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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
reduced Smad4 expression may predict responsiveness to regimens that contain DNA topoisomerase inhibitors in human non-small cell lung cancer
Our study showed that miR (show MLXIP Proteins)-205 decreased SMAD4 expression, thus promoting NSCLC cell growth.
Significantly, miR (show MLXIP Proteins)-4260 was increased in human colorectal cancer tissues with simultaneous downregulation of MCC (show MCC Proteins) and SMAD4.
Lung metastases from colorectal cancer patients revealed that CCL15 expression correlated with loss of SMAD4. In a mouse model, CCL15 secreted from SMAD4-deficient colorectal cancer cells recruited CCR1(+) cells, promoting their metastatic activities to the lung.
The stimulation of epithelial-mesenchymal transition (EMT (show ITK Proteins)) by miR196a5p in cancer stem-like cells was abolished by overexpression of Smad4. Collectively, these data demonstrate that miR196a5p has a key role in EMT (show ITK Proteins) and invasion by targeting Smad4 in gastric cancer stem cells(GCSCs). miR196a5p may serve as a potential target for gastric cancer therapy.
Biomarker expression in pancreatic ductal adenocarcinoma (PDAC) of CXCR4, SMAD4, SOX9 and IFIT3 will be prospectively assessed by immunohistochemistry and verified by rt.-PCR from tumor and adjacent healthy pancreatic tissue of surgical specimen.
Epstein Barr virus-encoded BARF1 promotes cell proliferation in stomach cancer by upregulating NFkappaB (show NFKB1 Proteins) and miR (show MLXIP Proteins)-146a and downregulating SMAD4, thereby contributing to EBV-induced stomach cancer progression.
miR (show MLXIP Proteins)-20a-5p, as an onco-miRNA, promoted the invasion and metastasis ability by suppressing Smad4 expression in colorectal cancer cells.
Findings illustrate the innovative mechanism by which PSG9 drives the progression of colorectal cancer and tumor angiogenesis. This occurs via nuclear translocation of PSG9/SMAD4, which activates angiogenic cytokines.
results characterized miR-1305-Smad4 axis as a major downstream functional mechanism of lncRNA DANCR in promoting the chondrogenesis in synovium-derived mesenchymal stem cells.
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 (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
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