression. "

Related Drugs and Biologics

1.	Proteins (Proteins, Gene)
2.	Messenger RNA (mRNA)
3.	Transforming Growth Factor beta1 (TGF beta 1)
4.	MicroRNAs (MicroRNA)
5.	Ubiquitin
6.	Collagen Type I (Type I Collagen)
7.	Transforming Growth Factor beta (TGF-beta)
8.	Collagen
9.	Long Noncoding RNA
10.	Proteasome Inhibitors

Related Therapies and Procedures

1.	Radiotherapy