TGF-β receptor levels regulate the specificity of signaling pathway activation and biological effects of TGF-β
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, ISSN: 0167-4889, Vol: 1793, Issue: 7, Page: 1165-1173
2009
- 89Citations
- 86Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations89
- Citation Indexes89
- 89
- CrossRef73
- Captures86
- Readers86
- 85
Article Description
TGF-β is a pluripotent cytokine that mediates its effects through a receptor composed of TGF-β receptor type II (TGFBR2) and type I (TGFBR1). The TGF-β receptor can regulate Smad and nonSmad signaling pathways, which then ultimately dictate TGF-β's biological effects. We postulated that control of the level of TGFBR2 is a mechanism for regulating the specificity of TGF-β signaling pathway activation and TGF-β's biological effects. We used a precisely regulatable TGFBR2 expression system to assess the effects of TGFBR2 expression levels on signaling and TGF-β mediated apoptosis. We found Smad signaling and MAPK–ERK signaling activation levels correlate directly with TGFBR2 expression levels. Furthermore, p21 levels and TGF-β induced apoptosis appear to depend on relatively high TGFBR2 expression and on the activation of the MAPK–ERK and Smad pathways. Thus, control of TGFBR2 expression and the differential activation of TGF-β signaling pathways appears to be a mechanism for regulating the specificity of the biological effects of TGF-β.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S016748890900038X; http://dx.doi.org/10.1016/j.bbamcr.2009.02.001; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=67649610073&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/19339207; https://linkinghub.elsevier.com/retrieve/pii/S016748890900038X
Elsevier BV
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