Evidence map›Paper›PMID 35721517›Full record

ArticleFrontiers in cell and developmental biology2022

ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.

Pragya Shah, Connor W McGuigan, Svea Cheng, Claire Vanpouille-Box, Sandra Demaria, Robert S Weiss, Jan Lammerding

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
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

19 citing papers in PubMed, 32 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Pragya ShahWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, United States.
Connor W McGuiganWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, United States.
Svea ChengWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, United States.
Claire Vanpouille-BoxDepartment of Radiation Oncology, Weill Cornell Medicine, New York City, NY, United States.
Sandra DemariaDepartment of Radiation Oncology, Weill Cornell Medicine, New York City, NY, United States.
Robert S WeissDepartment of Biomedical Sciences, Cornell University, Ithaca, NY, United States.
Jan LammerdingWeill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, United States.
Cornell University · USWeill Cornell Medicine · US

Funding

Project 3: Physical and Metabolic Constraints of Cancer Cell InvasionU54CA210184 · NCI · CORNELL UNIVERSITY · PI SCHAFFER, CHRIS B · 2016 to 2020
$10.2M
Nuclear mechanics and mechanotransduction in muscular laminopathiesR01HL082792 · NHLBI · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2007 to 2023
$4.8M
Cancer Cell Intrinsic Interferon-I pathway Activation by Fractionated RadiationR01CA201246 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DEMARIA, SANDRA · 2016 to 2025
$3.9M
Nuclear mechanobiology in confined migration (Equipment Supplement 2023)R01GM137605 · NIGMS · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2020 to 2023
$1.6M
NCI NIH HHS R01 CA201246NCI NIH HHS U54 CA210184NHLBI NIH HHS R01 HL082792NIGMS NIH HHS R01 GM137605
6 · The paper itself

Abstract

Ataxia-telangiectasia mutated (ATM) is one of the three main apical kinases at the crux of DNA damage response and repair in mammalian cells. ATM activates a cascade of downstream effector proteins to regulate DNA repair and cell cycle checkpoints in response to DNA double-strand breaks. While ATM is predominantly known for its role in DNA damage response and repair, new roles of ATM have recently begun to emerge, such as in regulating oxidative stress or metabolic pathways. Here, we report the surprising discovery that ATM inhibition and deletion lead to reduced expression of the nuclear envelope protein lamin A. Lamins are nuclear intermediate filaments that modulate nuclear shape, structure, and stiffness. Accordingly, inhibition or deletion of ATM resulted in increased nuclear deformability and enhanced cell migration through confined spaces, which requires substantial nuclear deformation. These findings point to a novel connection between ATM and lamin A and may have broad implications for cells with ATM mutations-as found in patients suffering from Ataxia Telangiectasia and many human cancers-which could lead to enhanced cell migration and increased metastatic potential.

Indexed as

ataxia-telangiectasia (AT)ATMcancer biologycell migrationconfined migrationlamin (A/C)mechanobiologynuclear mechanics

Identifiers

PMID35721517
PMCPMC9198445
OpenAlexW4281624846

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.