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Expression of Smad7 was negatively regulated by miR-17-5p; Smad7 expression inactivated NF-kappaB and Wnt/beta catenin pathways.
SMAD7 Polymorphisms Are Associated with Colorectal Cancer in Patients with Lynch Syndrome.
OTU deubiquitinase 1 (OTUD1) directly deubiquitinates Smad7 Protein (SMAD7) and prevents its degradation.
Periostin contributes to skin fibrosis by enhancing TGF-beta signaling via Smad 7 inhibition, which may lead to extracellular matrix deposition and periostin generation.
HO-1 plays a key role in protecting tumor cells from apoptosis, in a process that involves Smad7 and HDAC4/5 in apoptosis of B-ALL cells
Mechanistic studies reveal that TGFbeta activates the expression of microRNA-182 (miR-182), which suppresses SMAD7 protein. miR-182 silencing leads to SMAD7 upregulation on TGFbeta treatment and prevents TGFbeta-induced epithelial-mesenchymal transition and invasion of cancer cells.
This study reports a proinflammatory role for SMAD7 in human gestational tissues, with SMAD7 silencing attenuating the inflammatory response.
Smad7 enables STAT3 activation and promotes pluripotency independent of TGF-beta signaling.
Studied expression of microRNA-375 and its target gene SMAD-7 polymorphisms (rs4939827) in colorectal cancer (CRC) patients in comparison to control subjects. A very significant correlation was found between miRNA-375 level and mutant and heterozygotes genotypes of SMAD-7 rs4939827 polymorphism in CRC.
Studies indicate that the T allele of SMAD7 protein (SMAD7)single nucleotide polymorphism rs4939827 to be significantly related with an increase colorectal cancer (CRC) risk in Chinese population [Meta-analysis].
this large-scale meta-analysis indicated that SMAD7 polymorphisms (rs4464148, rs4939827, and rs12953717) correlate with CRC.
Collectively, these findings demonstrate that the miR-15a/Smad-7/TGF-beta pathway is important in HBV-associated liver cancer.
SMAD7 promoter is hyper-methylated both in human atherosclerotic plaques and atherosclerosis patients, which is positively associated with homocysteine levels and carotid plaque scores.
Furthermore, MERS coronavirus induced apoptosis through upregulation of Smad7 and fibroblast growth factor 2 (FGF2) expression in both kidney and lung cells.
findings demonstrate TGF-beta enhances expression of USP26 and reinforces SMAD7 stability by limiting the ubiquitin-mediated turnover of SMAD7; clinically, loss of USP26 correlates with high TGF-beta activity and confers poor prognosis in glioblastoma; data identify USP26 as a novel negative regulator of the TGF-beta pathway and suggest that loss of USP26 expression may be an important factor in glioblastoma pathogenesis
In conclusion, our study demonstrated that COL1A2-AS1/miR-21/Smad pathway plays an important role in inhibiting hypertrophic scar formation, and suggested this novel pathway may be a new target for hypertrophic scar treatment.
Our data revealed the SMAD7 loci is associated with hepatocellular carcinoma susceptibility and its clinicopathologic development.
Smad7 expression in necrotizing enterocolitis macrophages interrupts TGF-beta signaling and promotes NF-kappaB-mediated inflammatory signaling in these cells through increased expression of IKK-beta
SMAD7 gene and specifically the allele C could be protective for colorectal cancer (CRC). An independent protective association was also observed between high adherence Mediterranean diet pattern and CRC risk.
Smad7 inhibition diminishes interaction of PKR with protein kinase inhibitor p58 (p58(IPK)).
Smad7 overexpression causes severe iron overload in transgenic mice.
The response to chronic pancreatitis induction was significantly more severe in Smad7 mutants as indicated by a stronger accumulation of extracellular matrix, increased levels of inflammatory cells and an elevated number of mesenchymal cells/myofibroblasts in Smad7 mutant pancreata.
We confirmed that Smad7 was a direct target of miR-21. miR-21 knockout resulted in increased expression of Smad7 and impaired phosphorylation of the Smad2/3 complex
Eplerenone inhibited atrial fibrosis in MHC-TGFcys33ser transgenic mice. The underlying mechanism may involve increased protein expression of Smad7, which enhances the inhibitory feedback regulation of TGF-beta1/Smad signaling.
