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Cited by 277

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis

Open access
Akilesh, Shreeram, Suleiman, Hani, Yu, Haiyang, Stander, M. Christine, Lavin, Peter, Gbadegesin, Rasheed, Antignac, Corinne, Pollak, Martin, Kopp, Jeffrey B., Winn, Michelle P., Shaw, Andrey S.·2011·Journal of Clinical Investigation

Abstract

The specialized epithelial cell of the kidney, the podocyte, has a complex actin-based cytoskeleton. Dynamic regulation of this cytoskeleton is required for efficient barrier function of the kidney. Podocytes are a useful cell type to study the control of the actin cytoskeleton in vivo, because disruption of components of the cytoskeleton results in podocyte damage, cell loss, and a prototypic injury response called focal segmental glomerulosclerosis (FSGS). Searching for actin regulatory proteins that are expressed in podocytes, we identified a RhoA-activated Rac1 GTPase-activating protein (Rac1-GAP), Arhgap24, that was upregulated in podocytes as they differentiated, both in vitro and in vivo. Increased levels of active Rac1 and Cdc42 were measured in Arhgap24 knockdown experiments, which influenced podocyte cell shape and membrane dynamics. Consistent with a role for Arhgap24 in normal podocyte functioning in vivo, sequencing of the ARHGAP24 gene in patients with FSGS identified a mutation that impaired its Rac1-GAP activity and was associated with disease in a family with FSGS. Thus, Arhgap24 contributes to the careful balancing of RhoA and Rac1 signaling in podocytes, the disruption of which may lead to kidney disease.

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Crossref · 10.1172/jci46458

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Metadata

Authors
Akilesh, S., Suleiman, H., Yu, H., Stander, M. C., Lavin, P., Gbadegesin, R., Antignac, C., Pollak, M., Kopp, J. B., Winn, M. P., & Shaw, A. S.
Venue
Journal of Clinical Investigation
Published
2011-10-03
Volume
121
Issue
10
Pages
4127-4137
ISSN
0021-9738 (ISSN-L)
OpenAlex
W1976611664
Cited by
277
References
31
FWCI
15.79
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis. https://app.cochat.ai/papers/10.1172/jci46458
The paper
Akilesh, S., Suleiman, H., Yu, H., Stander, M. C., Lavin, P., Gbadegesin, R., Antignac, C., Pollak, M., Kopp, J. B., Winn, M. P., & Shaw, A. S. (2011). Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis. Journal of Clinical Investigation. https://doi.org/10.1172/jci46458

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.