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. 2021 Aug 2;129(6):669–683. doi: 10.1161/CIRCRESAHA.120.318577

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© 2021 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 8. — Molecular mechanism leading to cardiac hypertrophy in the absence of SRSF4 (serine/arginine splicing factor 4).A, GAS5 (growth arrest-specific 5) is a direct SRSF4 target. When SRSF4 is present, GAS5 binds to the GR (glucocorticoid receptor) and inhibits its binding to the GRE region in its target genes. B, In the absence of SRSF4, GAS5 is downregulated, and the GR induces the expression of target genes involved in cardiomyocyte hypertrophy. Moreover, the absence of SRSF4 produces the upregulation of SRSF6, which further contributes to an increase in GR targets.