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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. in Journal of virology 2011
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. in Translational research : the journal of laboratory and clinical medicine 2016
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.
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.
a constructed SMAD4 RNA interference experiment confirmed that the function of KCNQ1OT1 was to act on lens epithelial cell proliferation and EMT, and this was achieved via the SMAD4 signaling pathway. The findings of the present study may provide a novel target for molecular therapy of cataracts disease.
Serum BMP2 and Smad4 levels in patients with senile osteoporotic fracture were significantly lower than those in normal controls
The tumor suppressor gene SMAD4 (DPC4) may help predict which surgical patients are at higher risk for failure after definitive management and may benefit from intensified adjuvant therapy.
Smad4 could be considered as a central component of EMT transition in human colorectal cancer that combines with transcriptional factors to reduce E-cadherin and alter the expression of the epithelial phenotype.
LPS mediates intercellular tight junction destruction among TECs and RhoT1/SMAD-4/JAM-3 is a pivotal pathway to mediate the phenomenon.
the results indicated that miR3147 may serve an oncogenic role in vulvar squamous cell carcinoma (VSCC) by targeting Smad4. miR3147 may represent a novel potential therapeutic target marker for VSCC.
Data indicate that in pancreatic cancer cells, the expression of ENG may be controlled by a pathway mediated by SMAD4.
Data indicate that absence of KRAS, TP53 and SMAD4 genetic alterations may identify a subset of pancreatic carcinomas with better outcome.
Results demonstrated that SMAD4 is the direct target of miR-19b-3p in colon cancer. Its expression is downregulated in colon cancer contributing to oxaliplatin resistance.
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.
In SMAD4 deficiency, NK cells unexpectedly acquired an innate lymphoid cell type 1-like gene signature and were unable to control tumor metastasis or viral infection. Mechanistically, SMAD4 restrained non-canonical TGF-beta signaling mediated by the cytokine receptor TGFbetaR1 in NK cells.
The effect of Smad4 was at least partially mediated by the downstream effectors Syk and ROCK2 transcription in megakaryocytes
deletion of Smad4 in OBs differentially modulates HSC fate in a stage-dependent manner
Data suggest that ovarian Bmp4 levels are significantly decreased in a mouse model of polycystic ovary syndrome with hyperandrogenism; androgens inhibited Bmp4 expression via activation of androgen receptors; Smad4 signaling rather than p38 MAPK pathway regulates androgen and estrogen formation.
The authors demonstrated that ubiquitin-specific protease (USP) 4 strongly induces activin/BMP signaling by removing the inhibitory monoubiquitination from SMAD4.
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