ArticleMolecular and cellular biochemistry2012
Regulation of TGF-β signaling by PKC depends on Tsc-22 inducibility.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Bone Morphogenetic Proteins Shape TFrontiers in immunology · 2022Review
- Regulation and Signaling of TGF-β Autoinduction.International journal of molecular and cellular medicine · 2021Review
- Crucial role of TSC-22 in preventing the proteasomal degradation of p53 in cervical cancer.PloS one · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Interactions between various signaling pathways enable a fine control of cellular activities. When the cells are subjected to activation of TGF-β signaling and PKC signaling, PKC phosphorylation of Smad3 abrogates binding and transcriptional activity of Smad3 leading to suppression of TGF-β response. We studied this interaction between Smads and PKC in different cell types to examine cell specificity of the interaction. We found that the outcome of the interaction between Smads and PKC depends on cell types and inducibility of a regulatory molecule Tsc-22. In this report, we showed that induced Tsc-22 leads to enhancement of TGF-β-dependent signaling and the enhancement was blocked by expression of a dominant-negative Tsc-22 mutant. Its effect on cellular differentiation was also examined.
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