Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
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 ELISA Kits)-558 facilitates the progression of gastric cancer through directly targeting the HPSE (show HPSE ELISA Kits) promoter to attenuate Smad4-mediated repression of HPSE (show HPSE ELISA Kits) expression.
Smad4 may not directly induce thoracic aortic aneurysms; rather it may contribute to TAA in combination with other risk factors.
miR (show MLXIP ELISA Kits)-27a contributed to cell proliferation and invasion by inhibiting TGF-beta (show TGFB1 ELISA Kits)-induced cell cycle arrest. These results suggest that miR (show MLXIP ELISA Kits)-27a may function as an oncogene (show RAB1A ELISA Kits) by regulating SMAD2 (show SMAD2 ELISA Kits) and SMAD4 in lung cancer.
Genetic status of DPC4 contributes to the recurrence patterns in pancreatic ductal adenocarcinoma following pancreatectomy, and patients with an initially expressed DPC4 gene receive a greater benefit from intensive local control for locoregional recurrence
NK cells from a SMAD4-deficient person affected by polyposis were hyper-responsive to TGF-beta
SMAD4 mutation was commonly detected in pancreatic juice samples from patients with Pancreatic Ductal Adenocarcinoma, mutant SMAD4 concentrations could distinguish PDAC from Intraductal Papillary Mucinous neoplasm.
Phosphorylation of SMAD4 is associated with Breast Cancer Metastasis.
Several germline variants in Hamartomatous Polyposis Syndrome genes were detected, among them three in ENG (show ENG ELISA Kits), two in BMPR1A (show BMPR1A ELISA Kits), one in PTEN, and one in SMAD4. Although some of the detected variants have been reported previously none could be definitely pathogenic or likely pathogenic.
We discovered that Smad1 (show SMAD1 ELISA Kits)/5/4-Amhr2 (show AMHR2 ELISA Kits)-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1 (show SMAD1 ELISA Kits)/5/4-Amhr2 (show AMHR2 ELISA Kits)-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 ELISA Kits) signaling mediated by the cytokine receptor (show LEPR ELISA Kits) TGFbetaR1 in NK cells.
The effect of Smad4 was at least partially mediated by the downstream effectors Syk (show SYK ELISA Kits) and ROCK2 (show ROCK2 ELISA Kits) transcription in megakaryocytes
deletion of Smad4 in OBs (show LEP ELISA Kits) differentially modulates HSC (show FUT1 ELISA Kits) fate in a stage-dependent manner
Data suggest that ovarian Bmp4 (show BMP4 ELISA Kits) levels are significantly decreased in a mouse model of polycystic ovary syndrome with hyperandrogenism; androgens inhibited Bmp4 (show BMP4 ELISA Kits) expression via activation of androgen receptors; Smad4 signaling rather than p38 MAPK (show MAPK14 ELISA Kits) pathway regulates androgen and estrogen formation.
The authors demonstrated that ubiquitin-specific protease (USP) 4 (show USP4 ELISA Kits) strongly induces activin (show Actbeta ELISA Kits)/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 ELISA Kits) to induce the protein anabolism signature, which instead critically depends on the transcription factor Atf4 (show ATF4 ELISA Kits).
Smad4 may reduce lymphangiogenesis of colon cancer cell by attenuating VEGF-C (show VEGFC ELISA Kits) secretion and act as tumor suppressor by inhibiting migration, invasion and tumorigenicity.
MZF1 has a role in cellular migration of gastric cancer cells via promoting an increase in intracellular SMAD4 levels. This study might provide new evidence for the molecular basis of the tumor suppressive effect of the MZF1-SMAD4 axis, a new therapeutic target in advanced human gastric cancer.
Activated TGF-beta (show TGFB1 ELISA Kits) signaling rescued miR (show MYLIP ELISA Kits)-143-reduced FSHR (show FSHR ELISA Kits) and intracellular signaling molecules, and miR (show MYLIP ELISA Kits)-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 ELISA Kits).
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 ELISA Kits) are SMAD4 dependent.
ALK5 (show TGFBR1 ELISA Kits) and Smad4 have roles in TGF-beta1 (show TGFB1 ELISA Kits)-induced pulmonary endothelial permeability
TGF-beta (show TGFB1 ELISA Kits) 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