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SMAD family member 2
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 encoding the same protein have been observed. [provided by RefSeq, Jul 2008] (from
Muylkens et al., Namur, Belgium. In Vet J, 30 Sep 2015
Inhibition of expression of the pro-apoptotic factors JARID2 and SMAD2 by viral microRNAs may promote the survival and proliferation of GaHV-2 latently infected cells, thus enhancing tumorigenesis, while inhibition of interleukin 18 by viral microRNAs may be involved in evasion of immune surveillance.
Weber et al., Regensburg, Germany. In Hum Mol Genet, 26 Sep 2015
In addition, structurally altered HTRA1 led to an impaired autocrine TGF-β signaling in microglia, as measured by a strong down regulation of downstream effectors of the TGF-β cascade such as phosphorylated SMAD2 and PAI-1 expression.
Leung et al., Vancouver, Canada. In J Clin Endocrinol Metab, 25 Sep 2015
In HTR8/SVneo cells, activin A-induced production of SNAIL and MMP2 was abolished by pre-treatment with the TGF-β type I receptor (ALK4/5/7) inhibitor SB431542 or siRNA targeting ALK4, SMAD2/3 or common SMAD4.
Cool et al., Liverpool, United Kingdom. In Glycobiology, 24 Sep 2015
In cell-based assays heparin, 2-O-, 6-O- and N-desulphated re-N-acetylated heparin, and oligosaccharides 14-24 saccharides (dp14-24) in length all increased the phosphorylation of SMAD2 after 6 h stimulation with TGF-β1.
Semb et al., Copenhagen, Denmark. In Cell Stem Cell, 04 Jul 2015
β-catenin occupies regulatory regions in numerous PS and neural crest genes, and direct interactions between β-catenin and the Nodal effectors SMAD2/SMAD3 are required at these regions for PS gene activation.
Lahn et al., Bad Homburg vor der Höhe, Germany. In Drug Des Devel Ther, Dec 2014
Galunisertib (LY2157299 monohydrate) is an oral small molecule inhibitor of the TGF-β receptor I kinase that specifically downregulates the phosphorylation of SMAD2, abrogating activation of the canonical pathway.
Li et al., Kansas City, United States. In Nat Med, Nov 2014
MK ablation led to reduced levels of biologically active TGF-β1 protein in the bone marrow and nuclear-localized phosphorylated SMAD2/3 (pSMAD2/3) in HSCs, suggesting that MKs maintain HSC quiescence through TGF-β-SMAD signaling.
Zuo et al., Changsha, China. In Chin Med J (engl), 2013
Second, transforming growth factor receptor/SMAD2/3 signaling activation plays an important role in Treg/Th17 cell imbalance in T cells which toget converge to cause inflammation, endothelial dysfunction, and hypertension following tacrolimus treatment.
Furthermore, SMAD2/3 signaling pathway is involved in the control of both cumulus expansion and steroidogenesis in porcine OCCs, since SMAD2/3 activation by GDF9/ TGFβ produced by oocyte and/or cumulus cells, significantly affects gonadotropin-induced HA and progesterone synthesis by porcine cumulus cells.
Takashiba et al., Okayama, Japan. In J Dent Res, 2012
results indicated Smad2 has inhibitory effects in regulating keratinocyte migration during gingival wound healing. TGF-beta/Smad2 signaling mediating alteration of K16 expression must be tightly regulated during periodontal regeneration.
Derynck et al., San Francisco, United States. In Febs Lett, 2012
TGF-beta family signaling through Smads is conceptually a simple and linear signaling pathway, driven by sequential phosphorylation, with type II receptors activating type I receptors, which in turn activate R-Smads [review]