The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.
- Autores
- Gottifredi, Vanesa; Wiesmuller L
- Año de publicación
- 2018
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.Gottifredi V1, Wiesmüller L2.The tumor suppressor p53 is a transcriptional factor broadly mutated in cancer. Most inactivating and gain of function mutations disrupt the sequence-specific DNA binding domain, which activates target genes. This is perhaps the main reason why most research has focused on the relevance of such transcriptional activity for the prevention or elimination of cancer cells. Notwithstanding, transcriptional regulation may not be the only mechanism underlying its role in tumor suppression and therapeutic responses. In the past, a direct role of p53 in DNA repair transactions that include the regulation of homologous recombination has been suggested. More recently, the localization of p53 at replication forks has been demonstrated and the effect of p53 on nascent DNA elongation has been explored. While some data sets indicate that the regulation of ongoing replication forks by p53 may be mediated by p53 targets such as MDM2 (murine double minute 2) and polymerase (POL) eta other evidences demonstrate that p53 is capable of controlling DNA replication by directly interacting with the replisome and altering its composition. In addition to discussing such findings, this review will also analyze the impact that p53-mediated control of ongoing DNA replication has on treatment responses and tumor suppressor abilities of this important anti-oncogene.
Fil: Gottifredi, Vanesa. 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: Wiesmuller L. Universitat Ulm; Alemania - Materia
-
MRE11; POL iota; POL teta; RAD52;
ZRANB3; fork reversal; mutant p53;
template switching; translesion DNA synthesis
therapy resistance - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/88200
Ver los metadatos del registro completo
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The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.Gottifredi, VanesaWiesmuller LMRE11; POL iota; POL teta; RAD52;ZRANB3; fork reversal; mutant p53;template switching; translesion DNA synthesistherapy resistancehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.Gottifredi V1, Wiesmüller L2.The tumor suppressor p53 is a transcriptional factor broadly mutated in cancer. Most inactivating and gain of function mutations disrupt the sequence-specific DNA binding domain, which activates target genes. This is perhaps the main reason why most research has focused on the relevance of such transcriptional activity for the prevention or elimination of cancer cells. Notwithstanding, transcriptional regulation may not be the only mechanism underlying its role in tumor suppression and therapeutic responses. In the past, a direct role of p53 in DNA repair transactions that include the regulation of homologous recombination has been suggested. More recently, the localization of p53 at replication forks has been demonstrated and the effect of p53 on nascent DNA elongation has been explored. While some data sets indicate that the regulation of ongoing replication forks by p53 may be mediated by p53 targets such as MDM2 (murine double minute 2) and polymerase (POL) eta other evidences demonstrate that p53 is capable of controlling DNA replication by directly interacting with the replisome and altering its composition. In addition to discussing such findings, this review will also analyze the impact that p53-mediated control of ongoing DNA replication has on treatment responses and tumor suppressor abilities of this important anti-oncogene.Fil: Gottifredi, Vanesa. 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: Wiesmuller L. Universitat Ulm; AlemaniaMDPI2018-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/88200Gottifredi, Vanesa; Wiesmuller L; The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.; MDPI; Cancers; 10; 7-2018; 1-152072-6694CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.3390/cancers10080250info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2072-6694/10/8/250info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:03:50Zoai:ri.conicet.gov.ar:11336/88200instacron: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 10:03:50.487CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. |
title |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. |
spellingShingle |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. Gottifredi, Vanesa MRE11; POL iota; POL teta; RAD52; ZRANB3; fork reversal; mutant p53; template switching; translesion DNA synthesis therapy resistance |
title_short |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. |
title_full |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. |
title_fullStr |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. |
title_full_unstemmed |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. |
title_sort |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53. |
dc.creator.none.fl_str_mv |
Gottifredi, Vanesa Wiesmuller L |
author |
Gottifredi, Vanesa |
author_facet |
Gottifredi, Vanesa Wiesmuller L |
author_role |
author |
author2 |
Wiesmuller L |
author2_role |
author |
dc.subject.none.fl_str_mv |
MRE11; POL iota; POL teta; RAD52; ZRANB3; fork reversal; mutant p53; template switching; translesion DNA synthesis therapy resistance |
topic |
MRE11; POL iota; POL teta; RAD52; ZRANB3; fork reversal; mutant p53; template switching; translesion DNA synthesis therapy resistance |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.Gottifredi V1, Wiesmüller L2.The tumor suppressor p53 is a transcriptional factor broadly mutated in cancer. Most inactivating and gain of function mutations disrupt the sequence-specific DNA binding domain, which activates target genes. This is perhaps the main reason why most research has focused on the relevance of such transcriptional activity for the prevention or elimination of cancer cells. Notwithstanding, transcriptional regulation may not be the only mechanism underlying its role in tumor suppression and therapeutic responses. In the past, a direct role of p53 in DNA repair transactions that include the regulation of homologous recombination has been suggested. More recently, the localization of p53 at replication forks has been demonstrated and the effect of p53 on nascent DNA elongation has been explored. While some data sets indicate that the regulation of ongoing replication forks by p53 may be mediated by p53 targets such as MDM2 (murine double minute 2) and polymerase (POL) eta other evidences demonstrate that p53 is capable of controlling DNA replication by directly interacting with the replisome and altering its composition. In addition to discussing such findings, this review will also analyze the impact that p53-mediated control of ongoing DNA replication has on treatment responses and tumor suppressor abilities of this important anti-oncogene. Fil: Gottifredi, Vanesa. 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: Wiesmuller L. Universitat Ulm; Alemania |
description |
The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.Gottifredi V1, Wiesmüller L2.The tumor suppressor p53 is a transcriptional factor broadly mutated in cancer. Most inactivating and gain of function mutations disrupt the sequence-specific DNA binding domain, which activates target genes. This is perhaps the main reason why most research has focused on the relevance of such transcriptional activity for the prevention or elimination of cancer cells. Notwithstanding, transcriptional regulation may not be the only mechanism underlying its role in tumor suppression and therapeutic responses. In the past, a direct role of p53 in DNA repair transactions that include the regulation of homologous recombination has been suggested. More recently, the localization of p53 at replication forks has been demonstrated and the effect of p53 on nascent DNA elongation has been explored. While some data sets indicate that the regulation of ongoing replication forks by p53 may be mediated by p53 targets such as MDM2 (murine double minute 2) and polymerase (POL) eta other evidences demonstrate that p53 is capable of controlling DNA replication by directly interacting with the replisome and altering its composition. In addition to discussing such findings, this review will also analyze the impact that p53-mediated control of ongoing DNA replication has on treatment responses and tumor suppressor abilities of this important anti-oncogene. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-07 |
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/11336/88200 Gottifredi, Vanesa; Wiesmuller L; The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.; MDPI; Cancers; 10; 7-2018; 1-15 2072-6694 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/88200 |
identifier_str_mv |
Gottifredi, Vanesa; Wiesmuller L; The Tip of an Iceberg: Replication-Associated Functions of the Tumor Suppressor p53.; MDPI; Cancers; 10; 7-2018; 1-15 2072-6694 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.3390/cancers10080250 info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2072-6694/10/8/250 |
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 |
MDPI |
publisher.none.fl_str_mv |
MDPI |
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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1844613858621128704 |
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13.070432 |