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anti-Human SMAD6 Anticorps:
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Human Polyclonal SMAD6 Primary Antibody pour ICC, IF - ABIN252409
Hogg, Etherington, Young, McNeilly, Duncan: Inhibitor of differentiation (Id) genes are expressed in the steroidogenic cells of the ovine ovary and are differentially regulated by members of the transforming growth factor-beta family. dans Endocrinology 2010
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Human Polyclonal SMAD6 Primary Antibody pour WB - ABIN537519
Frullanti, Colombo, Falvella, Galvan, Noci, De Cecco, Incarbone, Alloisio, Santambrogio, Nosotti, Tosi, Pastorino, Dragani: Association of lung adenocarcinoma clinical stage with gene expression pattern in noninvolved lung tissue. dans International journal of cancer. Journal international du cancer 2012
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Human Monoclonal SMAD6 Primary Antibody pour ELISA, WB - ABIN969405
Shen, Chen, Wang, Kaneki, Xing, Okeefe, Chen: Smad6 interacts with Runx2 and mediates Smad ubiquitin regulatory factor 1-induced Runx2 degradation. dans The Journal of biological chemistry 2006
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SMAD6 overexpression leads to accelerated myogenic differentiation of LMNA mutated cells.
A novel SMAD6 variant was identified in a patient with severely calcified bicuspid aortic valve and thoracic aortic aneurysm.
Data indicate two individuals with biallelic missense variants in SMAD6 and a complex cardiac phenotype.
Study reports that SMAD6 is overexpressed in nuclei of glioma cells, which correlates with poor patient survival and regulates STAT3 activity via negatively regulating PIAS3. Mechanically, SMAD6 interacts directly with PIAS3, and this interaction is mediated through the Mad homology 2 domain of SMAD6 and the Ring domain of PIAS3.
Overexpression of miR186 mimic induced HUVEC apoptosis through mitogenactivated protein kinase (MAPK) activation by targeting and inhibiting SMAD family member 6 (SMAD6).
activation of AMPK upregulated Smad6 and Smurf1 and thereby enhanced their interactions, resulting in its proteosome-dependent degradation of ALK2.
Results show that high Smad6 expression is correlated with increased risk of metastasis in ER negative breast cancer and that Smad6 determines BMP-regulated invasive behavior of breast cancer cells in a zebrafish xenograft model.
evaluated the role of inherited genetic variation in Langerhans cell histiocytosis susceptibility and identified a novel risk variant in SMAD6
This search revealed that rare mutations that disable one copy of a gene called SMAD6 in combination with a common DNA variant near another gene called BMP2 account for about 7% of infants with midline forms of craniosynostosis.
Single Nucleotide Polymorphisms in SMAD6 gene is associated with brain metastasis in non-small-cell lung cancer
monoubiquitinated SMAD6 impairs the binding affinity of non-modified SMAD6 to the BMP type I receptor. Moreover, UBE2O and SMAD6 cooperated in the regulation of BMP7-induced adipogenesis
Smad6 indirectly maintains stemness by preventing spontaneous erythropoiesis in hematopoietic stem cells.
Loss of SMAD6 is associated with lung adenocarcinoma.
Congenital cardiovascular malformation is related to genetic variation in SMAD6
Haplotype analysis further revealed that two haplotype blocks within SMAD6 were significantly associated with decreased ovarian cancer risk, as compared to the most common haplotype.
results suggest that MyD88 degradation driven by the Smad6-Smurf pathway is a novel mechanism for TGF-beta1-mediated negative regulation of MyD88-dependent pro-inflammatory signalling
Data show that Runx1, in conjunction with Fli1, Gata2, and Scl, directly regulates the expression of Smad6 in the aorta-gonad-mesonephros region in the developing embryo, where hematopoietic stem cells originate.
Smad6 and Smad7, inhibitors of BMP signaling, were up-regulated in HFE-mutant hereditary hemochromatosis compared to controls, disruptin bone morphogenic protein signaling.
Smad6 together with Smad2 may be prognostic factors, independent of nodal status in oral SCC after curative resection
Smad6 has no role in TGF-beta response and injury in podocytes. In contrast, Smad6 is upregulated in the mesangium in human glomerular diseases and may be involved in functions independent of TGF-beta/Smad signaling.
A complex form of acute rheumatic heart disease with tissue hardening is seen in the absence of either Smad-6 (or NKX2-5).
These results indicate that PRIP is implicated in BMP-induced osteoblast differentiation by the negative regulation of Smad phosphorylation, through the methylation of inhibitory Smad6
These findings suggest that TNF-alpha induces valvular and vascular cell calcification, in part, by specifically reducing the expression of a BMP-2 signaling inhibitor, Smad6.
The Smad6 is a novel target of Arkadia, and that Arkadia positively regulates BMP signalling via degradation of Smad6, Smad7 and c-Ski/SnoN.
Smad6 inhibits non-canonical TGF-beta1 signaling by recruiting the deubiquitinase A20 to TRAF6.
Hepcidin, Smad6 and Smad7 mRNA expression is coordinated in a way that it correlates with the activity of the Bmp/Smad signaling pathway.
Sema7A positively regulates the production of transforming growth factor (TGF)-beta1 and Smad6 to facilitate West Nile virus pathogenesis in mice.
Results indicate that peptidyl-prolyl isomerase Pin1 Associates with Smad3 and Smad6.
JNK1 activation decreases binding of inhibitory Smad6 to the type I BMP receptor.
Increased Smad3 linker phosphorylation at Thr-179 and Ser-208 and was dependent on ERK1/2 activity via the TLR4-IRAK1-linked signaling cascade.
Smad7 and Smad6 significantly promoted the differentiation of mouse embryonic stem (ES) cells into ciliated cells.
Hoxc8, when over-expressed in C3H10T1/2 or C2C12 cells, suppressed basal Smad6 promoter activity and its mRNA expression
These results demonstrated that overexpression of Smad6 in acini enhanced the development of pancreatic fibrosis after chronic pancreatic injury.
Smad6 repressed bone morphogenetic protein-induced Id1 transcription through recruiting transcriptional corepressor C-terminal binding protein (CtBP).
Smad6 transgenic mice showed postnatal dwarfism with osteopenia and inhibition of Smad1/5/8 phosphorylation in chondrocytes.
Elevated intracellular cAMP might thus enhance BMP signaling by suppressing Smad6 induction and prolonging intracellular BMP signaling.
OAZ can alter the intensity and duration of the BMP4 stimulus through Smad6
The protein encoded by this gene belongs to the SMAD family of proteins, which are related to Drosophila 'mothers against decapentaplegic' (Mad) and C. elegans Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein functions in the negative regulation of BMP and TGF-beta/activin-signalling. Multiple transcript variants encoding different isoforms have been found for this gene.
SMAD, mothers against DPP homolog 6
, MAD homolog 6
, Mothers against decapentaplegic, drosophila, homolog of, 6
, SMAD 6
, mothers against DPP homolog 6
, mothers against decapentaplegic homolog 6
, Smad 6
, mad homolog 7
, MAD, mothers against decapentaplegic homolog 6