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10.1080/19420889.2017.1338990

http://scihub22266oqcxt.onion/10.1080/19420889.2017.1338990
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28919938!5595415!28919938
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suck abstract from ncbi

pmid28919938      Commun+Integr+Biol 2017 ; 10 (4): e1338990
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  • Keep it on the edge: The post-mitotic midbody as a polarity signal unit #MMPMID28919938
  • Lujan P; Rubio T; Varsano G; Kohn M
  • Commun Integr Biol 2017[]; 10 (4): e1338990 PMID28919938show ga
  • The maintenance of the epithelial architecture during tissue proliferation is achieved by apical positioning of the midbody after cell division. Consequently, midbody mislocalization contributes to epithelial architecture disruption, a fundamental event during epithelial tumorigenesis. Studies in 3D polarized epithelial MDCK or Caco2 cell models, where midbody misplacement leads to multiple ectopic but fully polarized lumen-containing cysts, revealed that this phenotype can be caused by 2 different scenarios: the loss of mitotic spindle orientation or the loss of asymmetric abscission. In addition, we have recently proposed a third cellular mechanism where the midbody mislocalization is achieved through cytokinesis acceleration driven by the cancer-promoting phosphatase of regenerating liver (PRL)-3. Here we critically review these findings, and we furthermore present new data indicating that midbodies themselves might act as signal unit for polarization since they can infer apical characteristics to a basal membrane.
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