All differential on the splicing front: Host alternative splicing alters the landscape of virus-host conflict

Mann, Joshua T.; Riley, Brent A.; Baker, Steven F.

doi:10.1016/j.semcdb.2023.01.013

Cited by 2 publications

(1 citation statement)

References 237 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Literature has presented many data on the involvement of abnormal AS in the occurrence of several biological processes, such as normal ageing ( Baralle and Romano 2023 ), premature ageing ( Lopez-Mejia, et al 2011 ) and age-related disorders, which range from hypertension to cardiovascular ( Hu, et al 2017 ; Gotthardt, et al 2023 ) and liver diseases ( Jobbins, et al 2023 ), neurodegeneration ( Nikom and Zheng 2023 ), and cancer ( Song, et al 2023 ; Temaj, et al 2023 ). Aberrant splicing is also implicated in processes that affect people of all ages, such as inflammatory bowel disease ( Zhou, et al 2023 ; Zou, et al 2023 ) and viral infection ( Mann, et al 2023 ). The mechanisms underlying the association of AS and diseases include alteration in splice site sequences and in cis- and trans-splicing regulatory elements ( Tang, et al 2020 ), chromatin modifications ( Gomez Acuna, et al 2013 ) and mutations that disrupt RNA secondary structure ( Warf and Berglund 2010 ), which can mediate mRNA decay or cause deletion of domains that are important for protein function.…”

Section: Introductionmentioning

confidence: 99%

Expression of Truncated Products at the 5′-Terminal Region of RIPK2 and Evolutive Aspects that Support Their Biological Importance

Villagra,

da Cunha,

Polachini

et al. 2024

Genome Biology and Evolution

View full text Add to dashboard Cite

Alternative splicing is the process of generating different mRNAs from the same primary transcript, which contributes to increase the transcriptome and proteome diversity. Abnormal splicing has been associated with the development of several diseases including cancer. Given that mutations and abnormal levels of the RIPK2 transcript and RIP-2 protein are frequent in tumors, and that RIP-2 modulates immune and inflammatory responses, we investigated alternative splicing events that result in partial deletions of the kinase domain at the N-terminus of RIP-2. We also investigated the structure and expression of the RIPK2 truncated variants and isoforms in different environments. In addition, we searched data throughout Supraprimates evolution that could support the biological importance of RIPK2 alternatively spliced products. We observed that human variants and isoforms were differentially regulated following temperature stress, and that the truncated transcript was more expressed than the long transcript in tumor samples. The inverse was found for the longer protein isoform. The truncated variant was also detected in chimpanzee, gorilla, hare, pika, mouse, rat and tree shrew. The fact that the same variant has been preserved in mammals with divergence times up to 70 million years raises the hypothesis that it may have a functional significance.

show abstract