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the role of SIRT7 (show SIRT7 ELISA Kits) in inhibiting SMAD4-mediated breast cancer metastasis providing a possible therapeutic avenue.
we propose that the Smad4-Pitx2 (show PITX2 ELISA Kits)-PPP2R2A (show PPP2R2A ELISA Kits) axis, a new signaling pathway, suppresses the pancreatic carcinogenesis
By downregulating TRAIL-R1, TGFbeta1 (show TGFB1 ELISA Kits) may not only promote tumor escape from immune surveillance but also negatively impact on TRAIL- or TRAIL-R1-based therapy regimens for treatment of Pancreatic ductal adenocarcinoma.
Sec8 (show EXOC4 ELISA Kits) regulates N-cadherin (show CDH2 ELISA Kits) expression by controlling Smad3 (show SMAD3 ELISA Kits) and Smad4 expression through CBP (show CREBBP ELISA Kits), thereby mediating the epithelial-mesenchymal transition.
miR (show MLXIP ELISA Kits)-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 (show CELSR1 ELISA Kits)
Our data indicated that colon cancer cell induced the expression of miR (show MLXIP ELISA Kits)-27a in HLECs, which promoted lymphangiogenesis by targeting SMAD4. Our finding implicated miR (show 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 (show 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 (show TAZ ELISA Kits) and miR (show 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.
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 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.
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