Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA

Autores
Federico, Maria Belén; Campodónico, Paola Bernadette; Paviolo, Natalia Soledad; Gottifredi, Vanesa
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Biallelic mutations of FANCD2 and other components of the Fanconi Anemia (FA) pathway cause a disease characterized by bone marrow failure, cancer predisposition and a striking sensitivity to agents that induce crosslinks between the two complementary DNA strands (inter-strand crosslinks-ICL). Such genotoxins were used to characterize the contribution of the FA pathway to the genomic stability of cells, thus unravelling the biological relevance of ICL repair in the context of the disease. Notwithstanding this, whether the defect in ICL repair as the sole trigger for the multiple physiological alterations observed in FA patients is still under investigation. Remarkably, ICL-independent functions of FANCD2 and other components of the FA pathway were recently reported. FANCD2 contributes to the processing of very challenging double strand ends (DSEs: one ended Double Strand Breaks -DSBs- created during DNA replication). Other ICL-independent functions of FANCD2 include prevention of DNA breakage at stalled replication forks and facilitation of chromosome segregation at the end of M phase. The current understanding of replication-associated functions of FANCD2 and its relevance for the survival of genomically stable cells is herein discussed.
Fil: Federico, Maria Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. Fundación Instituto Leloir; Argentina
Fil: Campodónico, Paola Bernadette. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Paviolo, Natalia Soledad. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Gottifredi, Vanesa. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Materia
Brca1
Brca2
Homologous-Directed Repair
Non-Homologous End Joining
Translesion Dna Synthesis
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/52560
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/52560
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNAFederico, Maria BelénCampodónico, Paola BernadettePaviolo, Natalia SoledadGottifredi, VanesaBrca1Brca2Homologous-Directed RepairNon-Homologous End JoiningTranslesion Dna Synthesishttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Biallelic mutations of FANCD2 and other components of the Fanconi Anemia (FA) pathway cause a disease characterized by bone marrow failure, cancer predisposition and a striking sensitivity to agents that induce crosslinks between the two complementary DNA strands (inter-strand crosslinks-ICL). Such genotoxins were used to characterize the contribution of the FA pathway to the genomic stability of cells, thus unravelling the biological relevance of ICL repair in the context of the disease. Notwithstanding this, whether the defect in ICL repair as the sole trigger for the multiple physiological alterations observed in FA patients is still under investigation. Remarkably, ICL-independent functions of FANCD2 and other components of the FA pathway were recently reported. FANCD2 contributes to the processing of very challenging double strand ends (DSEs: one ended Double Strand Breaks -DSBs- created during DNA replication). Other ICL-independent functions of FANCD2 include prevention of DNA breakage at stalled replication forks and facilitation of chromosome segregation at the end of M phase. The current understanding of replication-associated functions of FANCD2 and its relevance for the survival of genomically stable cells is herein discussed.Fil: Federico, Maria Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. Fundación Instituto Leloir; ArgentinaFil: Campodónico, Paola Bernadette. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Paviolo, Natalia Soledad. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Gottifredi, Vanesa. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaElsevier Science2018-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/52560Federico, Maria Belén; Campodónico, Paola Bernadette; Paviolo, Natalia Soledad; Gottifredi, Vanesa; Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA; Elsevier Science; Mutation Research-fundamental And Molecular Mechanisms Of Mutagenesis; 808; 3-2018; 83-920027-51071873-135XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0027510717301148info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mrfmmm.2017.09.004info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:38:42Zoai:ri.conicet.gov.ar:11336/52560instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:38:42.489CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
title Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
spellingShingle Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
Federico, Maria Belén
Brca1
Brca2
Homologous-Directed Repair
Non-Homologous End Joining
Translesion Dna Synthesis
title_short Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
