GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer

Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork prot...
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Autor*in:	Zu Ye [verfasserIn] Shengfeng Xu [verfasserIn] Yin Shi [verfasserIn] Xueqian Cheng [verfasserIn] Yuan Zhang [verfasserIn] Sunetra Roy [verfasserIn] Sarita Namjoshi [verfasserIn] Michael A. Longo [verfasserIn] Todd M. Link [verfasserIn] Katharina Schlacher [verfasserIn] Guang Peng [verfasserIn] Dihua Yu [verfasserIn] Bin Wang [verfasserIn] John A. Tainer [verfasserIn] Zamal Ahmed [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Übergeordnetes Werk:	In: Nature Communications - Nature Portfolio, 2016, 15(2024), 1, Seite 14
Übergeordnetes Werk:	volume:15 ; year:2024 ; number:1 ; pages:14

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1038/s41467-024-46283-y

Katalog-ID:	DOAJ092308724

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allfields	10.1038/s41467-024-46283-y doi (DE-627)DOAJ092308724 (DE-599)DOAJ34703b9f52584ec280d6534757e27d85 DE-627 ger DE-627 rakwb eng Zu Ye verfasserin aut GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination. Science Q Shengfeng Xu verfasserin aut Yin Shi verfasserin aut Xueqian Cheng verfasserin aut Yuan Zhang verfasserin aut Sunetra Roy verfasserin aut Sarita Namjoshi verfasserin aut Michael A. Longo verfasserin aut Todd M. Link verfasserin aut Katharina Schlacher verfasserin aut Guang Peng verfasserin aut Dihua Yu verfasserin aut Bin Wang verfasserin aut John A. Tainer verfasserin aut Zamal Ahmed verfasserin aut In Nature Communications Nature Portfolio, 2016 15(2024), 1, Seite 14 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:15 year:2024 number:1 pages:14 https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/article/34703b9f52584ec280d6534757e27d85 kostenfrei https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2024 1 14
spelling	10.1038/s41467-024-46283-y doi (DE-627)DOAJ092308724 (DE-599)DOAJ34703b9f52584ec280d6534757e27d85 DE-627 ger DE-627 rakwb eng Zu Ye verfasserin aut GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination. Science Q Shengfeng Xu verfasserin aut Yin Shi verfasserin aut Xueqian Cheng verfasserin aut Yuan Zhang verfasserin aut Sunetra Roy verfasserin aut Sarita Namjoshi verfasserin aut Michael A. Longo verfasserin aut Todd M. Link verfasserin aut Katharina Schlacher verfasserin aut Guang Peng verfasserin aut Dihua Yu verfasserin aut Bin Wang verfasserin aut John A. Tainer verfasserin aut Zamal Ahmed verfasserin aut In Nature Communications Nature Portfolio, 2016 15(2024), 1, Seite 14 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:15 year:2024 number:1 pages:14 https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/article/34703b9f52584ec280d6534757e27d85 kostenfrei https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2024 1 14
allfields_unstemmed	10.1038/s41467-024-46283-y doi (DE-627)DOAJ092308724 (DE-599)DOAJ34703b9f52584ec280d6534757e27d85 DE-627 ger DE-627 rakwb eng Zu Ye verfasserin aut GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination. Science Q Shengfeng Xu verfasserin aut Yin Shi verfasserin aut Xueqian Cheng verfasserin aut Yuan Zhang verfasserin aut Sunetra Roy verfasserin aut Sarita Namjoshi verfasserin aut Michael A. Longo verfasserin aut Todd M. Link verfasserin aut Katharina Schlacher verfasserin aut Guang Peng verfasserin aut Dihua Yu verfasserin aut Bin Wang verfasserin aut John A. Tainer verfasserin aut Zamal Ahmed verfasserin aut In Nature Communications Nature Portfolio, 2016 15(2024), 1, Seite 14 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:15 year:2024 number:1 pages:14 https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/article/34703b9f52584ec280d6534757e27d85 kostenfrei https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2024 1 14
allfieldsGer	10.1038/s41467-024-46283-y doi (DE-627)DOAJ092308724 (DE-599)DOAJ34703b9f52584ec280d6534757e27d85 DE-627 ger DE-627 rakwb eng Zu Ye verfasserin aut GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination. Science Q Shengfeng Xu verfasserin aut Yin Shi verfasserin aut Xueqian Cheng verfasserin aut Yuan Zhang verfasserin aut Sunetra Roy verfasserin aut Sarita Namjoshi verfasserin aut Michael A. Longo verfasserin aut Todd M. Link verfasserin aut Katharina Schlacher verfasserin aut Guang Peng verfasserin aut Dihua Yu verfasserin aut Bin Wang verfasserin aut John A. Tainer verfasserin aut Zamal Ahmed verfasserin aut In Nature Communications Nature Portfolio, 2016 15(2024), 1, Seite 14 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:15 year:2024 number:1 pages:14 https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/article/34703b9f52584ec280d6534757e27d85 kostenfrei https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2024 1 14
