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Molecules 2010, 15(10), 6974-6982;

LYRM1, a Gene that Promotes Proliferation and Inhibits Apoptosis during Heart Development

Department of Pediatrics, Nanjing Maternal and Child Health Hospital of Nanjing Medical University, No.123 Tianfei Road, Nanjing 210004, China
Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing 210029, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Received: 18 September 2010 / Revised: 28 September 2010 / Accepted: 2 October 2010 / Published: 11 October 2010
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Congenital heart disease (CHD) is the most common type of birth defect, but its underlying molecular mechanisms remain unidentified. Previous studies determined that Homo sapiens LYR motif containing 1 (LYRM1) is a novel nucleoprotein expressed at the highest level in adipose tissue and in high levels in heart tissue. The LYRM1 gene may play an important role in the development of the human heart. This study was designed to identify the biological characteristics of the LYRM1 gene in heart development. On the basis of expression-specific differentiation markers identified with quantitative real-time RT-PCR and the morphology of LYRM1-overexpressing cells during differentiation, ectopic expression was not found to significantly affect differentiation of P19 cells into cardiomyocytes. MTT assays and cell cycle analysis showed that LYRM1 dramatically increases the proliferation of P19 cells. Furthermore, data from annexin V-FITC binding and caspase-3 activity revealed that LYRM1 can inhibit the apoptosis of P19 cells. Our data suggest that LYRM1 might have the potential to modulate cell growth, apoptosis, and heart development. View Full-Text
Keywords: CHD; LYRM1; P19 cells; heart development CHD; LYRM1; P19 cells; heart development

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Zhu, C.; Liu, Y.-Q.; Chen, F.-K.; Hu, D.-L.; Yu, Z.-B.; Qian, L.-M. LYRM1, a Gene that Promotes Proliferation and Inhibits Apoptosis during Heart Development. Molecules 2010, 15, 6974-6982.

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