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anti-Human SMAD4 Antikörper:
anti-Mouse (Murine) SMAD4 Antikörper:
anti-Rat (Rattus) SMAD4 Antikörper:
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Human Polyclonal SMAD4 Primary Antibody für IF, IHC (p) - ABIN272224
Izumi, Nakamura, Tokumo, Mano: A minute pancreatic ductal adenocarcinoma with lipomatous pseudohypertrophy of the pancreas. in JOP : Journal of the pancreas 2011
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Human Monoclonal SMAD4 Primary Antibody für FACS, IF - ABIN967047
Smolander, Vogt, Maillard, Zweiacker, Littke, Hengelage, Burnier: Dose-dependent acute and sustained renal effects of the endothelin receptor antagonist avosentan in healthy subjects. in Clinical pharmacology and therapeutics 2009
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Human Polyclonal SMAD4 Primary Antibody für WB - ABIN3043341
Tang, Li, Yu, Gao, Liu, Chen, Xing, Liu, Yao: Quercetin prevents ethanol-induced iron overload by regulating hepcidin through the BMP6/SMAD4 signaling pathway. in The Journal of nutritional biochemistry 2014
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Human Monoclonal SMAD4 Primary Antibody für ICC, FACS - ABIN969403
Yao, Yin, Lian, Tian, Liu, Li, Sun: MicroRNA-224 is involved in transforming growth factor-beta-mediated mouse granulosa cell proliferation and granulosa cell function by targeting Smad4. in Molecular endocrinology (Baltimore, Md.) 2010
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Human Monoclonal SMAD4 Primary Antibody für ICC, WB - ABIN3043668
Chen, Kong, Wan, Xiao, Li, Wang, Lin, Wang: Effects of huogu I formula (I) on correlated factors of bone regeneration in chickens with steroid-induced necrosis of femoral head. in Chinese journal of integrative medicine 2012
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Human Polyclonal SMAD4 Primary Antibody für WB - ABIN4354704
Kidd, Modlin, Pfragner, Eick, Champaneria, Chan, Camp, Mane: Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor-beta1-mediated regulatory abnormalities including up-regulation of C-Myc and MTA1. in Cancer 2007
Human Monoclonal SMAD4 Primary Antibody für FACS - ABIN4895797
Geng, Chen, Yuan, Peng, Maitra, Diao, Chen, Zhang, Hu, Qi, Pierce, Ling, Xiong, Li: The persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis. in Nature communications 2016
Human Polyclonal SMAD4 Primary Antibody für IF, WB - ABIN392165
Lessard, Rivas, Alves-Wagner, Hirshman, Gallagher, Constantin-Teodosiu, Atkins, Greenhaff, Qi, Gustafsson, Fielding, Timmons, Britton, Koch, Goodyear: Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks. in Diabetes 2013
Epstein Barr virus-encoded BARF1 promotes cell proliferation in stomach cancer by upregulating NFkappaB (zeige NFKB1 Antikörper) and miR (zeige MLXIP Antikörper)-146a and downregulating SMAD4, thereby contributing to EBV-induced stomach cancer progression.
miR (zeige MLXIP Antikörper)-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 (zeige PSG4 Antikörper) drives the progression of colorectal cancer and tumor angiogenesis. This occurs via nuclear translocation of PSG9 (zeige PSG4 Antikörper)/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 Antikörper) in inhibiting SMAD4-mediated breast cancer metastasis providing a possible therapeutic avenue.
we propose that the Smad4-Pitx2 (zeige PITX2 Antikörper)-PPP2R2A (zeige PPP2R2A Antikörper) axis, a new signaling pathway, suppresses the pancreatic carcinogenesis
By downregulating TRAIL-R1, TGFbeta1 (zeige TGFB1 Antikörper) 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 Antikörper) regulates N-cadherin (zeige CDH2 Antikörper) expression by controlling Smad3 (zeige SMAD3 Antikörper) and Smad4 expression through CBP (zeige CREBBP Antikörper), thereby mediating the epithelial-mesenchymal transition.
miR (zeige MLXIP Antikörper)-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 Antikörper)
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 Antikörper)/5/4-Amhr2 (zeige AMHR2 Antikörper)-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1 (zeige SMAD1 Antikörper)/5/4-Amhr2 (zeige AMHR2 Antikörper)-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 Antikörper) signaling mediated by the cytokine receptor (zeige LEPR Antikörper) TGFbetaR1 in NK cells.
The effect of Smad4 was at least partially mediated by the downstream effectors Syk (zeige SYK Antikörper) and ROCK2 (zeige ROCK2 Antikörper) transcription in megakaryocytes
deletion of Smad4 in OBs (zeige LEP Antikörper) differentially modulates HSC (zeige FUT1 Antikörper) fate in a stage-dependent manner
Activated TGF-beta (zeige TGFB1 Antikörper) signaling rescued miR (zeige MYLIP Antikörper)-143-reduced FSHR (zeige FSHR Antikörper) and intracellular signaling molecules, and miR (zeige MYLIP Antikörper)-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 Antikörper).
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 Antikörper) are SMAD4 dependent.
ALK5 (zeige TGFBR1 Antikörper) and Smad4 have roles in TGF-beta1 (zeige TGFB1 Antikörper)-induced pulmonary endothelial permeability
TGF-beta (zeige TGFB1 Antikörper) 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