allfieldsSound	10.1038/s41467-024-46283-y doi (DE-627)DOAJ092308724 (DE-599)DOAJ34703b9f52584ec280d6534757e27d85 DE-627 ger DE-627 rakwb eng Zu Ye verfasserin aut GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination. Science Q Shengfeng Xu verfasserin aut Yin Shi verfasserin aut Xueqian Cheng verfasserin aut Yuan Zhang verfasserin aut Sunetra Roy verfasserin aut Sarita Namjoshi verfasserin aut Michael A. Longo verfasserin aut Todd M. Link verfasserin aut Katharina Schlacher verfasserin aut Guang Peng verfasserin aut Dihua Yu verfasserin aut Bin Wang verfasserin aut John A. Tainer verfasserin aut Zamal Ahmed verfasserin aut In Nature Communications Nature Portfolio, 2016 15(2024), 1, Seite 14 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:15 year:2024 number:1 pages:14 https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/article/34703b9f52584ec280d6534757e27d85 kostenfrei https://doi.org/10.1038/s41467-024-46283-y kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2024 1 14
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author	Zu Ye
spellingShingle	Zu Ye misc Science misc Q GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer
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topic_title	GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer
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title	GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer
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title_full	GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer
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author_browse	Zu Ye Shengfeng Xu Yin Shi Xueqian Cheng Yuan Zhang Sunetra Roy Sarita Namjoshi Michael A. Longo Todd M. Link Katharina Schlacher Guang Peng Dihua Yu Bin Wang John A. Tainer Zamal Ahmed
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title_sort	grb2 stabilizes rad51 at reversed replication forks suppressing genomic instability and innate immunity against cancer
title_auth	GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer
abstract	Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination.
abstractGer	Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination.
abstract_unstemmed	Abstract Growth factor receptor-bound protein 2 (GRB2) is a cytoplasmic adapter for tyrosine kinase signaling and a nuclear adapter for homology-directed-DNA repair. Here we find nuclear GRB2 protects DNA at stalled replication forks from MRE11-mediated degradation in the BRCA2 replication fork protection axis. Mechanistically, GRB2 binds and inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks. In GRB2-depleted cells, PARP inhibitor (PARPi) treatment releases DNA fragments from stalled forks into the cytoplasm that activate the cGAS–STING pathway to trigger pro-inflammatory cytokine production. Moreover in a syngeneic mouse metastatic ovarian cancer model, GRB2 depletion in the context of PARPi treatment reduced tumor burden and enabled high survival consistent with immune suppression of cancer growth. Collective findings unveil GRB2 function and mechanism for fork protection in the BRCA2-RAD51-MRE11 axis and suggest GRB2 as a potential therapeutic target and an enabling predictive biomarker for patient selection for PARPi and immunotherapy combination.
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title_short	GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer
url	https://doi.org/10.1038/s41467-024-46283-y https://doaj.org/article/34703b9f52584ec280d6534757e27d85 https://doaj.org/toc/2041-1723
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author2	Shengfeng Xu Yin Shi Xueqian Cheng Yuan Zhang Sunetra Roy Sarita Namjoshi Michael A. Longo Todd M. Link Katharina Schlacher Guang Peng Dihua Yu Bin Wang John A. Tainer Zamal Ahmed
author2Str	Shengfeng Xu Yin Shi Xueqian Cheng Yuan Zhang Sunetra Roy Sarita Namjoshi Michael A. Longo Todd M. Link Katharina Schlacher Guang Peng Dihua Yu Bin Wang John A. Tainer Zamal Ahmed
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GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer

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