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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
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 (zeige ITK Proteine), 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 (zeige BMP2 Proteine) 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 (zeige ITK Proteine) transition in human colorectal cancer that combines with transcriptional factors to reduce E-cadherin (zeige CDH1 Proteine) and alter the expression of the epithelial phenotype.
LPS (zeige IRF6 Proteine) mediates intercellular tight junction destruction among TECs and RhoT1 (zeige RHOT1 Proteine)/SMAD-4/JAM-3 (zeige JAM3 Proteine) 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 (zeige ENG Proteine) may be controlled by a pathway mediated by SMAD4.
Data indicate that absence of KRAS, TP53 (zeige TP53 Proteine) and SMAD4 genetic alterations may identify a subset of pancreatic carcinomas with better outcome.
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 (zeige PRDM1 Proteine) deletion. Administration of latent-TGFbeta1 (zeige TGFB1 Proteine)-Fc to wild-type mice antagonized LPS (zeige TLR4 Proteine)-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 (zeige TGFB1 Proteine) 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 (zeige TGFB1 Proteine) controls TH17 cell differentiation and uncovers the SKI (zeige SKI Proteine)-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.
Activated TGF-beta (zeige TGFB1 Proteine) signaling rescued miR (zeige MYLIP Proteine)-143-reduced FSHR (zeige FSHR Proteine) and intracellular signaling molecules, and miR (zeige MYLIP Proteine)-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 (zeige BRD2 Proteine).
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 (zeige FST Proteine) are SMAD4 dependent.
ALK5 (zeige TGFBR1 Proteine) and Smad4 have roles in TGF-beta1 (zeige TGFB1 Proteine)-induced pulmonary endothelial permeability
miR (zeige MYLIP Proteine)-183 positively regulates hircine preadipocyte differentiation by inhibiting expression of Smad4.
TGF-beta (zeige TGFB1 Proteine) 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