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SMAD7 Polymorphisms Are Associated with Colorectal Cancer in Patients with Lynch Syndrome.
OTU deubiquitinase 1 (OTUD1 (Montrer OTUD1 Protéines)) directly deubiquitinates Smad7 Protein (SMAD7) and prevents its degradation.
Periostin (Montrer POSTN Protéines) contributes to skin fibrosis by enhancing TGF-beta (Montrer TGFB1 Protéines) signaling via Smad 7 inhibition, which may lead to extracellular matrix deposition and periostin (Montrer POSTN Protéines) generation.
HO-1 (Montrer HMOX1 Protéines) plays a key role in protecting tumor cells from apoptosis, in a process that involves Smad7 and HDAC4 (Montrer HDAC4 Protéines)/5 in apoptosis of B-ALL cells
Mechanistic studies reveal that TGFbeta (Montrer TGFB1 Protéines) activates the expression of microRNA-182 (miR (Montrer MLXIP Protéines)-182), which suppresses SMAD7 protein. miR (Montrer MLXIP Protéines)-182 silencing leads to SMAD7 upregulation on TGFbeta (Montrer TGFB1 Protéines) treatment and prevents TGFbeta (Montrer TGFB1 Protéines)-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 (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).
We confirmed that Smad7 was a direct target of miR (Montrer MLXIP Protéines)-21. miR (Montrer MLXIP Protéines)-21 knockout resulted in increased expression of Smad7 and impaired phosphorylation of the Smad2 (Montrer SMAD2 Protéines)/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 (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
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
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 (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