Associated Papers
Nonmuscle α-Actinin-4 Couples Sarcomere Function to Cardiac Remodeling.
Hayes JB et al.
Circulation Research, 2026
Oxidative stress-driven transcriptomic remodeling in human astrocytes reveals network signatures associated with neurodegenerative and cardiovascular processes.
Bota PM et al.
Computational and Structural Biotechnology Journal, 2026
Early use of renin-angiotensin-aldosterone system inhibitors and stable renal function in familial focal segmental glomerulosclerosis with ACTN4 mutation: a case report and literature review.
Miyasako K et al.
Bmc Nephrology, 2025
A pediatric-onset case of chronic kidney disease caused by a novel sporadic ACTN4 variant and literature review.
Li W et al.
The Turkish Journal of Pediatrics, 2025
Functional assays in Drosophila facilitate classification of variants of uncertain significance associated with rare diseases.
Mok JW et al.
Genome Research, 2025
The mechanism of nesprin-2 accumulation at the nucleus front during confined cell migration.
Bos I et al.
Biophysical Journal, 2025
Functionally constrained human proteins are less prone to mutational instability from single amino acid substitutions.
May M et al.
Nature Communications, 2025
Structural and functional insights into α-actinin isoforms and their implications in cardiovascular disease.
Noureddine M et al.
The Journal of General Physiology, 2025
Association of ACTN4 Gene Mutation with Primary Nephrotic Syndrome in Children in Guangxi Autonomous Region, China.
Cao S et al.
Genetic Testing and Molecular Biomarkers, 2024
Actinin-4 controls survival signaling in B cells by limiting the lateral mobility of B-cell antigen receptors.
Alsouri S et al.
European Journal of Immunology, 2024
Analysis of the association of NPHS2 and ACTN4 genes polymorphism with nephrotic syndrome in Egyptian children.
Al-Azzawy MF et al.
Molecular Biology Reports, 2023
Modeling of ACTN4-Based Podocytopathy Using Drosophila Nephrocytes.
Odenthal J et al.
Kidney International Reports, 2023
α-Actinin-4 recruits Shp2 into focal adhesions to potentiate ROCK2 activation in podocytes.
Tseng CC et al.
Life Science Alliance, 2022
Case report and literature review: A de novo pathogenic missense variant in ACTN4 gene caused rapid progression to end-stage renal disease.
He Z et al.
Frontiers in Pediatrics, 2022
The Importance of Alpha-Actinin Proteins in Platelet Formation and Function, and Their Causative Role in Congenital Macrothrombocytopenia.
O'Sullivan LR et al.
International Journal of Molecular Sciences, 2021
Cytoskeleton Rearrangements Modulate TRPC6 Channel Activity in Podocytes.
Shalygin A et al.
International Journal of Molecular Sciences, 2021
Binding of alpha-ACTN4 to EGF receptor enables its rapid phosphorylation.
Shao H et al.
Heliyon, 2021
The mechanism of activation of the actin binding protein EHBP1 by Rab8 family members.
Rai A et al.
Nature Communications, 2020
Dynamic actin cross-linking governs the cytoplasm's transition to fluid-like behavior.
Chaubet L et al.
Molecular Biology of the Cell, 2020
Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis.
Feng D et al.
Journal of the American Society of Nephrology : Jasn, 2020
Steric regulation of tandem calponin homology domain actin-binding affinity.
Harris AR et al.
Molecular Biology of the Cell, 2019
Focal segmental glomerulosclerosis ACTN4 mutants binding to actin: regulation by phosphomimetic mutations.
Shao H et al.
Scientific Reports, 2019
Systematic analysis of the intersection of disease mutations with protein modifications.
Simpson CM et al.
Bmc Medical Genomics, 2019
Capturing variation impact on molecular interactions in the IMEx Consortium mutations data set.
Del-Toro N et al.
Nature Communications, 2019
Identification of a Novel ACTN4 Gene Mutation Which Is Resistant to Primary Nephrotic Syndrome Therapy.
Meng L et al.
Biomed Research International, 2019
Proteostasis as a therapeutic target in glomerular injury associated with mutant α-actinin-4.
Yee A et al.
American Journal of Physiology. Renal Physiology, 2018
Structural basis for high-affinity actin binding revealed by a β-III-spectrin SCA5 missense mutation.
Avery AW et al.
Nature Communications, 2017
Genetic basis of adult-onset nephrotic syndrome and focal segmental glomerulosclerosis.
Liu J et al.
Frontiers of Medicine, 2017
α Actinin 4 (ACTN4) Regulates Glucocorticoid Receptor-mediated Transactivation and Transrepression in Podocytes.
Zhao X et al.
The Journal of Biological Chemistry, 2017
Hypertrophic cardiomyopathy mutations in the calponin-homology domain of ACTN2 affect actin binding and cardiomyocyte Z-disc incorporation.
Haywood NJ et al.
The Biochemical Journal, 2016
Mechanoaccumulative Elements of the Mammalian Actin Cytoskeleton.
Schiffhauer ES et al.
Current Biology : Cb, 2016
Dynamic Regulation of α-Actinin's Calponin Homology Domains on F-Actin.
Shams H et al.
Biophysical Journal, 2016
Three-layered proteomic characterization of a novel ACTN4 mutation unravels its pathogenic potential in FSGS.
Bartram MP et al.
Human Molecular Genetics, 2016
Functional Validation of an Alpha-Actinin-4 Mutation as a Potential Cause of an Aggressive Presentation of Adolescent Focal Segmental Glomerulosclerosis: Implications for Genetic Testing.
Feng D et al.
Plos One, 2016
Genetic causes of proteinuria and nephrotic syndrome: impact on podocyte pathobiology.
Akchurin O et al.
Pediatric Nephrology (berlin, Germany), 2015
α-Actinin 4 potentiates nuclear factor κ-light-chain-enhancer of activated B-cell (NF-κB) activity in podocytes independent of its cytoplasmic actin binding function.
Zhao X et al.
The Journal of Biological Chemistry, 2015
The role of alpha-actinin-4 in human kidney disease.
Feng D et al.
Cell & Bioscience, 2015
The actinin family of actin cross-linking proteins - a genetic perspective.
Murphy AC et al.
Cell & Bioscience, 2015
Reproducible Analysis of Post-Translational Modifications in Proteomes--Application to Human Mutations.
Holehouse AS et al.
Plos One, 2015
Rapid progression to end-stage renal disease in a child with a sporadic ACTN4 mutation.
Kakajiwala AK et al.
Clinical Nephrology. Case Studies, 2015
Ubiquitin C-terminal hydrolase L1 deletion ameliorates glomerular injury in mice with ACTN4-associated focal segmental glomerulosclerosis.
Read NC et al.
Biochimica Et Biophysica Acta, 2014
FSGS3/CD2AP is a barbed-end capping protein that stabilizes actin and strengthens adherens junctions.
Tang VW et al.
The Journal of Cell Biology, 2013
The carboxyl tail of alpha-actinin-4 regulates its susceptibility to m-calpain and thus functions in cell migration and spreading.
Shao H et al.
The International Journal of Biochemistry & Cell Biology, 2013
Modeling the assembly of the multiple domains of α-actinin-4 and its role in actin cross-linking.
Travers T et al.
Biophysical Journal, 2013
Screening of ACTN4 and TRPC6 mutations in a Chinese cohort of patients with adult-onset familial focal segmental glomerulosclerosis.
Zhang Q et al.
Contributions to Nephrology, 2013
Current concepts of the podocyte in nephrotic syndrome.
Ding WY et al.
Kidney Research and Clinical Practice, 2012