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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 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 Polyclonal SMAD4 Primary Antibody für IHC (p), WB - ABIN3044024
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, 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 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
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
We found expression of pSmad2/3 and Smad4 in different liver tissues, with up-regulated expression of both antibodies in chronic hepatitis C with higher stage of fibrosis and higher grade of activity. Smad4 expression up-regulated in hepatocellular carcinoma compared to chronic hepatitis C lesions, so it could identify patients with high risk for hepatocellular carcinoma.
SMAD4 mutation is independently associated with worse outcomes among patients undergoing resection of colorectal liver metastases.
Our study demonstrates that loss of SMAD4 expression is a signature characterizing the cetuximab-resistant phenotype and suggests that SMAD4 expression may be a determinant of sensitivity/resistance to EGFR (zeige EGFR Antikörper)/MAPK (zeige MAPK1 Antikörper) or EGFR (zeige EGFR Antikörper)/JNK (zeige MAPK8 Antikörper) inhibition in HPV-negative head and neck squamous cell carcinoma tumors
Whole-genome sequencing and confirmatory Sanger sequencing of junction PCR products were used to show that in each of the 5 cases, the SMAD4 processed gene was integrated at the same position on chromosome 9, located within the last intron of the SCAI (zeige SCAI Antikörper) gene
SMAD4 which can form a SMAD3 (zeige SMAD3 Antikörper)/SMAD4 complex induced by TGFbeta (zeige TGFB1 Antikörper).
High Expression of smad4 is associated with liver cancer.
miR (zeige MLXIP Antikörper)-224 mediates HCT116 colorectal carcinoma cell line proliferation by targeting Smad4.
These results demonstrate that Smad4 suppresses the tumorigenesis and aggressiveness of neuroblastoma (zeige ARHGEF16 Antikörper) through repressing the HPSE (zeige HPSE Antikörper) expression.
SMAD4 gene mutation in hereditary hemorrhagic telangiectasia patients is independently associated with a higher risk of aortic root and ascending aorta dilation.
Smad4 expression negatively correlated with VEGF-A (zeige VEGFA Antikörper) and VEGF-C (zeige VEGFC Antikörper) in colon cancer
Loss of Smad4 in neural progenitor cells impairs adult neurogenesis in the subventricular zone.
Reduced bone-mass and accelerated osteoclastogenesis seen in Smad4-cKO were abrogated by Prdm1 (zeige PRDM1 Antikörper) deletion. Administration of latent-TGFbeta1 (zeige TGFB1 Antikörper)-Fc to wild-type mice antagonized LPS (zeige TLR4 Antikörper)-induced bone destruction in a model of activated osteoclast-mediated bone destruction
miR146b5p directly targeted Smad4 and negatively regulated the transforming growth factor (TGF)-beta (zeige TGFB1 Antikörper) signaling pathway, which contributed to the neural commitment of Pluripotent stem cells (PSCs). Collectively, our findings uncover the essential role of miR146b5p in the neural conversion of PSCs.
study reveals a critical mechanism by which TGFbeta (zeige TGFB1 Antikörper) controls TH17 cell differentiation and uncovers the SKI (zeige SKI Antikörper)-SMAD4 axis as a potential therapeutic target for treating TH17-related diseases
The binding motif of miR26b5p in the Smad4 3'UTR (zeige UTS2R Antikörper) was identified as UACUUGA at position 978-984.
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.
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
miR (zeige MYLIP Antikörper)-183 positively regulates hircine preadipocyte differentiation by inhibiting expression of Smad4.
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