2005
DOI: 10.1016/j.cell.2004.11.036
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Abstract: The transition from juvenile to adult life is accompanied by programmed remodeling in many tissues and organs, which is key for organisms to adapt to the demand of the environment. Here we report a novel regulated alternative splicing program that is crucial for postnatnal heart remodeling in the mouse. We identify the essential splicing factor ASF/SF2 as a key component of the program, regulating a restricted set of tissue-specific alternative splicing events during heart remodeling. Cardiomyocytes deficient … Show more

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Cited by 318 publications
(331 citation statements)
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References 52 publications
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“…1 and Supplementary Table 1). These observations markedly expand the number of known endogenous alternatively spliced gene targets of SR proteins 20,[35][36][37][38] .…”
Section: Mechanism Of Sf2/asf-driven Transformationmentioning
confidence: 84%
“…1 and Supplementary Table 1). These observations markedly expand the number of known endogenous alternatively spliced gene targets of SR proteins 20,[35][36][37][38] .…”
Section: Mechanism Of Sf2/asf-driven Transformationmentioning
confidence: 84%
“…The physiological changes that occur before and after birth are particularly important as the fetal heart adapts to birth and converts to adult function. This postnatal remodeling is accomplished through transcriptional and posttranscriptional networks, including AS (16,18).In the present study, splicing microarrays and computational screens were used to investigate regulatory networks of AS in vertebrate heart development. A large number of coordinated splicing transitions were identified that undergo dramatic changes during heart development.…”
mentioning
confidence: 99%
“…The physiological changes that occur before and after birth are particularly important as the fetal heart adapts to birth and converts to adult function. This postnatal remodeling is accomplished through transcriptional and posttranscriptional networks, including AS (16,18).…”
mentioning
confidence: 99%
“…SRSF1 is required for the cardiac-specific splicing of Cypher (also called Ldb3) pre-mRNA, and the regulation of alternative splicing of calcium/calmodulin-dependent protein kinase II delta (Camk2d) and cardiac Troponin T (cTnT) during heart development. In particular, the persistent splicing of a neuronal isoform of Camk2d and its ability to enhance excitation and contraction coupling (ECC) activity in Srsf1 mutant cardiomyocytes have been proposed as a possible cause of the phenotype in mutant mice (14). Ablation of another SR protein, SRSF10 (SRp38), from the mouse also leads to heart defects (15).…”
mentioning
confidence: 99%