AI Article Synopsis
- LVNC is a heart condition characterized by an abnormal growth of muscle tissue, and the role of the protein SORBS2 in exacerbating this condition is under investigation.
- Researchers used advanced techniques to identify proteins that interact with SORBS2, finding several potential links to the development of LVNC, including proteins like α-actinin and YWHAQ.
- The study highlights a novel mechanism where the interaction between SORBS2 and YWHAQ may disrupt the normal cell cycle, contributing to the pathology of LVNC.
Article Abstract
Background: Left ventricular noncompaction cardiomyopathy (LVNC) is a cardiac disorder characterized by an excessive trabecular meshwork of deep intertrabecular recesses within the ventricular myocardium. Sorbin and SH3 domain-containing protein 2 (SORBS2) converges on the actin and microtubule cytoskeleton. Here, we investigated the proteins interacting with SORBS2 to elucidate the pathogenic mechanism of LVNC. As reported in previous studies, SORBS2 enhances the occurrence of LVNC by potentiating heart failure, but the specific mechanism remains unclear.
Methods: Building from our previous finding of elevated SORBS2 levels in LVNC hearts, we screened for proteins interacting with SORBS2 by proteomics and conducting IP experiments. Co-IP and immunofluorescence were used to verify the effects.
Results: We selected several proteins with high scores and high coverage that could be closely related to SORBS2 according to earlier reports showing a correlation with LVNC for verification. We finally obtained several proteins that were related to the pathogenesis of LVNC and also interacted with SORBS2, such as α-actinin, β-tubulin, MYH7, FLNA, MYBPC3, YWHAQ and DES, and YWHAQ was the most associated.
Conclusions: We focused on the YWHAQ protein, and we identified a novel mechanism through which SORBS2 interacts with YWHAQ, having a negative effect on the cell cycle, potentially leading to LVNC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833133 | PMC |
| http://dx.doi.org/10.18632/aging.203841 | DOI Listing |
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