ArticleJournal of molecular biology2008
Crystal structure of the actin-binding domain of alpha-actinin-4 Lys255Glu mutant implicated in focal segmental glomerulosclerosis.
Article in Journal of molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Force-modulated structural landscape of the catch bonding F-actin crosslinker α-actinin-4.bioRxiv : the preprint server for biology · 2026Article
- Actin Bundles Dynamics and Architecture.Biomolecules · 2023Review
- Modeling ofKidney international reports · 2023Article
- Article
- The mechanism of activation of the actin binding protein EHBP1 by Rab8 family members.Nature communications · 2020Article
- Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis.Journal of the American Society of Nephrology : JASN · 2020Article
- Steric regulation of tandem calponin homology domain actin-binding affinity.Molecular biology of the cell · 2019Article
- Focal segmental glomerulosclerosis ACTN4 mutants binding to actin: regulation by phosphomimetic mutations.Scientific reports · 2019Article
- Dynamics of Dystrophin's Actin-Binding Domain.Biophysical journal · 2018Article
- Structural basis for high-affinity actin binding revealed by a β-III-spectrin SCA5 missense mutation.Nature communications · 2017Article
- Hypertrophic cardiomyopathy mutations in the calponin-homology domain of ACTN2 affect actin binding and cardiomyocyte Z-disc incorporation.The Biochemical journal · 2016Article
- The role of alpha-actinin-4 in human kidney disease.Cell & bioscience · 2015Article
- The biological role of actinin-4 (ACTN4) in malignant phenotypes of cancer.Cell & bioscience · 2015Article
- The carboxyl tail of alpha-actinin-4 regulates its susceptibility to m-calpain and thus functions in cell migration and spreading.The international journal of biochemistry & cell biology · 2013Article
- Modeling the assembly of the multiple domains of α-actinin-4 and its role in actin cross-linking.Biophysical journal · 2013Article
- Utrophin ABD binds to F-actin in an open conformation.FEBS open bio · 2012Article
- Limited digestion of α-actinin in the presence of F-actin.Biophysics (Nagoya-shi, Japan) · 2011Article
- Opening of tandem calponin homology domains regulates their affinity for F-actin.Nature structural & molecular biology · 2010Article
- Regulation of actin cytoskeleton dynamics in cells.Molecules and cells · 2010Review
- Phosphorylation of alpha-actinin 4 upon epidermal growth factor exposure regulates its interaction with actin.The Journal of biological chemistry · 2010Article
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5 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in alpha-actinin-4 have been linked to familial focal segmental glomerulosclerosis (FSGS), a common renal disorder in humans, and produce an apparent increase in the actin-binding affinity of alpha-actinin-4 in vitro. One of the mutations, in particular, Lys255Glu, falls in the middle of the actin-binding interface of the actin-binding domain (ABD). The ABD consists of tandem calponin homology (CH) domains (CH1 and CH2). The crystal structures of most ABDs display a compact conformation, characterized by extensive inter-CH interactions. However, the conformation of F-actin-bound ABDs is unsettled. Some electron microscopy studies find that the compact conformation is preserved upon binding to F-actin, whereas other studies suggest that the CHs separate and the ABD becomes extended. The Lys255Glu mutation in CH2 is significant in this regard since it removes a crucial inter-CH interaction with Trp147 of CH1, thought to stabilize the compact conformation. Together, the increased actin-binding affinity and the removal of this important inter-CH contact suggested that the Lys255Glu mutation might facilitate the transition toward the open ABD conformation proposed by some of the electron microscopy studies. However, the crystal structure of the ABD of alpha-actinin-4 Lys255Glu mutant described here displays the canonical compact conformation. Furthermore, the sedimentation coefficients by analytical ultracentrifugation of wild-type and FSGS mutant ABDs (Lys255Glu, Ser262Pro, and Thr259Ile) are nearly identical (2.50+/-0.03 S) and are in good agreement with the theoretical value calculated from the crystal structure (2.382 S), implying that the compact conformation is retained in solution. The absence of a structural change suggests that the compact ABD conformation observed in the majority of the structures is highly stable and is preserved in solution, even in FSGS mutant ABDs.
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