ArticleSmall GTPases2020
Unraveling a model of TCL/RhoJ allosterism using TC10 reverse chimeras.
Article in Small GTPases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- RhoJ: an emerging biomarker and target in cancer research and treatment.Cancer gene therapy · 2024Review
- Structure-based design of CDC42 effector interaction inhibitors for the treatment of cancer.Cell reports · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In addition to the classical regulation of GTPase activity by effector proteins, investigating the variations in the amino acid sequence and structures of GTPases often provides insights into regulatory mechanisms that are more GTPase-specific. TCL/RhoJ is a Rho GTPase most closely related to Cdc42 and TC10; however, its nucleotide exchange activity is distinctly influenced by N-terminal amino acids 17-20 and the more distal amino acids 121-129. In this short study, we have further explored the differences between TCL and its homolog TC10 and show that its unique mode of allosteric regulation requires broader diversification of its amino acid sequence than previously appreciated.
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