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proteins. Page last changed on 24 Oct 2014.
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
Li et al., Kansas City, United States. In Nat Med, 19 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), 31 Oct 2014
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.
Luo et al., Changsha, China. In Asian Pac J Cancer Prev, Dec 2013
The high-throughput analysis showed that the CCND1 and EGFR genes were outstanding in being significantly enriched, and the target genes cebpb and VCAM1 and the protein SMAD2 were also vital in mir-155-related immune reponse activities.
Higgins et al., Albany, United States. In Cell Signal, 2013
ROS generation in response to TGF-β1 stimulation is rapid and precedes PAI-1 induction; engagement of non-SMAD (e.g., EGFR, Src kinase, MAP kinases, p53) and SMAD2/3 pathways are both required for PAI-1 expression and are ROS-dependent.
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.
Cormier-Daire et al., Paris, France. In Am J Med Genet C Semin Med Genet, 2012
We found an increased level of active TGFβ in the fibroblast medium from patients with FBN1 or ADAMTSL2 mutations and an enhanced phosphorylated SMAD2 level, allowing us to conclude at an enhanced TGFβ signaling in GD and AD.
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]