ArticleACS omega2023
A Structural Network Analysis of Neuronal ArhGAP21/23 Interactors by Computational Modeling.
Article in ACS omega, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 4 citations in OpenAlex.
- ARHGAP21 enhances metastasis in hepatocellular carcinoma by inhibiting ubiquitination of filamin A.Cell death discovery · 2026Article
- C1-linker region of PARG1 RhoGAP promotes the catalytic recognition fold of RhoA substrate.PloS one · 2025Article
- Gene Expression and Alternative Splicing Analysis in a Large-Scale Multiple Sclerosis Study.International journal of molecular sciences · 2024Article
- Neutrophil-specific interactome of ARHGAP25 reveals novel partners and regulatory insights.Scientific reports · 2024Article
- Gene expression and alternative splicing analysis in a large-scale Multiple Sclerosis study.medRxiv : the preprint server for health sciences · 2024Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RhoGTPase-activating proteins (RhoGAPs) play multiple roles in neuronal development; however, details of their substrate recognition system remain elusive. ArhGAP21 and ArhGAP23 are RhoGAPs that contain N-terminal PDZ and pleckstrin homology domains. In the present study, the RhoGAP domain of these ArhGAPs was computationally modeled by template-based methods and the AlphaFold2 software program, and their intrinsic RhoGTPase recognition mechanism was analyzed from the domain structures using the protein docking programs HADDOCK and HDOCK. ArhGAP21 was predicted to preferentially catalyze Cdc42, RhoA, RhoB, RhoC, and RhoG and to downregulate RhoD and Tc10 activities. Regarding ArhGAP23, RhoA and Cdc42 were deduced to be its substrates, whereas RhoD downregulation was predicted to be less efficient. The PDZ domains of ArhGAP21/23 possess the FTLRXXXVY sequence, and similar globular folding consists of antiparalleled β-sheets and two α-helices that are conserved with PDZ domains of MAST-family proteins. A peptide docking analysis revealed the specific interaction of the ArhGAP23 PDZ domain with the PTEN C-terminus. The pleckstrin homology domain structure of ArhGAP23 was also predicted, and the functional selectivity for the interactors regulated by the folding and disordered domains in ArhGAP21 and ArhGAP23 was examined by an
Identifiers
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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 Socratic graph.