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Human SMAD4 Protein expressed in HEK-293 Cells - ABIN2732222
Atanelishvili, Shirai, Akter, Buckner, Noguchi, Silver, Bogatkevich: M10, a caspase cleavage product of the hepatocyte growth factor receptor, interacts with Smad2 and demonstrates antifibrotic properties in vitro and in vivo. dans Translational research : the journal of laboratory and clinical medicine 2016
Human SMAD4 Protein expressed in Wheat germ - ABIN1320605
Iempridee, Das, Xu, Mertz: Transforming growth factor beta-induced reactivation of Epstein-Barr virus involves multiple Smad-binding elements cooperatively activating expression of the latent-lytic switch BZLF1 gene. dans Journal of virology 2011
BRAF and SMAD4 genetic mutations might be important molecular markers to predict resistance to neoadjuvant chemoradiation therapy in locally advanced rectal cancer.
chromosomal SMAD4 loss is associated with head and neck squamous cell carcinomas.
TGIF1 homeodomain interacts with Smad2/Smad4 MH1 domains and represses TGF-beta signaling.
During iron deficiency, SMAD3 and SMAD4 expression was significantly decreased via proteasomal degradation, allowing for derepression of iron target genes.
This study revealed that miR-224-5p inhibited autophagy by targeting Smad4 in MDA-MB-231cells.
current study revealed that low FSTL1, BMP4, and Smad4 expression significantly predict poor prognosis in lung adenocarcinoma but not in squamous cell carcinoma.
Data suggest a mechanism by which SMAD4 protein (SMAD4) is inactivated in cancers and provides guidance for targeted therapies in anaplastic lymphoma kinase (ALK)-positive cancers.
findings revealed that S100A11 and TGF-beta1/SMAD4 signaling pathway were related but mutually independent in regulating PANC-1 cells proliferation and apoptosis.
Our data suggested miR-449c-5p could function as a new inhibitory regulator of VICs osteogenic differentiation, which may act by targeting Smad4. MiR-449c-5p may be a potential therapeutic target for CAVD.
RIP assay revealed that AWPPH could bind to EZH2 and ChIP assay showed SMAD4 was regulated by EZH2. LncRNA AWPPH can promote cell proliferation, autophagy, and migration, as well as inhibit cell apoptosis in bladder cancer by inhibiting SMAD4 via EZH2.
Concluded that SMAD4 inhibits the H2O2-induced apoptosis in osteoblast hFOB1.19 cells; such inhibition might depend on the SUMOylation by SUMO 2/3. It implies a promising role of SMAD4 in oxidative stress-promoted damage to osteoblasts.
Data show that miR-301a suppressed the expression of cyclin-dependent kinase inhibitor p21 (p21) and Smad4 protein, and subsequently promoted G1/S cell cycle transition and cell proliferation in vitro and xenograft growth in nude mice in vivo.
miR-422a suppressed SMAD4 expression and inhibited TGF-beta and bone morphogenetic protein-dependent luciferase activity in muscle cells.
as a direct target of miR-224, USP3 is a potent ceRNA of SMAD4 in CRC. Decreased expression of USP3 mRNA is associated with a poor prognosis and distal metastasis of CRC, which is attributed to further suppression of SMAD4 through the release of miR-224 from the USP3 3'UTR.
We report a 2-year-old girl diagnosed with Myhre syndrome by whole exome sequencing (WES) that revealed the recurrent p.Ile500Val mutation in the SMAD4 gene
ENG, ACVRL1, and SMAD4 mutations result in different phenotypes in hereditary hemorrhagic telangiectasia
Our results demonstrated that SMAD4 and NF1 mutations can serve as potential biomarkers for poor prognosis to cetuximab-based therapy in Chinese mCRC patients.
miRNA-34a suppressed the TGF-beta-induced epithelial mesenchymal transformation, invasion, and migration of nasopharyngeal carcinoma cells by directly targeting SMAD4.
Overall, these findings suggest a more dominant role for SMAD3 and SMAD4 than SMAD2 in TGFbeta-induced chondrogenesis of human bone marrow-derived mesenchymal stem cells.
miR-205 functions as an oncogenic miRNA by directly binding to SMAD4 and PTEN, providing a novel target for the molecular treatment of ovarian cancer.
This stimulation by BMP7 was lost in the combined TGFBR2 and SMAD4 double knockout fibroblasts, which included a profound decrease in HGF expression. Thus, Smad4-mediated signaling is required to initiate epithelial carcinogenesis subsequent to TGFBR2 deletion in FSP1(+) fibroblasts.
TGFbeta suppresses the expression of proinflammatory genes in the colon epithelium, and loss of its downstream mediator, SMAD4, is sufficient to initiate inflammation-driven colon cancer.
HNF4A acts redundantly with an intestine-restricted HNF4 paralog, HNF4G, to activate enhancer chromatin and upregulate the majority of transcripts in the differentiated epithelium; cells fail to differentiate on double knockout of both HNF4 paralogs. Furthermore, we show that SMAD4 and HNF4 function via a reinforcing feed-forward loop.
This review lists SMAD4 mutations in various types of cancer and summarizes recent advances on SMAD4 with focuses on the function, signaling pathway, and the possibility of SMAD4 as a prognostic indicator. [review]
To uncover the molecular changes induced by the concurrent targeting of E-cadherin, p53, and Smad4 loss.
