Cytokinesis failure in RhoA-deficient mouse erythroblasts involves actomyosin and midbody dysregulation and triggers p53 activation-Reference-Cited by-同舟云学术

Cytokinesis failure in RhoA-deficient mouse erythroblasts involves actomyosin and midbody dysregulation and triggers p53 activation

Published:2015-09-17 Issue:12 Volume:126 Page:1473-1482
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Konstantinidis Diamantis G.¹^ORCID,Giger Katie M.¹^ORCID,Risinger Mary²,Pushkaran Suvarnamala¹,Zhou Ping¹,Dexheimer Phillip³,Yerneni Satwica³,Andreassen Paul¹,Klingmüller Ursula⁴,Palis James⁵,Zheng Yi¹,Kalfa Theodosia A.¹^ORCID

Affiliation:

1. Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH;

2. College of Nursing, University of Cincinnati, Cincinnati, OH;

3. Biomedical Informatics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH;

4. Systems Biology of Signal Transduction, German Cancer Research Center, Center for Molecular Biology Alliance, Heidelberg, Germany; and

5. Department of Pediatrics, Center for Pediatric Biomedical Research, University of Rochester Medical Center, Rochester, NY

Abstract

Key Points RhoA GTPase activates pMRLC and localizes to the site of midbody formation to regulate erythroblast cytokinesis. Cytokinesis failure in erythroblasts caused by RhoA deficiency triggers p53-mediated DNA-damage response, cell-cycle arrest, and apoptosis.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/126/12/1473/1387991/1473.pdf

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