Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Select your species
Our data indicated that colon cancer cell induced the expression of miR (zeige MLXIP ELISA Kits)-27a in HLECs, which promoted lymphangiogenesis by targeting SMAD4. Our finding implicated miR (zeige MLXIP ELISA Kits)-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 (zeige MLXIP ELISA Kits)-224 functions by inhibiting the tumor suppressor, SMAD4, to support the proliferation and migration of osteosarcoma (OS) cells. Our findings indicate that targeting TAZ (zeige TAZ ELISA Kits) and miR (zeige MLXIP ELISA Kits)-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 (zeige MLXIP ELISA Kits)-558 facilitates the progression of gastric cancer through directly targeting the HPSE (zeige HPSE ELISA Kits) promoter to attenuate Smad4-mediated repression of HPSE (zeige 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 (zeige MLXIP ELISA Kits)-27a contributed to cell proliferation and invasion by inhibiting TGF-beta (zeige TGFB1 ELISA Kits)-induced cell cycle arrest. These results suggest that miR (zeige MLXIP ELISA Kits)-27a may function as an oncogene (zeige RAB1A ELISA Kits) by regulating SMAD2 (zeige 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
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 (zeige SMAD1 ELISA Kits)/5/4-Amhr2 (zeige AMHR2 ELISA Kits)-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1 (zeige SMAD1 ELISA Kits)/5/4-Amhr2 (zeige 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 (zeige TGFB1 ELISA Kits) signaling mediated by the cytokine receptor (zeige LEPR ELISA Kits) TGFbetaR1 in NK cells.
The effect of Smad4 was at least partially mediated by the downstream effectors Syk (zeige SYK ELISA Kits) and ROCK2 (zeige ROCK2 ELISA Kits) transcription in megakaryocytes
deletion of Smad4 in OBs (zeige LEP ELISA Kits) differentially modulates HSC (zeige FUT1 ELISA Kits) fate in a stage-dependent manner
Data suggest that ovarian Bmp4 (zeige BMP4 ELISA Kits) levels are significantly decreased in a mouse model of polycystic ovary syndrome with hyperandrogenism; androgens inhibited Bmp4 (zeige BMP4 ELISA Kits) expression via activation of androgen receptors; Smad4 signaling rather than p38 MAPK (zeige MAPK14 ELISA Kits) pathway regulates androgen and estrogen formation.
The authors demonstrated that ubiquitin-specific protease (USP) 4 (zeige USP4 ELISA Kits) strongly induces activin (zeige 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 (zeige BMP2 ELISA Kits) to induce the protein anabolism signature, which instead critically depends on the transcription factor Atf4 (zeige ATF4 ELISA Kits).
Smad4 may reduce lymphangiogenesis of colon cancer cell by attenuating VEGF-C (zeige VEGFC ELISA Kits) secretion and act as tumor suppressor by inhibiting migration, invasion and tumorigenicity.
Activated TGF-beta (zeige TGFB1 ELISA Kits) signaling rescued miR (zeige MYLIP ELISA Kits)-143-reduced FSHR (zeige FSHR ELISA Kits) and intracellular signaling molecules, and miR (zeige 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 (zeige 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 (zeige FST ELISA Kits) are SMAD4 dependent.
ALK5 (zeige TGFBR1 ELISA Kits) and Smad4 have roles in TGF-beta1 (zeige TGFB1 ELISA Kits)-induced pulmonary endothelial permeability
TGF-beta (zeige 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