Evidence map›Paper›PMID 42244525›Full record

ArticlebioRxiv : the preprint server for biology2026

ATR kinase inhibitors induce mitochondrial fission in CD8

Frank P Vendetti, Carina R Sclafani, Yunqi Zhang, Pinakin Pandya, Yvonne M Mowery, Su Hyeong Kim, Rachel L Cumberland, Satishkumar R Ganakammal, Thomas P Conrads, Michael J Calderon and 8 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

18 authors.

Frank P VendettiDepartment of Radiation Oncology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.ORCID 0009-0000-7480-355X
Carina R SclafaniDepartment of Radiation Oncology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.
Yunqi ZhangSchool of Medicine, Tsinghua University; Beijing, China.
Pinakin PandyaDepartment of Radiation Oncology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.
Yvonne M MoweryDepartment of Radiation Oncology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.ORCID 0000-0002-9839-2414
Su Hyeong KimDepartment of Radiation Oncology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.
Rachel L CumberlandDepartment of Immunology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.
Satishkumar R GanakammalWomen's Health Integrated Research Center, Women's Service Line, Inova Health System; Annandale, VA, USA.
Thomas P ConradsWomen's Health Integrated Research Center, Women's Service Line, Inova Health System; Annandale, VA, USA.ORCID 0000-0003-4742-3281
Michael J CalderonDepartment of Cell Biology, Center for Biologic Imaging, University of Pittsburgh School of Medicine; Pittsburgh, PA, USA.
Simon C WatkinsDepartment of Cell Biology, Center for Biologic Imaging, University of Pittsburgh School of Medicine; Pittsburgh, PA, USA.ORCID 0000-0003-4092-1552
Bennett Van HoutenDepartment of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine; Pittsburgh, PA, USA.ORCID 0000-0002-4009-2478
Ava ClumpDepartment of Radiation Oncology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.
Robert L FerrisDepartment of Otolaryngology-Head & Neck Surgery, University of North Carolina; Chapel Hill, NC, USA.ORCID 0000-0001-6605-2071
Jan H BeumerDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh; Pittsburgh, PA, USA.ORCID 0000-0002-8978-9401
Greg M DelgoffeDepartment of Immunology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.ORCID 0000-0002-2957-8135
Lawrence P KaneDepartment of Immunology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.ORCID 0000-0001-5198-516X
Christopher J BakkenistDepartment of Radiation Oncology, University of Pittsburgh School of Medicine; Pittsburgh, Pennsylvania, PA, USA.ORCID 0000-0001-9672-0886

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Leonard J. Appleman · 1988 to 2026
$158.0M
Watching cooperative interactions between base and nucleotide excision repair proteinsR35ES031638 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Bennett Van Houten · 2020 to 2026
$6.2M
Mechanisms of PD-1 and Tim-3 crosstalk in tumor-infiltrating lymphocytesR01CA206517 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Robert L. Ferris, Lawrence P. Kane · 2016 to 2026
$4.6M
Uncovering the metabolic underpinnings of T cell exhaustionR01AI166598 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DELGOFFE, GREG M. · 2022 to 2025
$3.2M
Dissecting the role of hypoxia in T cell differentiation in cancerR01CA277473 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Greg M. Delgoffe, Yana Najjar · 2023 to 2026
$2.4M
Metabolic control of regulatory T cell functional identityR01AI171483 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DELGOFFE, GREG M. · 2022 to 2025
$2.4M
The Impact of ATR Kinase Inhibitors on CD8+ T Cell Expansion and Memory DevelopmentR01CA266172 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 2022 to 2026
$2.3M
Deoxyuridine Contamination and Innate Immune SignalingR01CA294651 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 2025 to 2026
$1.3M
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA206517NCI NIH HHS R01 CA266172NCI NIH HHS R01 CA277473NCI NIH HHS R01 CA294651NIAID NIH HHS R01 AI166598NIAID NIH HHS R01 AI171483NIEHS NIH HHS R35 ES031638
6 · The paper itself

Abstract

The DNA damage response kinase ATR restrains CDK1 activity during S and G2 phases of the cell cycle, confining CDK1-driven processes to mitosis. ATR kinase inhibitors were originally developed to potentiate chemotherapy-induced DNA damage at stalled replication forks and to disrupt DNA damage-induced cell cycle checkpoints. Recent evidence, however, reveals that these inhibitors also disrupt cell cycle organization in cells that have not sustained any DNA damage. We show that ATR kinase inhibitors potently trigger unscheduled mitochondrial fission, causing loss of mitochondrial mass in actively dividing CD8

Identifiers

PMID42244525
PMCPMC13232094

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.