Evidence map›Paper›PMID 39868202›Full record

ArticlebioRxiv : the preprint server for biology2025

REV7 associates with ATRIP and inhibits ATR kinase activity.

Megan Biller, Sara Kabir, Sarah Nipper, Sydney Allen, Yara Kayali, Skyler Kuncik, Hiroyuki Sasanuma, Pei Zhou, Cyrus Vaziri, Junya Tomida

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. 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

5 · Who and what money

Authors and funding

10 authors.

Megan Biller
Sara Kabir
Sarah Nipper
Sydney Allen
Yara Kayali
Skyler Kuncik
Hiroyuki Sasanuma
Pei Zhou
Cyrus Vaziri
Junya Tomida

Funding

Synergistic DNA repair genes and sensitivity to radiation therapy in prostate cancerR15CA263784 · NCI · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI TOMIDA, JUNYA · 2021 to 2021
$447k
NCI NIH HHS R15 CA263784
6 · The paper itself

Abstract

Integration of DNA replication with DNA repair, cell cycle progression, and other biological processes is crucial for preserving genome stability and fundamentally important for all life. Ataxia-telangiectasia mutated and RAD3-related (ATR) and its partner ATR-interacting protein (ATRIP) function as a critical proximal sensor and transducer of the DNA Damage Response (DDR). Several ATR substrates, including p53 and CHK1, are crucial for coordination of cell cycle phase transitions, transcription, and DNA repair when cells sustain DNA damage. While much is known about ATR activation mechanisms, it is less clear how ATR signaling is negatively regulated in cells. Here, we identify the DNA repair protein REV7 as a novel direct binding partner of ATRIP. We define a REV7-interaction motif in ATRIP, which when mutated abrogates the REV7-ATRIP interaction

Identifiers

PMID39868202
PMCPMC11761088

What OpenQuestion holds

Textmetadata
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.