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Article: KIF5B modulates central spindle organization in late-stage cytokinesis in chondrocytes

TitleKIF5B modulates central spindle organization in late-stage cytokinesis in chondrocytes
Authors
KeywordsKinesin-1
Cytokinesis
Chondrocytes
Central spindle
Issue Date2019
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.cellandbioscience.com
Citation
Cell & Bioscience, 2019, v. 9, p. article no. 85 How to Cite?
AbstractBackground: The growth plate is a special region of the cartilage that drives longitudinal growth of long bones. Proliferating chondrocytes in the growth plate, arranged in columns, divide perpendicular to the long axis of the growth plate then intercalate to re-align with parental columns. Which molecular partners maintain growth plate columnar structures and chondrocyte cytokinesis has not been fully revealed. It is reported that kinesin family member 3A (KIF3A), a subunit of kinesin-2, plays an important role in maintaining columnar organization in growth plates via controlling primary cilia formation and cell proliferation. Result: Here we identify kinesin family member 5B (KIF5B), the heavy chain of kinesin-1, a ubiquitously expressed motor protein for anterograde intracellular transport along the microtubule network, as a key modulator of cytokinesis in chondrocytes via maintenance of central spindle organization. We show that KIF5B is concentrated in the central spindle during cytokinesis in both primary chondrocytes and chondrogenic ATDC5 cells. Conclusion: The failure of cytokinesis in KIF5B null chondrocytes leads to incomplete cell rotation, disrupting proliferation and differentiation, and results in a disorganized growth plate.
Persistent Identifierhttp://hdl.handle.net/10722/283991
ISSN
2018 Impact Factor: 3.355
2015 SCImago Journal Rankings: 1.593

 

DC FieldValueLanguage
dc.contributor.authorGan, H-
dc.contributor.authorXue, W-
dc.contributor.authorGAO, Y-
dc.contributor.authorZhu, GX-
dc.contributor.authorChan, D-
dc.contributor.authorCheah, KSE-
dc.contributor.authorHuang, J-
dc.date.accessioned2020-07-20T05:55:09Z-
dc.date.available2020-07-20T05:55:09Z-
dc.date.issued2019-
dc.identifier.citationCell & Bioscience, 2019, v. 9, p. article no. 85-
dc.identifier.issn2045-3701-
dc.identifier.urihttp://hdl.handle.net/10722/283991-
dc.description.abstractBackground: The growth plate is a special region of the cartilage that drives longitudinal growth of long bones. Proliferating chondrocytes in the growth plate, arranged in columns, divide perpendicular to the long axis of the growth plate then intercalate to re-align with parental columns. Which molecular partners maintain growth plate columnar structures and chondrocyte cytokinesis has not been fully revealed. It is reported that kinesin family member 3A (KIF3A), a subunit of kinesin-2, plays an important role in maintaining columnar organization in growth plates via controlling primary cilia formation and cell proliferation. Result: Here we identify kinesin family member 5B (KIF5B), the heavy chain of kinesin-1, a ubiquitously expressed motor protein for anterograde intracellular transport along the microtubule network, as a key modulator of cytokinesis in chondrocytes via maintenance of central spindle organization. We show that KIF5B is concentrated in the central spindle during cytokinesis in both primary chondrocytes and chondrogenic ATDC5 cells. Conclusion: The failure of cytokinesis in KIF5B null chondrocytes leads to incomplete cell rotation, disrupting proliferation and differentiation, and results in a disorganized growth plate.-
dc.languageeng-
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.cellandbioscience.com-
dc.relation.ispartofCell & Bioscience-
dc.rightsCell & Bioscience. Copyright © BioMed Central Ltd.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectKinesin-1-
dc.subjectCytokinesis-
dc.subjectChondrocytes-
dc.subjectCentral spindle-
dc.titleKIF5B modulates central spindle organization in late-stage cytokinesis in chondrocytes-
dc.typeArticle-
dc.identifier.emailGan, H: huiyan2@hku.hk-
dc.identifier.emailChan, D: chand@hku.hk-
dc.identifier.emailCheah, KSE: hrmbdkc@hku.hk-
dc.identifier.emailHuang, J: jdhuang@hku.hk-
dc.identifier.authorityChan, D=rp00540-
dc.identifier.authorityCheah, KSE=rp00342-
dc.identifier.authorityHuang, J=rp00451-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/s13578-019-0344-5-
dc.identifier.scopuseid_2-s2.0-85073621467-
dc.identifier.hkuros311105-
dc.identifier.volume9-
dc.identifier.spagearticle no. 85-
dc.identifier.epagearticle no. 85-
dc.publisher.placeUnited Kingdom-

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