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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 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 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 Polyclonal SMAD4 Primary Antibody für IHC (p), WB - ABIN3044024
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
reduced Smad4 expression may predict responsiveness to regimens that contain DNA topoisomerase inhibitors in human non-small cell lung cancer
Our study showed that miR (zeige MLXIP Antikörper)-205 decreased SMAD4 expression, thus promoting NSCLC cell growth.
Significantly, miR (zeige MLXIP Antikörper)-4260 was increased in human colorectal cancer tissues with simultaneous downregulation of MCC (zeige MCC Antikörper) and SMAD4.
Lung metastases from colorectal cancer patients revealed that CCL15 expression correlated with loss of SMAD4. In a mouse model, CCL15 secreted from SMAD4-deficient colorectal cancer cells recruited CCR1(+) cells, promoting their metastatic activities to the lung.
The stimulation of epithelial-mesenchymal transition (EMT (zeige ITK Antikörper)) by miR196a5p in cancer stem-like cells was abolished by overexpression of Smad4. Collectively, these data demonstrate that miR196a5p has a key role in EMT (zeige ITK Antikörper) and invasion by targeting Smad4 in gastric cancer stem cells(GCSCs). miR196a5p may serve as a potential target for gastric cancer therapy.
Biomarker expression in pancreatic ductal adenocarcinoma (PDAC) of CXCR4, SMAD4, SOX9 and IFIT3 will be prospectively assessed by immunohistochemistry and verified by rt.-PCR from tumor and adjacent healthy pancreatic tissue of surgical specimen.
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 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.
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
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