ArticleScientific reports2022
Structural modeling of human AKAP3 protein and in silico analysis of single nucleotide polymorphisms associated with sperm motility.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Alterations in the protein lactylation landscape of sperm from patients with varicocele-associated asthenozoospermia.Frontiers in endocrinology · 2026Article
- Efficacy of butylated hydroxytoluene nanoparticles in enhancing the quality and preservation of stallion chilled semen.Veterinary research communications · 2025Article
- Computational screening of damaging nsSNPs in human SOD1 genes associated with amyotrophic lateral sclerosis identifies destabilising effects of G38R and G42D mutations through in silico evaluation.In silico pharmacology · 2024Article
- Computational analysis of missense variant CYP4F2*3 (V433M) in association with human CYP4F2 dysfunction: a functional and structural impact.BMC molecular and cell biology · 2023Article
- An In Silico Functional Analysis of Non-Synonymous Single-Nucleotide Polymorphisms of BovinePathogens (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKAP3 is a member of the A-kinase anchoring proteins and it is a constituent of the sperm fibrous sheath. AKAP3 is needed for the formation of sperm flagellum structure, sperm motility, and male fertility. This study aims to model the AKAP3 tertiary structure and identify the probable impact of four mutations characterized in infertile men on the AKAP3 structure. The T464S, I500T, E525K, and I661T substitutions were analyzed using in silico methods. The secondary structure and three-dimensional model of AKAP3 were determined using PSI-BLAST based secondary structure prediction and Robetta servers. The TM-score was used to quantitatively measure the structural similarities between native and mutated models. All of the desired substitutions were classified as benign. I-Mutant results showed all of the substitutions decreased AKAP3 stability; however, the I500T and I661T were more effective. Superposition and secondary structure comparisons between native and mutants showed no dramatic deviations. Our study provided an appropriate model for AKAP3. Destabilization of AKAP3 caused by these substitutions did not appear to induce structural disturbances. As AKAP3 is involved in male infertility, providing more structural insights and the impact of mutations that cause protein functional diversity could elucidate the etiology of male fertility problems at molecular level.
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