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Human SMAD2 ELISA Kit for Sandwich ELISA - ABIN417849
Piotrowski, Kiszałkiewicz, Górski, Antczak, Górski, Pastuszak-Lewandoska, Migdalska-Sęk, Domańska-Senderowska, Nawrot, Czarnecka, Kurmanowska, Brzeziańska-Lasota: Immunoexpression of TGF-β/Smad and VEGF-A proteins in serum and BAL fluid of sarcoidosis patients. in BMC immunology 2015
Rat (Rattus) SMAD2 ELISA Kit for Sandwich ELISA - ABIN432538
Kabel, Abd Elmaaboud, Albarraq: Ameliorative potential of omega 3 fatty acids and HMG-CoA reductase inhibitors on experimentally-induced non-alcoholic steatohepatitis. in Prostaglandins, leukotrienes, and essential fatty acids 2015
The results of this study found that Bptf and TGF-beta (show TGFB1 ELISA Kits)/Smad2 mediate nucleosome remodeling to regulate wnt8a (show WNT8A ELISA Kits) expression and hence neural posteriorization.
Smad2 and Eomesodermin (show EOMES ELISA Kits) a (Eomesa (show EOMES ELISA Kits)) bind common genomic regions proximal to genes involved in mesoderm and endoderm formation, suggesting Eomesa (show EOMES ELISA Kits) forms a general component of the Smad2 signalling complex in zebrafish.
These results reveal that kinesin-mediated transport of Smad2 along microtubules to the receptors is an essential step in ligand-induced Smad2 activation.
study systemically uncovers a large number of Smad2 targets in early gastrulas and suggests cooperative roles of Smad2 and other transcription factors in controlling target gene transcription
Nodal signaling and mesendoderm induction depend on Smad2/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2/3 signaling and embryonic patterning.
Smad2/3 activities play important roles not only in mesendodermal development but also in neural development during early vertebrate embryogenesis
Low SMAD2 expression is associated with progression of hepatic fibrosis.
In order to study the translation between mouse model and patients, we evaluated the signature of phosphorylated Sma- and Mad-related protein 2 (pSmad2), as molecular marker of TGF-beta/activin activity, in the kidneys of streptozotocin (STZ)-treated mice compared to that of type 1 diabetes (T1D) patients.
SMAD2/SMAD3 (show SMAD3 ELISA Kits) signaling by bone morphogenetic proteins causes disproportionate induction of HAS2 (show HAS2 ELISA Kits) expression and hyaluronan production in immortalized human granulosa cells.
miR (show MLXIP ELISA Kits)-27a contributed to cell proliferation and invasion by inhibiting TGF-beta (show TGFB1 ELISA Kits)-induced cell cycle arrest. These results suggest that miR (show MLXIP ELISA Kits)-27a may function as an oncogene (show RAB1A ELISA Kits) by regulating SMAD2 and SMAD4 (show SMAD4 ELISA Kits) in lung cancer.
cPLA2alpha (show PLA2G4A ELISA Kits) activates PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) and inhibits Smad2/3 during epithelial-mesenchymal transition of hepatocellular carcinoma cells.
selective inhibition of SMAD3 (show SMAD3 ELISA Kits) or CCT6A (show CCT6A ELISA Kits) efficiently suppresses TGF-beta (show TGFB1 ELISA Kits)-mediated metastasis. Findings provide a mechanism that directs TGF-beta (show TGFB1 ELISA Kits) signaling toward its prometastatic arm and may contribute to the development of therapeutic strategies targeting TGF-beta (show TGFB1 ELISA Kits) for non-small-cell lung carcinoma.
In response to TGF-beta (show TGFB1 ELISA Kits), RASSF1A (show RASSF1 ELISA Kits) is recruited to TGF-beta (show TGFB1 ELISA Kits) receptor I and targeted for degradation by the co-recruited E3 ubiquitin ligase ITCH. RASSF1A (show RASSF1 ELISA Kits) degradation is necessary to permit Hippo pathway effector YAP1 (show YAP1 ELISA Kits) association with SMADs and subsequent nuclear translocation of receptor-activated SMAD2.
Smad2 is a key scaffold, allowing RIN1 (show RIN1 ELISA Kits) to act as a GTP (show AK3 ELISA Kits) exchange factor for MFN2 (show MFN2 ELISA Kits)-GTPase (show RACGAP1 ELISA Kits) activation to promote mitochondrial ATP synthesis and suppress superoxide production during mitochondrial fusion.
Ang (show ANG ELISA Kits) down-regulate the expression of Col (show HDAC1 ELISA Kits)-I, alpha-SMA (show SMN1 ELISA Kits) and TGF-beta1 (show TGFB1 ELISA Kits)/Smad2/3 and subsequently inhibits fibroblast-myofibroblast transition.
