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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. in 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. in Journal of virology 2011
miR (show MLXIP Proteins)-483 suppresses chondrogenic differentiation of bone marrow-derived mesenchymal stem cells by targeting SMAD4
The chromosome 18q21 deletion in nearly one third of pancreatic adenocarcinomas eliminates not only the tumor suppressor SMAD4, but also neighboring genes with important cellular roles, such as ME2
Our data indicated that colon cancer cell induced the expression of miR (show MLXIP Proteins)-27a in HLECs, which promoted lymphangiogenesis by targeting SMAD4. Our finding implicated miR (show MLXIP Proteins)-27a as a potential target for new anticancer therapies in colon cancer
Results provide evidence that not only epithelial SMAD4 loss, but also stromal features, may regulate the risk of malignant transformation of oral leukoplakia.
mechanistic study revealed that miR (show MLXIP Proteins)-224 functions by inhibiting the tumor suppressor, SMAD4, to support the proliferation and migration of osteosarcoma (OS) cells. Our findings indicate that targeting TAZ (show TAZ Proteins) and miR (show MLXIP Proteins)-224 could be a promising approach for the treatment of OS.
We hypothesize that the expanded spectrum of cardiovascular abnormalities relates to the ability of the SMAD4 protein to integrate diverse signaling pathways. The co-occurrence of congenital and acquired phenotypes demonstrates that the gene product of SMAD4 is required for both developmental and postnatal cardiovascular homeostasis.
Loss of heterozygosity and high cytoplasmic localization of SMAD4 expression in Stage II and low nuclear SMAD4 in Stage III are associated with colorectal cancer.
miR (show MLXIP Proteins)-558 facilitates the progression of gastric cancer through directly targeting the HPSE (show HPSE Proteins) promoter to attenuate Smad4-mediated repression of HPSE (show HPSE Proteins) expression.
Smad4 may not directly induce thoracic aortic aneurysms; rather it may contribute to TAA in combination with other risk factors.
miR (show MLXIP Proteins)-27a contributed to cell proliferation and invasion by inhibiting TGF-beta (show TGFB1 Proteins)-induced cell cycle arrest. These results suggest that miR (show MLXIP Proteins)-27a may function as an oncogene (show RAB1A Proteins) by regulating SMAD2 (show SMAD2 Proteins) and SMAD4 in lung cancer.
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 (show SMAD1 Proteins)/5/4-Amhr2 (show AMHR2 Proteins)-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1 (show SMAD1 Proteins)/5/4-Amhr2 (show AMHR2 Proteins)-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 (show TGFB1 Proteins) signaling mediated by the cytokine receptor (show LEPR Proteins) TGFbetaR1 in NK cells.
The effect of Smad4 was at least partially mediated by the downstream effectors Syk (show SYK Proteins) and ROCK2 (show ROCK2 Proteins) transcription in megakaryocytes
deletion of Smad4 in OBs (show LEP Proteins) differentially modulates HSC (show FUT1 Proteins) fate in a stage-dependent manner
Data suggest that ovarian Bmp4 (show BMP4 Proteins) levels are significantly decreased in a mouse model of polycystic ovary syndrome with hyperandrogenism; androgens inhibited Bmp4 (show BMP4 Proteins) expression via activation of androgen receptors; Smad4 signaling rather than p38 MAPK (show MAPK14 Proteins) pathway regulates androgen and estrogen formation.
The authors demonstrated that ubiquitin-specific protease (USP) 4 (show USP4 Proteins) strongly induces activin/BMP signaling by removing the inhibitory monoubiquitination from SMAD4.
SMAD4 and STRA8 are essential factors that regulate the female fate of germ cells.
Smad4 is necessary for the activation of the mineralization-related genes, it is dispensable for BMP2 (show BMP2 Proteins) to induce the protein anabolism signature, which instead critically depends on the transcription factor Atf4 (show ATF4 Proteins).
Activated TGF-beta (show TGFB1 Proteins) signaling rescued miR (show MYLIP Proteins)-143-reduced FSHR (show FSHR Proteins) and intracellular signaling molecules, and miR (show MYLIP Proteins)-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 (show BRD2 Proteins).
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 (show FST Proteins) are SMAD4 dependent.
ALK5 (show TGFBR1 Proteins) and Smad4 have roles in TGF-beta1 (show TGFB1 Proteins)-induced pulmonary endothelial permeability
TGF-beta (show TGFB1 Proteins) 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