Evidence map›Paper›PMID 20188671›Full record

ArticleMolecular cell2010

The matrix peptide exporter HAF-1 signals a mitochondrial UPR by activating the transcription factor ZC376.7 in C. elegans.

Cole M Haynes, Yun Yang, Steven P Blais, Thomas A Neubert, David Ron

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 302 papers.

0numbers the graph read from it
0cells of the map it votes in
302citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

302 citing papers in PubMed, 491 citations in OpenAlex.

  1. HSP60 and HSP10 depletion provoke distinct biological responses.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
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  11. Molecular mechanisms of mitochondrial AAA+ proteases.The Journal of biological chemistry · 2026
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242 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Cole M HaynesKimmel Center for Biology and Medicine of the Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USA. haynesc@mskcc.org
Yun Yang
Steven P Blais
Thomas A Neubert
David Ron
New York University · US

Funding

Protein Mass Spectrometry Core Facility for NeuroscienceP30NS050276 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NEUBERT, THOMAS A · 2005 to 2015
$7.9M
THE CELLULAR RESPONSE TO NON-MUTAGENIC CARCINOGENSR01ES008681 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHMAN, GLENN I · 1996 to 2010
$4.4M
Metabolic Regulation in the Acute PhaseR37DK047119 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RON, DAVID · 2003 to 2009
$3.0M
METABOLIC REGULATION IN THE ACUTE PHASER01DK047119 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RYOO, HYUNG D · 1999 to 2010
$1.5M
Q-TOF Mass SpectrometerS10RR017990 · NCRR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NEUBERT, THOMAS A · 2003 to 2003
$500k
Mitochondrial Unfolded Proteins and Cell DegenerationF32NS050901 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HAYNES, COLE MICHAEL · 2005 to 2007
$143k
METABOLIC REGULATION IN THE ACUTE-PHASE RESPONSER29DK047119 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RON, DAVID · 1993 to 1997
–
Medical Research Council G0600717NCRR NIH HHS RR017990NIDDK NIH HHS DK47119NIDDK NIH HHS R01 DK047119NIDDK NIH HHS R37 DK047119NIEHS NIH HHS ES08681NIEHS NIH HHS R01 ES008681NINDS NIH HHS F32 NS050901NINDS NIH HHS F32-NS050901NINDS NIH HHS NS050279NINDS NIH HHS P30 NS050276
6 · The paper itself

Abstract

Genetic analyses previously implicated the matrix-localized protease ClpP in signaling the stress of protein misfolding in the mitochondrial matrix to activate nuclear-encoded mitochondrial chaperone genes in C. elegans (UPR(mt)). Here, we report that haf-1, a gene encoding a mitochondria-localized ATP-binding cassette protein, is required for signaling within the UPR(mt) and for coping with misfolded protein stress. Peptide efflux from isolated mitochondria was ATP dependent and required HAF-1 and the protease ClpP. Defective UPR(mt) signaling in the haf-1-deleted worms was associated with failure of the bZIP protein, ZC376.7, to localize to nuclei in worms with perturbed mitochondrial protein folding, whereas zc376.7(RNAi) strongly inhibited the UPR(mt). These observations suggest a simple model whereby perturbation of the protein-folding environment in the mitochondrial matrix promotes ClpP-mediated generation of peptides whose haf-1-dependent export from the matrix contributes to UPR(mt) signaling across the mitochondrial inner membrane.

Indexed as

Signal TransductionUnfolded Protein ResponseAnimalsATP-Binding Cassette TransportersCaenorhabditis elegansCaenorhabditis elegans ProteinsMitochondriaMitochondrial ProteinsProtein FoldingRNA InterferenceTranscription FactorsATFS-1 protein, C elegansATP-Binding Cassette TransportersCaenorhabditis elegans ProteinsHAF-1 protein, C elegansMitochondrial ProteinsTranscription Factors

Identifiers

PMID20188671
PMCPMC2846537
OpenAlexW1989108323

What OpenQuestion holds

Textmetadata
LicenceTDM
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.