Proteomics

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Identification of proteins that interact with the lncRNA Sarrah

ABSTRACT: Long non-coding RNAs (lncRNAs) contribute to (patho)physiological processes in the heart. Aging is the major risk factor for cardiovascular disease. Apoptosis of individual cardiomyocytes is one of the underlying causes for age-related cardiac dysfunction. Here, we identified the lncRNA Sarrah that is regulated during aging in cardiomyocytes and show that it has a protective effect on the myocardium. We used an RNA pulldown approach to identify proteins interacting with endogenous Sarrah to determine the mechanism by which Sarrah induces a cardioprotective gene expression pattern.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Ilka Wittig  

LAB HEAD: Reinier Boon

PROVIDER: PXD018315 | Pride | 2020-04-01

REPOSITORIES: Pride

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Publications

Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.

Trembinski D Julia DJ   Bink Diewertje I DI   Theodorou Kosta K   Sommer Janina J   Fischer Ariane A   van Bergen Anke A   Kuo Chao-Chung CC   Costa Ivan G IG   Schürmann Christoph C   Leisegang Matthias S MS   Brandes Ralf P RP   Alekseeva Tijna T   Brill Boris B   Wietelmann Astrid A   Johnson Christopher N CN   Spring-Connell Alexander A   Kaulich Manuel M   Werfel Stanislas S   Engelhardt Stefan S   Hirt Marc N MN   Yorgan Kaja K   Eschenhagen Thomas T   Kirchhof Luisa L   Hofmann Patrick P   Jaé Nicolas N   Wittig Ilka I   Hamdani Nazha N   Bischof Corinne C   Krishnan Jaya J   Houtkooper Riekelt H RH   Dimmeler Stefanie S   Boon Reinier A RA  

Nature communications 20200427 1

Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes. Importantly, loss of SARRAH (OXCT1-AS1) in human engineered heart tissue results in impaired contractile force development. SARRAH directly binds to the promoters of genes downregul  ...[more]

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