Response by Cho and Yoon to Letter Regarding Article, “Polycomb Group Protein CBX7 Represses Cardiomyocyte Proliferation Through Modulation of the TARDBP/RBM38 Axis”
Author:
Affiliation:
1. Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA (K-W.C.; Y-s.Y.).
2. Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Republic of Korea (Y-s.Y.).
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine
Reference5 articles.
1. Mammalian CBX7 isoforms p36 and p22 exhibit differential responses to serum, varying functions for proliferation, and distinct subcellular localization
2. CBX7 Induces Self-Renewal of Human Normal and Malignant Hematopoietic Stem and Progenitor Cells by Canonical and Non-canonical Interactions
3. c-kit+ cells minimally contribute cardiomyocytes to the heart
4. Genetic Lineage Tracing of Sca-1 + Cells Reveals Endothelial but Not Myogenic Contribution to the Murine Heart
5. The RNF26/CBX7 axis modulates the TNF pathway to promote cell proliferation and regulate sensitivity to TKIs in ccRCC
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