@ARTICLE{Kodani2022-lj,
  title    = "Zika virus alters centrosome organization to suppress the innate
              immune response",
  author   = "Kodani, Andrew and Knopp, Kristeene A and Di Lullo, Elizabeth and
              Retallack, Hanna and Kriegstein, Arnold R and DeRisi, Joseph L
              and Reiter, Jeremy F",
  abstract = "Zika virus (ZIKV) is a flavivirus transmitted via mosquitoes and
              sex to cause congenital neurodevelopmental defects, including
              microcephaly. Inherited forms of microcephaly (MCPH) are
              associated with disrupted centrosome organization. Similarly, we
              found that ZIKV infection disrupted centrosome organization. ZIKV
              infection disrupted the organization of centrosomal proteins
              including CEP63, a MCPH-associated protein. The ZIKV
              nonstructural protein NS3 bound CEP63, and expression of NS3 was
              sufficient to alter centrosome architecture and CEP63
              localization. Loss of CEP63 suppressed ZIKV-induced centrosome
              disorganization, indicating that ZIKV requires CEP63 to disrupt
              centrosome organization. ZIKV infection or CEP63 loss decreased
              the centrosomal localization and stability of TANK-binding kinase
              1 (TBK1), a regulator of the innate immune response. ZIKV
              infection also increased the centrosomal accumulation of the
              CEP63 interactor DTX4, a ubiquitin ligase that degrades TBK1.
              Therefore, we propose that ZIKV disrupts CEP63 function to
              increase centrosomal DTX4 localization and destabilization of
              TBK1, thereby tempering the innate immune response.",
  journal  = "EMBO Rep",
  volume   =  23,
  number   =  9,
  pages    = "e52211",
  month    =  jul,
  year     =  2022,
  keywords = "Zika virus; centrosome; innate immunity; microcephaly",
  language = "en"
}

{"_id":"zTZR92aewWbisd2vM","bibbaseid":"kodani-knopp-dilullo-retallack-kriegstein-derisi-reiter-zikavirusalterscentrosomeorganizationtosuppresstheinnateimmuneresponse-2022","author_short":["Kodani, A.","Knopp, K. A","Di Lullo, E.","Retallack, H.","Kriegstein, A. R","DeRisi, J. L","Reiter, J. F"],"bibdata":{"bibtype":"article","type":"article","title":"Zika virus alters centrosome organization to suppress the innate immune response","author":[{"propositions":[],"lastnames":["Kodani"],"firstnames":["Andrew"],"suffixes":[]},{"propositions":[],"lastnames":["Knopp"],"firstnames":["Kristeene","A"],"suffixes":[]},{"propositions":[],"lastnames":["Di","Lullo"],"firstnames":["Elizabeth"],"suffixes":[]},{"propositions":[],"lastnames":["Retallack"],"firstnames":["Hanna"],"suffixes":[]},{"propositions":[],"lastnames":["Kriegstein"],"firstnames":["Arnold","R"],"suffixes":[]},{"propositions":[],"lastnames":["DeRisi"],"firstnames":["Joseph","L"],"suffixes":[]},{"propositions":[],"lastnames":["Reiter"],"firstnames":["Jeremy","F"],"suffixes":[]}],"abstract":"Zika virus (ZIKV) is a flavivirus transmitted via mosquitoes and sex to cause congenital neurodevelopmental defects, including microcephaly. Inherited forms of microcephaly (MCPH) are associated with disrupted centrosome organization. Similarly, we found that ZIKV infection disrupted centrosome organization. ZIKV infection disrupted the organization of centrosomal proteins including CEP63, a MCPH-associated protein. The ZIKV nonstructural protein NS3 bound CEP63, and expression of NS3 was sufficient to alter centrosome architecture and CEP63 localization. Loss of CEP63 suppressed ZIKV-induced centrosome disorganization, indicating that ZIKV requires CEP63 to disrupt centrosome organization. ZIKV infection or CEP63 loss decreased the centrosomal localization and stability of TANK-binding kinase 1 (TBK1), a regulator of the innate immune response. ZIKV infection also increased the centrosomal accumulation of the CEP63 interactor DTX4, a ubiquitin ligase that degrades TBK1. Therefore, we propose that ZIKV disrupts CEP63 function to increase centrosomal DTX4 localization and destabilization of TBK1, thereby tempering the innate immune response.","journal":"EMBO Rep","volume":"23","number":"9","pages":"e52211","month":"July","year":"2022","keywords":"Zika virus; centrosome; innate immunity; microcephaly","language":"en","bibtex":"@ARTICLE{Kodani2022-lj,\n title = \"Zika virus alters centrosome organization to suppress the innate\n immune response\",\n author = \"Kodani, Andrew and Knopp, Kristeene A and Di Lullo, Elizabeth and\n Retallack, Hanna and Kriegstein, Arnold R and DeRisi, Joseph L\n and Reiter, Jeremy F\",\n abstract = \"Zika virus (ZIKV) is a flavivirus transmitted via mosquitoes and\n sex to cause congenital neurodevelopmental defects, including\n microcephaly. Inherited forms of microcephaly (MCPH) are\n associated with disrupted centrosome organization. Similarly, we\n found that ZIKV infection disrupted centrosome organization. ZIKV\n infection disrupted the organization of centrosomal proteins\n including CEP63, a MCPH-associated protein. The ZIKV\n nonstructural protein NS3 bound CEP63, and expression of NS3 was\n sufficient to alter centrosome architecture and CEP63\n localization. Loss of CEP63 suppressed ZIKV-induced centrosome\n disorganization, indicating that ZIKV requires CEP63 to disrupt\n centrosome organization. ZIKV infection or CEP63 loss decreased\n the centrosomal localization and stability of TANK-binding kinase\n 1 (TBK1), a regulator of the innate immune response. ZIKV\n infection also increased the centrosomal accumulation of the\n CEP63 interactor DTX4, a ubiquitin ligase that degrades TBK1.\n Therefore, we propose that ZIKV disrupts CEP63 function to\n increase centrosomal DTX4 localization and destabilization of\n TBK1, thereby tempering the innate immune response.\",\n journal = \"EMBO Rep\",\n volume = 23,\n number = 9,\n pages = \"e52211\",\n month = jul,\n year = 2022,\n keywords = \"Zika virus; centrosome; innate immunity; microcephaly\",\n language = \"en\"\n}\n\n","author_short":["Kodani, A.","Knopp, K. A","Di Lullo, E.","Retallack, H.","Kriegstein, A. R","DeRisi, J. L","Reiter, J. F"],"key":"Kodani2022-lj","id":"Kodani2022-lj","bibbaseid":"kodani-knopp-dilullo-retallack-kriegstein-derisi-reiter-zikavirusalterscentrosomeorganizationtosuppresstheinnateimmuneresponse-2022","role":"author","urls":{},"keyword":["Zika virus; centrosome; innate immunity; microcephaly"],"metadata":{"authorlinks":{}}},"bibtype":"article","biburl":"https://bibbase.org/f/EJMp3HRuxirjxpcXh/references.bib","dataSources":["sAFYeB74DpbdXM9NN","4zx9n2tbeLTix3Wxr","k3cdWrThyTh5o59Rm","hq9pebjzmsTuyxGGx","h8Atv2SAy4PmShg5j"],"keywords":["zika virus; centrosome; innate immunity; microcephaly"],"search_terms":["zika","virus","alters","centrosome","organization","suppress","innate","immune","response","kodani","knopp","di lullo","retallack","kriegstein","derisi","reiter"],"title":"Zika virus alters centrosome organization to suppress the innate immune response","year":2022}