title_full Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
title_fullStr Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
title_full_unstemmed Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
title_sort Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA
dc.creator.none.fl_str_mv Federico, Maria Belén
Campodónico, Paola Bernadette
Paviolo, Natalia Soledad
Gottifredi, Vanesa
author Federico, Maria Belén
author_facet Federico, Maria Belén
Campodónico, Paola Bernadette
Paviolo, Natalia Soledad
Gottifredi, Vanesa
author_role author
author2 Campodónico, Paola Bernadette
Paviolo, Natalia Soledad
Gottifredi, Vanesa
author2_role author
author
author
dc.subject.none.fl_str_mv Brca1
Brca2
Homologous-Directed Repair
Non-Homologous End Joining
Translesion Dna Synthesis
topic Brca1
Brca2
Homologous-Directed Repair
Non-Homologous End Joining
Translesion Dna Synthesis
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Biallelic mutations of FANCD2 and other components of the Fanconi Anemia (FA) pathway cause a disease characterized by bone marrow failure, cancer predisposition and a striking sensitivity to agents that induce crosslinks between the two complementary DNA strands (inter-strand crosslinks-ICL). Such genotoxins were used to characterize the contribution of the FA pathway to the genomic stability of cells, thus unravelling the biological relevance of ICL repair in the context of the disease. Notwithstanding this, whether the defect in ICL repair as the sole trigger for the multiple physiological alterations observed in FA patients is still under investigation. Remarkably, ICL-independent functions of FANCD2 and other components of the FA pathway were recently reported. FANCD2 contributes to the processing of very challenging double strand ends (DSEs: one ended Double Strand Breaks -DSBs- created during DNA replication). Other ICL-independent functions of FANCD2 include prevention of DNA breakage at stalled replication forks and facilitation of chromosome segregation at the end of M phase. The current understanding of replication-associated functions of FANCD2 and its relevance for the survival of genomically stable cells is herein discussed.
Fil: Federico, Maria Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina. Fundación Instituto Leloir; Argentina
Fil: Campodónico, Paola Bernadette. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Paviolo, Natalia Soledad. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Gottifredi, Vanesa. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
description Biallelic mutations of FANCD2 and other components of the Fanconi Anemia (FA) pathway cause a disease characterized by bone marrow failure, cancer predisposition and a striking sensitivity to agents that induce crosslinks between the two complementary DNA strands (inter-strand crosslinks-ICL). Such genotoxins were used to characterize the contribution of the FA pathway to the genomic stability of cells, thus unravelling the biological relevance of ICL repair in the context of the disease. Notwithstanding this, whether the defect in ICL repair as the sole trigger for the multiple physiological alterations observed in FA patients is still under investigation. Remarkably, ICL-independent functions of FANCD2 and other components of the FA pathway were recently reported. FANCD2 contributes to the processing of very challenging double strand ends (DSEs: one ended Double Strand Breaks -DSBs- created during DNA replication). Other ICL-independent functions of FANCD2 include prevention of DNA breakage at stalled replication forks and facilitation of chromosome segregation at the end of M phase. The current understanding of replication-associated functions of FANCD2 and its relevance for the survival of genomically stable cells is herein discussed.
publishDate 2018
dc.date.none.fl_str_mv 2018-03
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/52560
Federico, Maria Belén; Campodónico, Paola Bernadette; Paviolo, Natalia Soledad; Gottifredi, Vanesa; Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA; Elsevier Science; Mutation Research-fundamental And Molecular Mechanisms Of Mutagenesis; 808; 3-2018; 83-92
0027-5107
1873-135X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/52560
identifier_str_mv Federico, Maria Belén; Campodónico, Paola Bernadette; Paviolo, Natalia Soledad; Gottifredi, Vanesa; Beyond interstrand crosslinks repair: contribution of FANCD2 and other Fanconi Anemia proteins to the replication of DNA; Elsevier Science; Mutation Research-fundamental And Molecular Mechanisms Of Mutagenesis; 808; 3-2018; 83-92
0027-5107
1873-135X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0027510717301148
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mrfmmm.2017.09.004
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Science
publisher.none.fl_str_mv Elsevier Science
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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