Literature DB >> 21224392

The pericentriolar satellite protein CEP90 is crucial for integrity of the mitotic spindle pole.

Kyeongmi Kim1, Kunsoo Rhee.   

Abstract

Pericentriolar satellites are electron-dense granules that are concentrated around the centrosome. They are involved in the recruitment of centrosomal proteins and microtubule organization in interphase cells, but their mitotic functions are largely unknown. In this study, we characterize CEP90 as a component of pericentriolar satellites. CEP90 is present both in the centrosome and in the cytoplasm, but is transiently concentrated at the centrosome once cells enter mitosis. Depletion of CEP90 caused mitotic arrest with misaligned chromosomes. Spindle pole fragmentation was the most characteristic phenotype in CEP90-depleted cells. Spindle poles were fragmented as soon as the spindles attached, suggesting that the mechanical forces of spindle microtubules physically stress the structure of CEP90-depleted spindle poles. Based on these results, we propose that CEP90 is crucial for maintaining the integrity of spindle poles during mitosis.

Entities:  

Mesh:

Substances:

Year:  2011        PMID: 21224392     DOI: 10.1242/jcs.078329

Source DB:  PubMed          Journal:  J Cell Sci        ISSN: 0021-9533            Impact factor:   5.285


  43 in total

1.  CLASPs prevent irreversible multipolarity by ensuring spindle-pole resistance to traction forces during chromosome alignment.

Authors:  Elsa Logarinho; Stefano Maffini; Marin Barisic; Andrea Marques; Alberto Toso; Patrick Meraldi; Helder Maiato
Journal:  Nat Cell Biol       Date:  2012-02-05       Impact factor: 28.824

2.  Cep57, a NEDD1-binding pericentriolar material component, is essential for spindle pole integrity.

Authors:  Qixi Wu; Runsheng He; Haining Zhou; Albert C H Yu; Bo Zhang; Junlin Teng; Jianguo Chen
Journal:  Cell Res       Date:  2012-04-17       Impact factor: 25.617

3.  The centriolar satellite protein CCDC66 interacts with CEP290 and functions in cilium formation and trafficking.

Authors:  Deniz Conkar; Efraim Culfa; Ezgi Odabasi; Navin Rauniyar; John R Yates; Elif N Firat-Karalar
Journal:  J Cell Sci       Date:  2017-02-24       Impact factor: 5.285

Review 4.  CEP proteins: the knights of centrosome dynasty.

Authors:  Ambuj Kumar; Vidya Rajendran; Rao Sethumadhavan; Rituraj Purohit
Journal:  Protoplasma       Date:  2013-02-28       Impact factor: 3.356

5.  Progesterone-induced blocking factor differentially regulates trophoblast and tumor invasion by altering matrix metalloproteinase activity.

Authors:  Melinda Halasz; Beata Polgar; Gergely Berta; Livia Czimbalek; Julia Szekeres-Bartho
Journal:  Cell Mol Life Sci       Date:  2013-06-27       Impact factor: 9.261

6.  Centriolar satellites assemble centrosomal microcephaly proteins to recruit CDK2 and promote centriole duplication.

Authors:  Andrew Kodani; Timothy W Yu; Jeffrey R Johnson; Divya Jayaraman; Tasha L Johnson; Lihadh Al-Gazali; Lāszló Sztriha; Jennifer N Partlow; Hanjun Kim; Alexis L Krup; Alexander Dammermann; Nevan J Krogan; Christopher A Walsh; Jeremy F Reiter
Journal:  Elife       Date:  2015-08-22       Impact factor: 8.140

Review 7.  Centriolar satellites: key mediators of centrosome functions.

Authors:  Maxim A X Tollenaere; Niels Mailand; Simon Bekker-Jensen
Journal:  Cell Mol Life Sci       Date:  2014-08-31       Impact factor: 9.261

Review 8.  Mitotic spindle multipolarity without centrosome amplification.

Authors:  Helder Maiato; Elsa Logarinho
Journal:  Nat Cell Biol       Date:  2014-05       Impact factor: 28.824

Review 9.  The Role of Progesterone in Feto-Maternal Immunological Cross Talk.

Authors:  Julia Szekeres-Bartho
Journal:  Med Princ Pract       Date:  2018-06-27       Impact factor: 1.927

10.  The DNA replication protein Cdc6 inhibits the microtubule-organizing activity of the centrosome.

Authors:  Inyoung Lee; Gwang Su Kim; Jun Sung Bae; Jaeyoun Kim; Kunsoo Rhee; Deog Su Hwang
Journal:  J Biol Chem       Date:  2017-08-21       Impact factor: 5.157

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.