The nuclear importin IPO5 (show IPO5 ELISA Kits) was identified as a novel interacting protein of SMAD1 (show GARS ELISA Kits). Overexpression of IPO5 (show IPO5 ELISA Kits) in various cell lines specifically increases nuclear localization of BMP receptor (show BMPR1A ELISA Kits)-activated SMADs (R-SMADs) confirming a functional relationship between IPO5 (show IPO5 ELISA Kits) and BMP but not TGF-beta (show TGFB1 ELISA Kits) R-SMADs.
Grg4 occupancy at the Xnr1 (show NODAL ELISA Kits) enhancer significantly decreases with Smad2 overexpression.Nodal-activated Smad2 physically displaces Grg4 from FoxH1 (show FOXH1 ELISA Kits) at the Xnr1 (show NODAL ELISA Kits) enhancer, an essential feature of the transcriptional switch mechanism.
E2a (show TCF3 ELISA Kits) is necessary to drive transcription of Smad2/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
GDF11 (show GDF11 ELISA Kits) has a central role in the activation of Smad2 phosphorylation in tailbud stage Xenopus embryos.
XPIASy functions as an essential negative regulator of the XSmad2 pathway to ensure proper mesoderm induction at the appropriate time and in the appropriate region.
Activin A (show INHBA ELISA Kits) and overexpression of SMAD2/3 significantly promoted expressions of porcine NANOG (show NANOG ELISA Kits) and OCT4 (show POU5F1 ELISA Kits),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (show NANOG ELISA Kits)/OCT4 (show POU5F1 ELISA Kits) expression.
the present work provides evidence supporting a functional role of SMAD2/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2/3P signaling, which is known to be protective for articular cartilage and to block chondrocyte terminal differentiation.
a detailed computational model for TGF-beta (show TGFB1 ELISA Kits) signalling that incorporates elements of previous models together with crosstalking between Smad1 (show SMAD1 ELISA Kits)/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7 (show SMAD7 ELISA Kits).
These findings implicate TGF-beta (show TGFB1 ELISA Kits)-Smad2/3 signaling in activated tissue-resident cardiac fibroblasts as principal mediators of the fibrotic response.
results demonstrate that TGF-beta1 (show TGFB1 ELISA Kits)-induced autophagy links beta-catenin (show CTNNB1 ELISA Kits) and Smad (show SMAD1 ELISA Kits) signaling to promote epithelial-mesenchymal transition in C1.1 cells through a novel pY654-beta-catenin (show CTNNB1 ELISA Kits)/p-Smad2/ILK (show ILK ELISA Kits) pathway.
These results suggest that Nedd9 (show NEDD9 ELISA Kits) is a Smad2/3 target gene implicated in RANKL (show TNFSF11 ELISA Kits)-induced osteoclastogenesis.
In conclusion, TGF-beta (show TGFB1 ELISA Kits) signaling pathway may influence liver fibrosis by incorporating with YB-1 (show YBX1 ELISA Kits), indicating that YB-1 (show YBX1 ELISA Kits) could be a potential target for therapies against liver fibrosis.
miR (show MLXIP ELISA Kits)-27b is an anti-fibrotic microRNA that inhibits fibroblast activation by targeting TGFbeta (show TGFB1 ELISA Kits) receptor 1 and SMAD2.
hese studies revealed that Smad2 plays an essential role in the development of the growth plate, that both Smads 2 and 3 inhibit Ihh (show IHH ELISA Kits) expression in the neonatal growth plate, and suggested they accomplish this by binding to distinct SBEs, mediating assembly of distinct repressive complexes.
This study found evidence of increased leukocyte phosphorylated-Smad2/3 staining in both single leukocytes and platelet-leukocyte aggregates in mice that developed aortic valve stenosis, suggesting the presence of increased circulating active TGF-beta1 (show TGFB1 ELISA Kits).
Data show that muscle-specific (show EIF3K ELISA Kits) Smad (show SMAD1 ELISA Kits) proteins Smad2/3-deficient mice exhibited significant resistance to denervation-induced muscle atrophy.
The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein mediates the signal of the transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4. The association with SMAD4 is important for the translocation of this protein into the nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors. This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants have been observed for this gene.
SMAD, mothers against DPP homolog 2
, MAD (mothers against decapentaplegic, Drosophila) homolog 2
, SMA- and MAD-related protein 2
, SMAD 2
, SMAD family member 2
, mothers against DPP homolog 2
, mothers against decapentaplegic homolog 2
, MAD homolog 2
, Sma- and Mad-related protein 2
, mother against DPP homolog 2
, mothers against decapentaplegic-like 2
, Smad 2
, mad-related protein 2