Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Sélectionnez vos espèces d'intérêt
This study reports a proinflammatory role for SMAD7 in human gestational tissues, with SMAD7 silencing attenuating the inflammatory response.
Smad7 enables STAT3 (Montrer STAT3 Protéines) activation and promotes pluripotency independent of TGF-beta (Montrer TGFB1 Protéines) signaling.
Studied expression of microRNA-375 and its target gene SMAD-7 polymorphisms (rs4939827) in colorectal cancer (CRC (Montrer CALR Protéines)) 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 (Montrer CALR Protéines).
Studies indicate that the T allele of SMAD7 protein (SMAD7)single nucleotide polymorphism rs4939827 to be significantly related with an increase colorectal cancer (CRC (Montrer CALR Protéines)) risk in Chinese population [Meta-analysis].
this large-scale meta-analysis indicated that SMAD7 polymorphisms (rs4464148, rs4939827, and rs12953717) correlate with CRC (Montrer CALR Protéines).
Collectively, these findings demonstrate that the miR (Montrer MLXIP Protéines)-15a/Smad-7/TGF-beta (Montrer TGFB1 Protéines) 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 (Montrer FGF2 Protéines)) 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 (Montrer COL1A2 Protéines)-AS1 (Montrer PTGDR Protéines)/miR (Montrer MLXIP Protéines)-21/Smad (Montrer SMAD1 Protéines) pathway plays an important role in inhibiting hypertrophic scar formation, and suggested this novel pathway may be a new target for hypertrophic scar treatment.
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 (Montrer TGFB1 Protéines)/Smad (Montrer SMAD1 Protéines) signaling.
Smad7 enables STAT3 (Montrer STAT3 Protéines) activation and promotes pluripotency independent of TGF-beta (Montrer TGFB1 Protéines) 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 (Montrer MLXIP Protéines)-212-3p facilitates the activation of HSCs and TGF-beta (Montrer TGFB1 Protéines) 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 (Montrer SPHK2 Protéines)(-/-) 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 (Montrer TGFB1 Protéines) and CLIC4 (Montrer CLIC4 Protéines), is a dominant inhibitor of Smad7 and enhances TGF-beta (Montrer TGFB1 Protéines) signaling
Pancreatic depletion of SMAD7 resulted in age-dependent increases in beta cell dysfunction with accelerated glucose intolerance, followed by overt diabetes.
Tril (Montrer TRIL Protéines) is a novel component of a Bmp-Gata2 (Montrer GATA2 Protéines) 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 (Montrer SMAD1 Protéines) family and that highest binding activity occurs with the negative regulatory Smad7, through the conserved MH2 (Montrer SCN4A Protéines) 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 (Montrer MYLIP Protéines)-92a inhibits porcine ovarian granulosa cell apoptosis by targeting Smad7 gene
a detailed computational model for TGF-beta (Montrer TGFB1 Protéines) signalling that incorporates elements of previous models together with crosstalking between Smad1 (Montrer SMAD1 Protéines)/5/8 and Smad2 (Montrer SMAD2 Protéines)/3 channels through a negative feedback loop dependent on Smad7.
Results suggest that myostatin (Montrer MSTN Protéines) 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