Results 31 to 40 of about 81,731 (259)
Smad2 Overexpression Reduces the Proliferation of the Junctional Epithelium [PDF]
The overexpression of the intracellular signaling molecule of the transforming growth factor–beta family (TGF-β) Smad2 was found to induce apoptosis and inhibit the proliferation rate of oral epithelial cells. Therefore, the aim of this study was to investigate in vivo the effect of Smad2 overexpression on the proliferation rate of
M K, Alotaibi, Y, Kitase, C F, Shuler
openaire +2 more sources
Cancer-induced myeloid-derived suppressor cells (MDSC) play an important role in tumor immune evasion. MDSC programming or polarization has been proposed as a strategy for leveraging the developmental plasticity of myeloid cells to reverse MDSC immune ...
Padmini Jayaraman +15 more
doaj +1 more source
Smad2 and Smad4 gene mutations in hepatocellular carcinoma [PDF]
TGF-beta is a negative regulator of liver growth. Smad family of genes, as mediators of TGF-beta pathway, are candidate tumor suppressor genes in hepatocellular carcinoma (HCC). We studied 35 HCC and non-tumour liver tissues for possible mutations in Smad2 and Smad4 genes. Three tumours displayed somatic mutations; two in Smad4 (Asp332Gly and Cys401Arg)
Yakicier, M.C. +4 more
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During placental development, cytotrophoblast progenitor cells differentiate into the syncytiotrophoblast and invasive extravillous trophoblasts (EVTs).
Jelena Brkić +11 more
doaj +1 more source
Involvement of Rho-associated coiled-coil kinase signaling inhibition in TGF-β1/Smad2, 3 signal transduction in vitro [PDF]
AIM: To research the effect of Y-27632, a selective Rho-associated coiled-coil kinase (ROCK) inhibitor, on TGF-β1/Smad2, 3 signal transduction in ocular Tenon’s capsule fibroblasts (OTFs).
Zhao-Hui Feng +3 more
doaj +1 more source
Fluorofenidone alleviates liver fibrosis by inhibiting hepatic stellate cell autophagy via the TGF-β1/Smad pathway: implications for liver cancer [PDF]
Objectives Liver fibrosis is a key stage in the progression of various chronic liver diseases to cirrhosis and liver cancer, but at present, there is no effective treatment.
Xiongqun Peng +8 more
doaj +2 more sources
NODAL/Activin signaling orchestrates key processes during embryonic development via SMAD2. How SMAD2 activates programs of gene expression that are modulated over time however, is not known.
Davide M Coda +8 more
doaj +1 more source
Formation of a Stable Heterodimer between Smad2 and Smad4 [PDF]
Smad proteins mediate transforming growth factor beta signaling from the cell membrane to the nucleus. Upon phosphorylation by the activated receptor kinases, the receptor-regulated Smad, such as Smad2, forms a heterocomplex with the co-mediator Smad, Smad4.
Wu, J. W. +3 more
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Mechanism for Mutational Inactivation of the Tumor Suppressor Smad2 [PDF]
Transforming growth factor beta (TGF-beta) is a potent natural antiproliferative agent that plays an important role in suppressing tumorigenicity. In numerous tumors, loss of TGF-beta responsiveness is associated with inactivating mutations that can occur in components of this signaling pathway, such as the tumor suppressor Smad2.
C, Prunier +4 more
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Background Hepatocellular carcinoma (HCC) is one of the most prevalent common cancer worldwide with high mortality. Transforming growth factor-β (TGF-β) signaling pathway was reported dysregulated during liver cancer formation and progression.
Zhao Huang +9 more
doaj +1 more source