Smad7 enables STAT3 activation and promotes pluripotency independent of TGF-beta signaling
lentiviral vector-mediated i.a. overexpression of Smad7 can ameliorate rheumatoid joint, implicating a pharmacological development of Smad7-based molecular strategy in collagen-induced arthritis
Smad7 expression governs splenic DC subset differentiation.
Our results indicate that miR-212-3p facilitates the activation of HSCs and TGF-beta pathway by targeting SMAD7, highlighting that it can be served as a novel biomarker or therapeutic target for liver fibrosis.
a heterozygous deletion of SMAD7 results in an increased proliferation of Muller cell progenitors in the central retina at postnatal day 4, the time window when Muller cells differentiate in the mouse retina; this in turn results in a thickened retina and inner nuclear layer and a higher number of differentiated Muller cells in the more developed retina
changes were associated with increased expression of the antifibrotic protein Smad7 and higher levels of sphingosine in Sphk2(-/-) unilateral ureteral obstruction kidneys
Smad7 plays a protective role in acute kidney injury by preventing tubular epithelial cells from the G1 cell cycle arrest.
study reports an alternately-spliced form of Smad7, Smad7Delta, that is induced by TGF-beta and CLIC4, is a dominant inhibitor of Smad7 and enhances TGF-beta signaling
Pancreatic depletion of SMAD7 resulted in age-dependent increases in beta cell dysfunction with accelerated glucose intolerance, followed by overt diabetes.
The inverse correlation between Smad7 and AhR expression helps to propagate inflammatory signals in the gut in Crohn's disease.
results indicate that miR-181a-5p promotes 3T3-L1 preadipocyte differentiation and adipogenesis through regulating TGFbeta/Smad and Wnt signaling pathway by directly targeting Smad7 and Tcf7l2
microRNA-497 modulates breast cancer cell proliferation, invasion, and survival by targeting SMAD7.
results indicate that miR-195a-5p inhibits MTEC1 proliferation, at least in part, via down-regulation of Smad7
Data indicate that, in irritable bowel disease, high Smad7 contributes to sustain detrimental immune responses and knockdown of this molecule can help attenuate the ongoing mucosal inflammation in patients with such disorders
Hic-5 deficiency attenuates the activation of hepatic stellate cells and liver fibrosis though reducing the TGF-beta/Smad2 signaling by upregulation of Smad7
Data show that microRNA miR-21 was significantly upregulated by bone morphogenetic protein 9 (BMP9) during the osteogenesis the multilineage cells (MMCs) by suppressing Smad7 protein.
The fibronectin type III (FN) domain and the intracellular domain of Tril are required to trigger Smad7 degradation in Xenopus embryos.
Tril is a novel component of a Bmp-Gata2 positive-feedback loop that plays an essential role in hematopoietic specification, by targeting Smad7 for degradation.
cTid1 can bind to other members of the Smad family and that highest binding activity occurs with the negative regulatory Smad7, through the conserved MH2 domain
Smad7 has a role in Xenopus mesodermal and neural induction
SMAD7 plays a potentially important role in mammalian prenatal skeletal muscle development and is a candidate gene for promoting greater weaning weight in pig breeding.
MiR-92a inhibits porcine ovarian granulosa cell apoptosis by targeting Smad7 gene
miRNA-424/503 cluster members target the SMAD7 and ACVR2A genes which are involved in the activin signalling pathway
a detailed computational model for TGF-beta signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7.
Results suggest that myostatin auto-regulates its gene expression through a Smad7 dependent mechanism in myogenic cells.
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.
MAD (mothers against decapentaplegic, Drosophila) homolog 7
, MAD homolog 8
, Mothers against decapentaplegic, drosophila, homolog of, 7
, SMAD, mothers against DPP homolog 7
, mothers against DPP homolog 8
, mothers against decapentaplegic homolog 7
, MAD homolog 7
, SMAD 7
, mothers against DPP homolog 7
, mothers against decapentaplegic homolog 8
, MAD, mothers against decapentaplegic homolog 7
, mothers against DPP 7
, mothers against decapentaplegic-like protein 7
, SMAD family member 7