Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Alternative Mechanisms of p53 Action During the Unfolded Protein Response

LTS. Fusée, M. Marín, R. Fåhraeus, I. López,

. 2020 ; 12 (2) : . [pub] 20200210

Jazyk angličtina Země Švýcarsko

Typ dokumentu časopisecké články, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/bmc20005191

Grantová podpora
MEYS - NPS I - LO1413 Ministerstvo Školství, Mládeže a Tělovýchovy
MH CZ - DRO (MMCI, 00209805) Ministerstvo Zdravotnictví Ceské Republiky
180296 Cancerfonden

The tumor suppressor protein p53 orchestrates cellular responses to a vast number of stresses, with DNA damage and oncogenic activation being some of the best described. The capacity of p53 to control cellular events such as cell cycle progression, DNA repair, and apoptosis, to mention some, has been mostly linked to its role as a transcription factor. However, how p53 integrates different signaling cascades to promote a particular pathway remains an open question. One way to broaden its capacity to respond to different stimuli is by the expression of isoforms that can modulate the activities of the full-length protein. One of these isoforms is p47 (p53/47, Δ40p53, p53ΔN40), an alternative translation initiation variant whose expression is specifically induced by the PERK kinase during the Unfolded Protein Response (UPR) following Endoplasmic Reticulum stress. Despite the increasing knowledge on the p53 pathway, its activity when the translation machinery is globally suppressed during the UPR remains poorly understood. Here, we focus on the expression of p47 and we propose that the alternative initiation of p53 mRNA translation offers a unique condition-dependent mechanism to differentiate p53 activity to control cell homeostasis during the UPR. We also discuss how the manipulation of these processes may influence cancer cell physiology in light of therapeutic approaches.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc20005191
003      
CZ-PrNML
005      
20200518104352.0
007      
ta
008      
200511s2020 sz f 000 0|eng||
009      
AR
024    7_
$a 10.3390/cancers12020401 $2 doi
035    __
$a (PubMed)32050651
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a sz
100    1_
$a Fusée, Leïla T S $u INSERM U1162, 27 rue Juliette Dodu, 75010 Paris, France.
245    10
$a Alternative Mechanisms of p53 Action During the Unfolded Protein Response / $c LTS. Fusée, M. Marín, R. Fåhraeus, I. López,
520    9_
$a The tumor suppressor protein p53 orchestrates cellular responses to a vast number of stresses, with DNA damage and oncogenic activation being some of the best described. The capacity of p53 to control cellular events such as cell cycle progression, DNA repair, and apoptosis, to mention some, has been mostly linked to its role as a transcription factor. However, how p53 integrates different signaling cascades to promote a particular pathway remains an open question. One way to broaden its capacity to respond to different stimuli is by the expression of isoforms that can modulate the activities of the full-length protein. One of these isoforms is p47 (p53/47, Δ40p53, p53ΔN40), an alternative translation initiation variant whose expression is specifically induced by the PERK kinase during the Unfolded Protein Response (UPR) following Endoplasmic Reticulum stress. Despite the increasing knowledge on the p53 pathway, its activity when the translation machinery is globally suppressed during the UPR remains poorly understood. Here, we focus on the expression of p47 and we propose that the alternative initiation of p53 mRNA translation offers a unique condition-dependent mechanism to differentiate p53 activity to control cell homeostasis during the UPR. We also discuss how the manipulation of these processes may influence cancer cell physiology in light of therapeutic approaches.
655    _2
$a časopisecké články $7 D016428
655    _2
$a přehledy $7 D016454
700    1_
$a Marín, Mónica $u Biochemistry-Molecular Biology, Faculty of Science, Universidad de la República, Iguá 4225, Montevideo 11400, Uruguay.
700    1_
$a Fåhraeus, Robin $u INSERM U1162, 27 rue Juliette Dodu, 75010 Paris, France. RECAMO, Masaryk Memorial Cancer Institute, Zluty kopec 7, 656 53 Brno, Czech Republic. Department of Medical Biosciences, Umeå University, 90185 Umeå, Sweden. ICCVS, University of Gdańsk, Science, ul. Wita Stwosza 63, 80-308 Gdańsk, Poland.
700    1_
$a López, Ignacio $u Biochemistry-Molecular Biology, Faculty of Science, Universidad de la República, Iguá 4225, Montevideo 11400, Uruguay.
773    0_
$w MED00173178 $t Cancers $x 2072-6694 $g Roč. 12, č. 2 (2020)
856    41
$u https://pubmed.ncbi.nlm.nih.gov/32050651 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20200511 $b ABA008
991    __
$a 20200518104352 $b ABA008
999    __
$a ind $b bmc $g 1524121 $s 1095246
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2020 $b 12 $c 2 $e 20200210 $i 2072-6694 $m Cancers $n Cancers $x MED00173178
GRA    __
$a MEYS - NPS I - LO1413 $p Ministerstvo Školství, Mládeže a Tělovýchovy
GRA    __
$a MH CZ - DRO (MMCI, 00209805) $p Ministerstvo Zdravotnictví Ceské Republiky
GRA    __
$a 180296 $p Cancerfonden
LZP    __
$a Pubmed-20200511

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...