Evidence map›Paper›PMID 36516772›Full record

ArticleCell reports2022

Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD

Dane T Sessions, Kee-Beom Kim, Jennifer A Kashatus, Nikolas Churchill, Kwon-Sik Park, Marty W Mayo, Hiromi Sesaki, David F Kashatus

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 40 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

8 authors at 2 institutions in 1 country.

Dane T SessionsDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Kee-Beom KimDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Jennifer A KashatusDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Nikolas ChurchillDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Kwon-Sik ParkDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA.
Marty W MayoDepartment of Biochemistry and Molecular Genetics, University of Virginia Health System, Charlottesville, VA 22908, USA.
Hiromi SesakiDepartment of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
David F KashatusDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA. Electronic address: kashatus@virginia.edu.
University of Virginia Health System · USJohns Hopkins University · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
Systems Analysis of Stress-adapted Cancer Organelles (SASCO) CenterU54CA274499 · NCI · UNIVERSITY OF VIRGINIA · PI Gustavo Kunde Rohde · 2022 to 2026
$13.4M
Exploring the Role of Mitochondrial Fission in Pancreatic TumorigenesisR01CA200755 · NCI · UNIVERSITY OF VIRGINIA · PI KASHATUS, DAVID FRANCIS · 2016 to 2020
$2.2M
Identifying tumor suppressor targets of SIRT6 in lung cancerR01CA192399 · NCI · UNIVERSITY OF VIRGINIA · PI MAYO, MARTY W · 2015 to 2019
$1.9M
Interdisciplinary Training in Systems & Biomolecular Data ScienceT32GM145443 · NIGMS · UNIVERSITY OF VIRGINIA · PI Kevin A Janes, Jason Papin · 2022 to 2026
$1.5M
NCI NIH HHS P30 CA044579NCI NIH HHS R01 CA192399NCI NIH HHS R01 CA200755NCI NIH HHS U54 CA274499NIGMS NIH HHS T32 GM145443
6 · The paper itself

Abstract

Oncogenic KRas activates mitochondrial fission through Erk-mediated phosphorylation of the mitochondrial fission GTPase Drp1. Drp1 deletion inhibits tumorigenesis of KRas-driven pancreatic cancer, but the role of mitochondrial dynamics in other Ras-driven malignancies is poorly defined. Here we show that in vitro and in vivo growth of KRas-driven lung adenocarcinoma is unaffected by deletion of Drp1 but is inhibited by deletion of Opa1, the GTPase that regulates inner membrane fusion and proper cristae morphology. Mechanistically, Opa1 knockout disrupts cristae morphology and inhibits electron transport chain (ETC) assembly and activity, which inhibits tumor cell proliferation through loss of NAD

Indexed as

Adenocarcinoma of LungNADDynaminsGTP PhosphohydrolasesHumansMitochondriaMitochondrial DynamicsMitochondrial MembranesMitochondrial ProteinsProto-Oncogene Proteins p21(ras)DynaminsGTP PhosphohydrolasesKRAS protein, humanMitochondrial ProteinsNADOPA1 protein, humanProto-Oncogene Proteins p21(ras)cancerCP: CancercristaeDrp1ETCfissionfusionKRasmitochondriaNADOpa1

Identifiers

PMID36516772
PMCPMC10265649
OpenAlexW4311676948

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.