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anti-Human SMAD4 Antikörper:
anti-Mouse (Murine) 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 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 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
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
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)
These results suggest an important role for cross talk among Smad (zeige SMAD1 Antikörper), p38 MAPK (zeige MAPK14 Antikörper), JNK (zeige MAPK8 Antikörper), and PI3K (zeige PIK3CA Antikörper) pathways in mediating the augmented expression of hAT(1 (zeige HAT1 Antikörper))R following TGF-beta1 (zeige TGFB1 Antikörper) treatment in human fetal pulmonary fibroblasts.
Our data indicated that colon cancer cell induced the expression of miR (zeige MLXIP Antikörper)-27a in HLECs, which promoted lymphangiogenesis by targeting SMAD4. Our finding implicated miR (zeige MLXIP Antikörper)-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 Antikörper)-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 Antikörper) and miR (zeige MLXIP Antikörper)-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 Antikörper)-558 facilitates the progression of gastric cancer through directly targeting the HPSE (zeige HPSE Antikörper) promoter to attenuate Smad4-mediated repression of HPSE (zeige HPSE Antikörper) expression.
Smad4 may not directly induce thoracic aortic aneurysms; rather it may contribute to TAA in combination with other risk factors.
miR (zeige MLXIP Antikörper)-27a contributed to cell proliferation and invasion by inhibiting TGF-beta (zeige TGFB1 Antikörper)-induced cell cycle arrest. These results suggest that miR (zeige MLXIP Antikörper)-27a may function as an oncogene (zeige RAB1A Antikörper) by regulating SMAD2 (zeige SMAD2 Antikörper) and SMAD4 in lung cancer.
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
Data suggest that ovarian Bmp4 (zeige BMP4 Antikörper) levels are significantly decreased in a mouse model of polycystic ovary syndrome with hyperandrogenism; androgens inhibited Bmp4 (zeige BMP4 Antikörper) expression via activation of androgen receptors; Smad4 signaling rather than p38 MAPK (zeige MAPK14 Antikörper) pathway regulates androgen and estrogen formation.
The authors demonstrated that ubiquitin-specific protease (USP) 4 (zeige USP4 Antikörper) strongly induces activin (zeige Actbeta Antikörper)/BMP signaling by removing the inhibitory monoubiquitination from SMAD4.
SMAD4 and STRA8 (zeige STRA8 Antikörper) 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 Antikörper) to induce the protein anabolism signature, which instead critically depends on the transcription factor Atf4 (zeige ATF4 Antikörper).
Smad4 may reduce lymphangiogenesis of colon cancer cell by attenuating VEGF-C (zeige VEGFC Antikörper) secretion and act as tumor suppressor by inhibiting migration, invasion and tumorigenicity.
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