| COQUEL, Flavie, Maria Joao SILVA, Hervé TECHER, Karina ZADOROZHNY, Sushma SHARMA, Jadwiga NIEMINUSZCZY, Clément METTLING, Elodie DARDILLAC, Antoine BARTHE, Anne Lyne SCHMITZ, Alexy PROMONET, Alexandra CRIBIER, Amélie SARRAZIN, Wojciech NIEDZWIEDZ, Bernard LOPEZ, Vincenzo COSTANZO, Lumír KREJČÍ, Andrei CHABES, Monsef BENKIRANE, Lin YEA-LIH a Philippe PASERO. SAMHD1 acts at stalled replication forks to prevent interferon induction. Nature. LONDON: NATURE PUBLISHING GROUP, 2018, roč. 557, č. 7703, s. "57"-"+", 26 s. ISSN 0028-0836. Dostupné z: https://dx.doi.org/10.1038/s41586-018-0050-1. |
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@article{1504937,
author = {Coquel, Flavie and Silva, Maria Joao and Techer, Hervé and Zadorozhny, Karina and Sharma, Sushma and Nieminuszczy, Jadwiga and Mettling, Clément and Dardillac, Elodie and Barthe, Antoine and Schmitz, Anne Lyne and Promonet, Alexy and Cribier, Alexandra and Sarrazin, Amélie and Niedzwiedz, Wojciech and Lopez, Bernard and Costanzo, Vincenzo and Krejčí, Lumír and Chabes, Andrei and Benkirane, Monsef and YeaandLih, Lin and Pasero, Philippe},
article_location = {LONDON},
article_number = {7703},
doi = {http://dx.doi.org/10.1038/s41586-018-0050-1},
keywords = {SAMHD1},
language = {eng},
issn = {0028-0836},
journal = {Nature},
title = {SAMHD1 acts at stalled replication forks to prevent interferon induction},
volume = {557},
year = {2018}
}
TY - JOUR
ID - 1504937
AU - Coquel, Flavie - Silva, Maria Joao - Techer, Hervé - Zadorozhny, Karina - Sharma, Sushma - Nieminuszczy, Jadwiga - Mettling, Clément - Dardillac, Elodie - Barthe, Antoine - Schmitz, Anne Lyne - Promonet, Alexy - Cribier, Alexandra - Sarrazin, Amélie - Niedzwiedz, Wojciech - Lopez, Bernard - Costanzo, Vincenzo - Krejčí, Lumír - Chabes, Andrei - Benkirane, Monsef - Yea-Lih, Lin - Pasero, Philippe
PY - 2018
TI - SAMHD1 acts at stalled replication forks to prevent interferon induction
JF - Nature
VL - 557
IS - 7703
SP - "57"-"+"
EP - "57"-"+"
PB - NATURE PUBLISHING GROUP
SN - 00280836
KW - SAMHD1
N2 - SAMHD1 was previously characterized as a dNTPase that protects cells from viral infections. Mutations in SAMHD1 are implicated in cancer development and in a severe congenital inflammatory disease known as Aicardi-Goutieres syndrome. The mechanism by which SAMHD1 protects against cancer and chronic inflammation is unknown. Here we show that SAMHD1 promotes degradation of nascent DNA at stalled replication forks in human cell lines by stimulating the exonuclease activity of MRE11. This function activates the ATR-CHK1 checkpoint and allows the forks to restart replication. In SAMHD1-depleted cells, single-stranded DNA fragments are released from stalled forks and accumulate in the cytosol, where they activate the cGAS-STING pathway to induce expression of pro-inflammatory type I interferons. SAMHD1 is thus an important player in the replication stress response, which prevents chronic inflammation by limiting the release of single-stranded DNA from stalled replication forks.
ER -
COQUEL, Flavie, Maria Joao SILVA, Hervé TECHER, Karina ZADOROZHNY, Sushma SHARMA, Jadwiga NIEMINUSZCZY, Clément METTLING, Elodie DARDILLAC, Antoine BARTHE, Anne Lyne SCHMITZ, Alexy PROMONET, Alexandra CRIBIER, Amélie SARRAZIN, Wojciech NIEDZWIEDZ, Bernard LOPEZ, Vincenzo COSTANZO, Lumír KREJČÍ, Andrei CHABES, Monsef BENKIRANE, Lin YEA-LIH a Philippe PASERO. SAMHD1 acts at stalled replication forks to prevent interferon induction. \textit{Nature}. LONDON: NATURE PUBLISHING GROUP, 2018, roč.~557, č.~7703, s.~''57''-''+'', 26 s. ISSN~0028-0836. Dostupné z: https://dx.doi.org/10.1038/s41586-018-0050-1.
|
