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Here, we found that myostatin increased the phosphorylation of Smad3 in soleus and EDL muscles and promoted an increase in proteolysis in soleus and a decrease in protein turnover in EDL and C2C12 cell culture.
A novel 17 bpindel in the SMAD3 gene alters transcription level, contributing to phenotypic traits in Chinese cattle.
These changes include cell growth arrest due to an increased expression of transforming growth factor beta (TGF[beta]1 and TGF[beta]2) followed by the inactivation of c-Myc through SMAD3 in human mesenchymal stem cells, (26) downregulation of cell-cycle quiescence and stemness-related genes and upregulation of signal transduction, cell adhesion, and cytoskeletal-related genes in human stromal stem cells.
Kaempferol Suppresses Transforming Growth Factor-[beta]-Induced Epithelial-to-Mesenchymal Transition and Migration of A549 Lung Cancer Cells by Inhibiting Aktl-Mediated Phosphorylation of Smad3 at Threonine-179.
Human Smad3 and Smad4 are sequence-specific transcription activators.
Cloning and expression pattern of a Smad3 homolog from the pearl oyster, Pinctada fucata.
The CAGA boxes were found in the promoter of plasminogen activator inhibitor-type 1, and serve as binding sites to transcription factors Smad3 and/or Smad4, participating in the signaling pathway of TGF-[beta]S (Dennler ef a/.
Transforming growth factor-[beta] (TGF-[beta]) signaling has been widely postulated to be excessively activated as the final common pathway causing fibroproliferative disease and fibrosis including the pulmonary fibrosis [3, 4], via Smad3 signaling .
MAN1, an integral protein of the inner nuclear membrane, binds Smad2 and Smad3 and antagonizes transforming growth factor-beta signaling.
Although the functional role of some famous transcription factors such as AR, SMAD3 and VDR are well known as genes linked to prostate cancer (40-42), the 9 transcription factors (CAMTA1, ISL1, MNX1, NHLH2, NKX2-2, STAT2, ZNF146, ZNF205, and ZNF529) are new candidates that may have critical roles in prostate cancer based on topological significance and regulatory changes during cancer progression.
SMAD3 gene mutation cause LDS type III and TGFB2 gene mutation cause LDS type IV.
Alternatively, IL-6 activates IL-1ra, which allows TGF-[beta] to phosphorylate and induce the expression of activating signaling protein genes Smad2 and Smad3, resulting in the full expression of multiple genes.
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- SMAD (mothers against decapentaplegic) homolog 2
- SMAD (mothers against DPP) homolog 3
- SMAD (mothers against DPP) homolog 5
- SMAD (mothers against DPP) homolog 6
- SMAD (mothers against DPP) homolog 7
- SMAD 1
- SMAD 2
- SMAD 3
- SMAD 4
- SMAD 5
- SMAD 6
- SMAD 7
- SMAD anchor for receptor activation
- SMAD family member 1
- SMAD family member 2
- SMAD family member 3
- SMAD family member 4
- SMAD family member 5
- SMAD family member 6, SMAD
- SMAD family member 7
- smad ubiqiutination regulatory factor
- SMAD Ubiquitination Regulatory Factor 1
- SMAD, mothers against DPP homolog 1
- SMAD, mothers against DPP homolog 4
- SMAD, mothers against DPP homolog 7
- SMAD-Interacting Protein 1
- SMAD-Interacting Protein 1
- Smad1 protein
- SMAD4-Interacting Transcription Factor
- Smaf Sound Decorator
- Smagorinsky model