Cep63 Recruits Cdk1 to the Centrosome—Letter

Alsara, Mohammad; Löffler, Harald; Fechter, Anne; Bártek, Jiří; Krämer, Alwin

doi:10.1158/0008-5472.can-14-3431

Cited by 2 publications

(1 citation statement)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, this issue will require further investigation since some of the CDK1 antibodies used for cytology cross-react with CEP152, that we, and others, have shown is dependent on CEP63 for centrosomal recruitment ( Fig. 2a and 6a ) 5 , 22 , 46 – 48 .…”

Section: Discussionmentioning

confidence: 89%

CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination

et al. 2015

View full text Add to dashboard Cite

CEP63 is a centrosomal protein that facilitates centriole duplication and is regulated by the DNA damage response. Mutations in CEP63 cause Seckel syndrome, a human disease characterized by microcephaly and dwarfism. Here we demonstrate that Cep63 deficient mice recapitulate Seckel syndrome pathology. The attrition of neural progenitor cells involves p53-dependent cell death and brain size is rescued by the deletion of p53. Cell death is not the result of an aberrant DNA damage response but is triggered by centrosome-based mitotic errors. In addition, Cep63 loss severely impairs meiotic recombination, leading to profound male infertility. Cep63 deficient spermatocytes display numerical and structural centrosome aberrations, chromosome entanglements and defective telomere clustering, suggesting that a reduction in centrosome-mediated chromosome movements underlies recombination failure. Our results provide novel insight into the molecular pathology of microcephaly and establish a role for the centrosome in meiotic recombination.

show abstract

Section: Discussionmentioning

confidence: 89%

CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination

et al. 2015

View full text Add to dashboard Cite

show abstract

Zika virus: An emerging challenge for obstetrics and gynecology

Lin¹,

Chin²,

Chen³

et al. 2017

Taiwanese Journal of Obstetrics and Gynecology

View full text Add to dashboard Cite

Microcephaly is a rare birth defect, however, the re-emerging mosquito and sexual transmitted flavivirus, Zika virus (ZIKV), had changed the situation and caused an urgent challenge for the obstetrics and gynecology. This review will brief summarize the epidemiology and virology of ZIKV. And compared the animal models that had developed for the ZIKV infections. These animal models will be benefit for the development of vaccines and anti-ZIKV drugs. Furthermore, the genes that are involved in the causation of microcephaly were also summarized. Finally, the Wnt signal is critical for the brain development as well as innate immune response. Based on previous literatures, we proposed that ZIKV-induced microcephaly might result from the influence of Wnt/β-catenin signaling pathway through the regulation of miRNA-34.

show abstract

Cep63 Recruits Cdk1 to the Centrosome—Letter

Cited by 2 publications

References 5 publications

CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination

CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination

Zika virus: An emerging challenge for obstetrics and gynecology

Contact Info

Product

Resources

About