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Epstein Barr virus-encoded BARF1 promotes cell proliferation in stomach cancer by upregulating NFkappaB (zeige NFKB1 ELISA Kits) and miR (zeige MLXIP ELISA Kits)-146a and downregulating SMAD4, thereby contributing to EBV-induced stomach cancer progression.
miR (zeige MLXIP ELISA Kits)-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 role of SIRT7 (zeige SIRT7 ELISA Kits) in inhibiting SMAD4-mediated breast cancer metastasis providing a possible therapeutic avenue.
we propose that the Smad4-Pitx2 (zeige PITX2 ELISA Kits)-PPP2R2A (zeige PPP2R2A ELISA Kits) axis, a new signaling pathway, suppresses the pancreatic carcinogenesis
By downregulating TRAIL-R1, TGFbeta1 (zeige 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 (zeige EXOC4 ELISA Kits) regulates N-cadherin (zeige CDH2 ELISA Kits) expression by controlling Smad3 (zeige SMAD3 ELISA Kits) and Smad4 expression through CBP (zeige CREBBP ELISA Kits), thereby mediating the epithelial-mesenchymal transition.
miR (zeige 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 (zeige CELSR1 ELISA Kits)
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 (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
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