Evidence map›Paper›PMID 42181247›Full record

ArticleiScience2026

The modulation of AUF1 regulates the R-loop resolution activating the immune response in DDR.

Maria Carmen Ragosta, Alessandro di Vaio, Maria Cuomo, Margherita D'angelo, Annamaria Medugno, Andrea Russo, Giulio Mazzarotti, Giuseppe Maria Napolitano, Carmelina Antonella Iannuzzi, Iris Maria Forte and 5 more

Abstract read
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Maria Carmen RagostaScuola Superiore Meridionale (SSM, School of Advanced Studies), Clinical and Translational Oncology Program, University of Naples Federico II, Naples, Italy.
Alessandro di VaioDepartment of Medical Biotechnologies, University of Siena, Siena, Italy.
Maria CuomoDepartment of Medical Biotechnologies, University of Siena, Siena, Italy.
Margherita D'angeloDipartimento di Salute Mentale, Fisica e Medicina Preventiva, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Annamaria MedugnoDepartment of Medical Biotechnologies, University of Siena, Siena, Italy.
Andrea RussoScuola Superiore Meridionale (SSM, School of Advanced Studies), Clinical and Translational Oncology Program, University of Naples Federico II, Naples, Italy.
Giulio MazzarottiDepartment of Medical Biotechnologies, University of Siena, Siena, Italy.
Giuseppe Maria NapolitanoScuola Superiore Meridionale (SSM, School of Advanced Studies), Clinical and Translational Oncology Program, University of Naples Federico II, Naples, Italy.
Carmelina Antonella IannuzziDepartment of Breast and Thoracic Oncology, Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, Napoli, Italy.
Iris Maria ForteDepartment of Breast and Thoracic Oncology, Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, Napoli, Italy.
Rosa CamerlingoCell Biology and Biotherapy Unit, Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, Napoli, Italy.
Canio MartinelliCell Biology and Biotherapy Unit, Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, Napoli, Italy.
Michelino De LaurentiisDepartment of Breast and Thoracic Oncology, Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, Napoli, Italy.
Antonio GiordanoDepartment of Medical Biotechnologies, University of Siena, Siena, Italy.
Luigi AlfanoSbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA damage response (DDR) is a global cellular process that affects multiple cellular compartments, including the tumor microenvironment (TME). After DNA damage, unrepaired DNA fragments or DNA-RNA hybrids can be exported from the nucleus to the cytoplasm, where they activate immune responses, suggesting a new potential readout for cancer therapy. We previously showed that loss of AUF1, an RNA-binding protein, impairs homologous recombination by promoting the accumulation of R -loops. In this study, we investigate the role of AUF1 in DNA repair and immune activation. We demonstrate that AUF1 deregulation leads to accumulation and cytoplasmic export of R loops following DNA damage, resulting in activation of the cGAS-STING signaling pathway. These findings highlight the critical role of R loops in maintaining genome stability and reveal how their deregulation links defective DNA repair to innate immune signaling, opening to a possible therapeutic relevance for cancer.

Indexed as

ImmunologyMolecular biology

Identifiers

PMID42181247
PMCPMC13196424

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.