| Online-Ressource |
Verfasst von: | Boeckel, Jes-Niels [VerfasserIn]  |
| Möbius-Winkler, Maximilian Nicolas Werner [VerfasserIn]  |
| Müller, Marion [VerfasserIn]  |
| Rebs, Sabine [VerfasserIn]  |
| Eger, Nicole [VerfasserIn]  |
| Schoppe, Laura [VerfasserIn]  |
| Tappu, Rewati [VerfasserIn]  |
| Kokot, Karoline E. [VerfasserIn]  |
| Kneuer, Jasmin M. [VerfasserIn]  |
| Gaul, Susanne [VerfasserIn]  |
| Bordalo, Diana M. [VerfasserIn]  |
| Lai, Alan [VerfasserIn]  |
| Haas, Jan [VerfasserIn]  |
| Ghanbari, Mahsa [VerfasserIn]  |
| Drewe-Boss, Philipp [VerfasserIn]  |
| Liss, Martin [VerfasserIn]  |
| Katus, Hugo [VerfasserIn]  |
| Ohler, Uwe [VerfasserIn]  |
| Gotthardt, Michael [VerfasserIn]  |
| Laufs, Ulrich [VerfasserIn]  |
| Streckfuss-Bömeke, Katrin [VerfasserIn]  |
| Meder, Benjamin [VerfasserIn]  |
Titel: | SLM2 is a novel cardiac splicing factor involved in heart failure due to dilated cardiomyopathy |
Verf.angabe: | Jes-Niels Boeckel, Maximilian Möbius-Winkler, Marion Müller, Sabine Rebs, Nicole Eger, Laura Schoppe, Rewati Tappu, Karoline E. Kokot, Jasmin M. Kneuer, Susanne Gaul, Diana M. Bordalo, Alan Lai, Jan Haas, Mahsa Ghanbari, Philipp Drewe-Boss, Martin Liss, Hugo A. Katus, Uwe Ohler, Michael Gotthardt, Ulrich Laufs, Katrin Streckfuss-Bömeke, Benjamin Meder |
E-Jahr: | 2022 |
Jahr: | 15 July 2021 |
Umfang: | 18 S. |
Fussnoten: | Gesehen am 13.12.2022 |
Titel Quelle: | Enthalten in: Genomics, proteomics & bioinformatics |
Ort Quelle: | Amsterdam [u.a.] : Elsevier, 2006 |
Jahr Quelle: | 2022 |
Band/Heft Quelle: | 20(2022), 1, Seite 129-146 |
ISSN Quelle: | 2210-3244 |
Abstract: | Alternative mRNA splicing is a fundamental process to increase the versatility of the genome. In humans, cardiac mRNA splicing is involved in the pathophysiology of heart failure. Mutations in the splicing factor RNA binding motif protein 20 (RBM20) cause severe forms of cardiomyopathy. To identify novel cardiomyopathy-associated splicing factors, RNA-seq and tissue-enrichment analyses were performed, which identified up-regulated expression of Sam68-Like mammalian protein 2 (SLM2) in the left ventricle of dilated cardiomyopathy (DCM) patients. In the human heart, SLM2 binds to important transcripts of sarcomere constituents, such as those encoding myosin light chain 2 (MYL2), troponin I3 (TNNI3), troponin T2 (TNNT2), tropomyosin 1/2 (TPM1/2), and titin (TTN). Mechanistically, SLM2 mediates intron retention, prevents exon exclusion, and thereby mediates alternative splicing of the mRNA regions encoding the variable proline-, glutamate-, valine-, and lysine-rich (PEVK) domain and another part of the I-band region of titin. In summary, SLM2 is a novel cardiac splicing regulator with essential functions for maintaining cardiomyocyte integrity by binding to and processing the mRNAs of essential cardiac constituents such as titin. |
DOI: | doi:10.1016/j.gpb.2021.01.006 |
URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext ; Verlag: https://doi.org/10.1016/j.gpb.2021.01.006 |
| Volltext: https://www.sciencedirect.com/science/article/pii/S1672022921001467 |
| DOI: https://doi.org/10.1016/j.gpb.2021.01.006 |
Datenträger: | Online-Ressource |
Sprache: | eng |
Sach-SW: | Dilated cardiomyopathy |
| KHDRBS3 |
| SLM2 |
| Splicing |
| Titin |
K10plus-PPN: | 1826882154 |
Verknüpfungen: | → Zeitschrift |
SLM2 is a novel cardiac splicing factor involved in heart failure due to dilated cardiomyopathy / Boeckel, Jes-Niels [VerfasserIn]; 15 July 2021 (Online-Ressource)