ArticleSmall GTPases2011
Rho family GTPase Chp/RhoV induces PC12 apoptotic cell death via JNK activation.
Article in Small GTPases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- A prognostic model for lung adenocarcinoma based on cuproptosis and disulfidptosis related genes revealing the key prognostic role of FURIN.Scientific reports · 2025Article
- Atypical RhoUV GTPases in development and disease.Biochemical Society transactions · 2024Review
- Molecular basis and current insights of atypical Rho small GTPase in cancer.Molecular biology reports · 2024Review
- Prognostic significance of the rho GTPase RHOV and its role in tumor immune cell infiltration: a comprehensive pan-cancer analysis.FEBS open bio · 2023Article
- In vivo CRISPR screens identify RhoV as a pro-metastasis factor of triple-negative breast cancer.Cancer science · 2023Article
- RHOV promotes lung adenocarcinoma cell growth and metastasis through JNK/c-Jun pathway.International journal of biological sciences · 2021Article
- Regulation and functions of RhoU and RhoV.Small GTPases · 2020Review
- The Atypical Rho GTPase CHW-1 Works with SAX-3/Robo To Mediate Axon Guidance inG3 (Bethesda, Md.) · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Rho GTPases regulate numerous cellular processes including apoptosis. Chp/RhoV is an atypical Rho GTPase which functions are poorly understood. Here we investigated the role of Chp in regulation of cell viability using PC12 cells with inducible expression of Chp as a model. We found that expression of Chp results in apoptosis in PC12 cells. Chp-induced apoptosis was accompanied by activation of JNK signaling and both death receptor-mediated and mitochondrial apoptotic pathways as justified by caspase-8 and caspase-9 activation, respectively. Moreover, inhibition of JNK by SP600125 rescued PC12 cells from Chp-triggered cell death and attenuated activation of caspases-9 and -3/7 suggesting that activation of JNK mediates pro-apoptotic effect of Chp. Expression of Chp resulted in increased phosphorylation of c-Jun in PC12 cells, and Chp expression in HE K293 cells upregulated AP-1-dependent transcription in a JNK-dependent manner. Together results of our study reveal the role of Chp GTPase as a putative regulator of JNK-dependent apoptotic death in PC12 cells, similarly to previously described pro-apoptotic activity of the related Cdc42 and Rac1 GTPases.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.