Evidence map›Paper›PMID 35663400›Full record

ArticleFrontiers in cell and developmental biology2022

Reduction of

Maithili Saoji, Courtney E Petersen, Aditya Sen, Benjamin A Tripoli, Jeremy T Smyth, Rachel T Cox

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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

6 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
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

6 authors at 2 institutions in 1 country.

Maithili SaojiDepartment of Biochemistry and Molecular Biology, Uniformed Services University, Bethesda, MD, United States.
Courtney E PetersenHenry M. Jackson Foundation, Bethesda, MD, United States.
Aditya SenDepartment of Biochemistry and Molecular Biology, Uniformed Services University, Bethesda, MD, United States.
Benjamin A TripoliDepartment of Anatomy, Physiology and Genetics, Uniformed Services University, Bethesda, MD, United States.
Jeremy T SmythDepartment of Anatomy, Physiology and Genetics, Uniformed Services University, Bethesda, MD, United States.
Rachel T CoxDepartment of Biochemistry and Molecular Biology, Uniformed Services University, Bethesda, MD, United States.
Henry M. Jackson Foundation · USUniformed Services University of the Health Sciences · US

Funding

Drosophila Transgenic RNAi Resource ProjectR01GM084947 · NIGMS · HARVARD MEDICAL SCHOOL · PI PERRIMON, NORBERT · 2008 to 2019
$9.8M
Clu forms a dynamic new ribonucleoprotein particle directly involved in mitochondrial functionR01GM127938 · NIGMS · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI COX, RACHEL TAFEL · 2019 to 2022
$1.3M
NIGMS NIH HHS R01 GM084947NIGMS NIH HHS R01 GM127938
6 · The paper itself

Abstract

In this study, we examine the cause and progression of mitochondrial diseases linked to the loss of mtRNase P, a three-protein complex responsible for processing and cleaving mitochondrial transfer RNAs (tRNA) from their nascent transcripts. When mtRNase P function is missing, mature mitochondrial tRNA levels are decreased, resulting in mitochondrial dysfunction. mtRNase P is composed of Mitochondrial RNase P Protein (MRPP) 1, 2, and 3. MRPP1 and 2 have their own enzymatic activity separate from MRPP3, which is the endonuclease responsible for cleaving tRNA. Human mutations in all subunits cause mitochondrial disease. The loss of mitochondrial function can cause devastating, often multisystemic failures. When mitochondria do not provide enough energy and metabolites, the result can be skeletal muscle weakness, cardiomyopathy, and heart arrhythmias. These symptoms are complex and often difficult to interpret, making disease models useful for diagnosing disease onset and progression. Previously, we identified

Indexed as

arrythmiacardiomyopathydrosophilaintravital imagingmitochondrial diseasemitochondrial RNase PMRPPskeletal muscle

Identifiers

PMID35663400
PMCPMC9162060
OpenAlexW4280542946

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.