These results suggest a new mechanism whereby Smad4 controls chondrocyte hypertrophy by up-regulating Runx2 expression during skeletal development. The regulatory mechanism involving Smad4-mediated Runx2 activation uncovered here provides critical insights into bone development and pathogenesis of chondrodysplasia.
The significant insight into synergistic role of Pten and Smad4 in SGT.
Smad4 deletion may inhibit lipogenesis, stimulate beta-oxidation, improve lipid metabolism and liver function, alleviate inflammation and fibrosis, and reduce cell apoptosis in nonalcoholic steatohepatitis
Loss of Smad4 in neural progenitor cells impairs adult neurogenesis in the subventricular zone.
Reduced bone-mass and accelerated osteoclastogenesis seen in Smad4-cKO were abrogated by Prdm1 deletion. Administration of latent-TGFbeta1-Fc to wild-type mice antagonized LPS-induced bone destruction in a model of activated osteoclast-mediated bone destruction
miR146b5p directly targeted Smad4 and negatively regulated the transforming growth factor (TGF)-beta signaling pathway, which contributed to the neural commitment of Pluripotent stem cells (PSCs). Collectively, our findings uncover the essential role of miR146b5p in the neural conversion of PSCs.
study reveals a critical mechanism by which TGFbeta controls TH17 cell differentiation and uncovers the SKI-SMAD4 axis as a potential therapeutic target for treating TH17-related diseases
The binding motif of miR26b5p in the Smad4 3'UTR was identified as UACUUGA at position 978-984.
Smad4 expression in T lymphocytes plays a protective role in the development of autoimmune Sjogren's syndrome in the nonobese diabetic mouse.
SMAD4 defect causes auditory neuropathy via specialized disruption of cochlear ribbon synapses.
germ-cell-knockout mice were fertile and did not exhibit any detectable abnormalities in spermatogenesis, indicating that Smad4 is not required for the production of sperm; instead, these data indicate a cell type-specific requirement of Smad4 primarily during testis development.
Smad4 deletion in T cells of NOD mice accelerated the development of autoimmune diabetes.
Smad4 regulates osteoblast apoptosis and mineralization in vitro.
Specific deletion of Smad4 in adult mouse satellite cells led to increased propensity for terminal myogenic commitment connected to impaired proliferative potential.
We discovered that Smad1/5/4-Amhr2-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1/5/4-Amhr2-cre KO females exhibit multiple defects in stroma, epithelium, and smooth muscle layers and fail to assemble a closed uterine lumen upon embryo implantation, with defective uterine decidualization that led to pregnancy loss at early to mid-gestation.
SMAD4, a core component of the canonical TGF-beta signaling pathway, regulates the canonical TGF-beta signaling pathway in porcine granulosa cells (GCs) through a feedback mechanism.
CYP19A1 is an inhibitor of follicular atresia and is regulated by both SMAD4 and miR-10b.
Activated TGF-beta signaling rescued miR-143-reduced FSHR and intracellular signaling molecules, and miR-143-induced porcine granulosa cell apoptosis.
miR26b may have a proapoptotic role in granulosa cells by regulating SMAD4 expression.
These observations establish an important role of SMAD4 in the regulation of the response of porcine granulosa cells to FSH.
Data suggest SMAD4 mRNA is increased in oocytes during maturation, is maximal in 2-cell blastocysts, remains elevated through 8-cell stage, and is decreased in remaining ectogenesis; embryotrophic actions of follistatin are SMAD4 dependent.
ALK5 and Smad4 have roles in TGF-beta1-induced pulmonary endothelial permeability
miR-183 positively regulates hircine preadipocyte differentiation by inhibiting expression of Smad4.
TGF-beta signaling has a role in nuclear localization of transcription factor Smad4
This gene encodes a member of the Smad family of signal transduction proteins. Smad proteins are phosphorylated and activated by transmembrane serine-threonine receptor kinases in response to TGF-beta signaling. The product of this gene forms homomeric complexes and heteromeric complexes with other activated Smad proteins, which then accumulate in the nucleus and regulate the transcription of target genes. This protein binds to DNA and recognizes an 8-bp palindromic sequence (GTCTAGAC) called the Smad-binding element (SBE). The Smad proteins are subject to complex regulation by post-translational modifications. Mutations or deletions in this gene have been shown to result in pancreatic cancer, juvenile polyposis syndrome, and hereditary hemorrhagic telangiectasia syndrome.
Mothers against decapentaplegic-like protein 4
, mothers against decapentaplegic homolog 4
, Smad4 protein
, SMAD family member 4
, mothers against decapentaplegic homolog 4-like
, MAD homolog 4
, SMAD, mothers against DPP homolog 4
, deleted in pancreatic carcinoma locus 4
, deletion target in pancreatic carcinoma 4
, mothers against decapentaplegic, Drosophila, homolog of, 4
, Smad 4
, deletion target in pancreatic carcinoma 4 homolog
, mothers against DPP homolog 4
, MAD (mothers against decapentaplegic Drosophila) homolog 4
, SMAD 4
, MAD, mothers against decapentaplegic homolog 4
, mothers against DPP-like 4
, mothers against decapentaplegic-like 4