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Articles

Cardiac fibroblast deletion of PTBP1 modulates the profibrotic response by alternative splicing

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By Shea Ricketts, Gregory Farber, sunil verma, Yanhan Dong, Yifang Xie, Paige Takasugi, Shufen Chen, Luping Du, Haofei Wang, Wei Hui, Celine Keles, Sergey Tsoy, Grace Fuller, Michael Wang, Gabrielle M. Gentile, Jimena Giudice, Muge N. Kuyumcu-Martinez, Jiandong Liu, Li Qian
| Nature Verified
Abstract Dynamic cardiac fibroblast phenotypes drive pathological remodeling and fibrosis, yet post-transcriptional mechanisms controlling fibroblast activation remain poorly defined. Here, we identify the RNA-binding protein polypyrimidine tract binding protein 1 (PTBP1) as a regulator of cardiac fibroblast activation and fibrotic remodeling.
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How RNA splicing decisions shape and break the developing heart

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By sunil verma, Rachel L. DeLancey, Muge N. Kuyumcu-Martinez
| Nature Verified
Splice-altering genetic variants are found in individuals with infantile cardiomyopathy, but the consequences are unclear. A study now shows that aberrant splicing of only one exon in the AARS2 gene can cause devastating heart development defects, phenocopying patient congenital cardiomyopathy.
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RBFOX2 is critical for maintaining alternative polyadenylation patterns and mitochondrial health in rat myoblasts

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By Jun Cao, sunil verma, Elizabeth A. Jaworski, Stephanie Mohan
| Cell Reports Verified
Highlights • Loss of RBFOX2 is linked to human heart diseases • RBFOX2 depletion in rat myoblasts alters alternative polyadenylation (APA) patterns • RBFOX2-mediated APA modulates contractile and mitochondrial gene expression • RBFOX2 loss impacts mitochondrial health Summary RBFOX2, which has a well-established role in alternative splicing, is linked to heart diseases.
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