Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Rebecca A. Boisvert"'
Autor:
Michael A. Longo, Sunetra Roy, Yue Chen, Karl-Heinz Tomaszowski, Andrew S. Arvai, Jordan T. Pepper, Rebecca A. Boisvert, Selvi Kunnimalaiyaan, Caezanne Keshvani, David Schild, Albino Bacolla, Gareth J. Williams, John A. Tainer, Katharina Schlacher
Publikováno v:
Nature Communications, Vol 14, Iss 1, Pp 1-16 (2023)
Abstract RAD51C is an enigmatic predisposition gene for breast, ovarian, and prostate cancer. Currently, missing structural and related functional understanding limits patient mutation interpretation to homology-directed repair (HDR) function analysi
Externí odkaz:
https://doaj.org/article/3d21ced31b7c4fa39d8b21ed94cd204f
Autor:
Jessica W. Luzwick, Eszter Dombi, Rebecca A. Boisvert, Sunetra Roy, Soyoung Park, Selvi Kunnimalaiyaan, Steffi Goffart, Detlev Schindler, Katharina Schlacher
Publikováno v:
Science Advances
Description
MRE11 activates mitochondrial DNA–dependent cGAS immune signaling in cells with BRCA/FANC gene defects.
Mitochondrial DNA (mtDNA) instability activates cGAS-dependent innate immune signaling by unknown mechanisms. Here, we fin
MRE11 activates mitochondrial DNA–dependent cGAS immune signaling in cells with BRCA/FANC gene defects.
Mitochondrial DNA (mtDNA) instability activates cGAS-dependent innate immune signaling by unknown mechanisms. Here, we fin
Autor:
Benjamin Piraino, Justin L. Blaize, Juan A. Cantres-Velez, Rebecca A. Boisvert, Winnie Tan, David A. Vierra, Niall G. Howlett, Andrew J. Deans, Jada L Garzon
Publikováno v:
Mol Cell Biol
Fanconi anemia (FA) is a rare genetic disease characterized by increased risk for bone marrow failure and cancer. The FA proteins function together to repair damaged DNA. A central step in the activation of the FA pathway is the monoubiquitination of
Publikováno v:
PLoS ONE, Vol 8, Iss 11, p e81387 (2013)
Fanconi anemia (FA) is a rare recessive disease, characterized by congenital defects, bone marrow failure, and increased cancer susceptibility. FA is caused by biallelic mutation of any one of sixteen genes. The protein products of these genes functi
Externí odkaz:
https://doaj.org/article/8e1eb78d59c94aae87e4ae5e4ac3e7a4
Autor:
Rebecca Anne Boisvert
Fanconi anemia (FA) is a rare autosomal and X-linked recessive disorder, characterized by congenital abnormalities, pediatric bone marrow failure and cancer susceptibility. FA is caused by biallelic mutations in any one of 16 genes. The FA proteins f
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::2dea508bd8266ca7dcb30d592099ca70
https://doi.org/10.23860/diss-boisvert-rebecca-2015
https://doi.org/10.23860/diss-boisvert-rebecca-2015
Autor:
Selvi Kunnimalaiyaan, Sunetra Roy, Jessica w. Luzwick, Rebecca A. Boisvert, Soyoung Park, Steffi Goffart, Katharina Schlacher, Detlev Schindler
Publikováno v:
SSRN Electronic Journal.
Mitochondrial DNA instability activates cGAS and the innate immune system by unknown mechanisms. Here, we find that Fanconi anemia suppressor genes are acting in the mitochondria to protect mitochondrial DNA replication forks from instability. Specif
Autor:
Rebecca A. Boisvert, Francesca Cavallo, Meghan A. Rego, Niall G. Howlett, Fumiko Esashi, Maurizio Mauro, Maria Jasin
Publikováno v:
Nucleic Acids Research
p21 is a well-established regulator of cell cycle progression. The role of p21 in DNA repair, however, remains poorly characterized. Here, we describe a critical role of p21 in a replication-coupled DNA double-strand break (DSB) repair that is mechan
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::59950a2210d6e6679b41b164f610c2a3
https://ora.ox.ac.uk/objects/uuid:86d55a26-08f8-4a12-b4b4-be4a98edf5c0
https://ora.ox.ac.uk/objects/uuid:86d55a26-08f8-4a12-b4b4-be4a98edf5c0
Autor:
Niall G. Howlett, Rebecca A. Boisvert
Publikováno v:
Cell cycle (Georgetown, Tex.). 13(19)
Fanconi anemia (FA) is a rare recessive genetic disease characterized by congenital abnormalities, bone marrow failure and heightened cancer susceptibility in early adulthood. FA is caused by biallelic germ-line mutation of any one of 16 genes. While
Publikováno v:
The FASEB Journal. 27