Evidence map›Paper›PMID 22228767›Full record

ArticleThe Journal of biological chemistry2012

CHCM1/CHCHD6, novel mitochondrial protein linked to regulation of mitofilin and mitochondrial cristae morphology.

Jie An, Jingxue Shi, Qin He, Ki Lui, Yuxin Liu, Ying Huang, M Saeed Sheikh

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
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  5. In and out of the mitochondrial intermembrane space.Protein science : a publication of the Protein Society · 2026
    Review
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  9. Metabolic stress-mediated cell death and autophagy in human lung cancer cells.The Journal of pharmacology and experimental therapeutics · 2025
    Article
  10. Review
  11. HThe Journal of biological chemistry · 2025
    Article
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10 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jie AnDepartment of Pharmacology, State University of New York, Upstate Medical University, Syracuse, New York 13210, USA.
Jingxue Shi
Qin He
Ki Lui
Yuxin Liu
Ying Huang
M Saeed Sheikh
SUNY Upstate Medical University · US

Funding

Characterization of a novel stress-regulated anti-apoptotic ubiquitin ligaseR21ES016668 · NIEHS · UPSTATE MEDICAL UNIVERSITY · PI SHEIKH, M. SAEED · 2008 to 2009
$432k
A novel biomarker and therapeutic target for breast cancerR21CA157168 · NCI · UPSTATE MEDICAL UNIVERSITY · PI SHEIKH, M. SAEED · 2011 to 2012
$381k
NCI NIH HHS CA157168NCI NIH HHS R21 CA157168NIEHS NIH HHS ES016668NIEHS NIH HHS R21 ES016668
6 · The paper itself

Abstract

The structural integrity of mitochondrial cristae is crucial for mitochondrial functions; however, the molecular events controlling the structural integrity and biogenesis of mitochondrial cristae remain to be fully elucidated. Here, we report the functional characterization of a novel mitochondrial protein named CHCM1 (coiled coil helix cristae morphology 1)/CHCHD6. CHCM1/CHCHD6 harbors a coiled coil helix-coiled coil helix domain at its C-terminal end and predominantly localizes to mitochondrial inner membrane. CHCM1/CHCHD6 knockdown causes severe defects in mitochondrial cristae morphology. The mitochondrial cristae in CHCM1/CHCHD6-deficient cells become hollow with loss of structural definitions and reduction in electron-dense matrix. CHCM1/CHCHD6 depletion also leads to reductions in cell growth, ATP production, and oxygen consumption. CHCM1/CHCHD6 through its C-terminal end strongly and directly interacts with the mitochondrial inner membrane protein mitofilin, which is known to also control mitochondrial cristae morphology. CHCM1/CHCHD6 also interacts with other mitofilin-associated proteins, including DISC1 and CHCHD3. Knockdown of CHCM1/CHCHD6 reduces mitofilin protein levels; conversely, mitofilin knockdown leads to reduction in CHCM1 levels, suggesting coordinate regulation between these proteins. Our results further indicate that genotoxic anticancer drugs that induce DNA damage down-regulate CHCM1/CHCHD6 expression in multiple human cancer cells, whereas mitochondrial respiratory chain inhibitors do not affect CHCM1/CHCHD6 levels. CHCM1/CHCHD6 knockdown in human cancer cells enhances chemosensitivity to genotoxic anticancer drugs, whereas its overexpression increases resistance. Collectively, our results indicate that CHCM1/CHCHD6 is linked to regulation of mitochondrial cristae morphology, cell growth, ATP production, and oxygen consumption and highlight its potential as a possible target for cancer therapeutics.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticAdenosine TriphosphateAmino Acid SequenceAntineoplastic AgentsCell Line, TumorGene Knockdown TechniquesHumansMitochondriaMitochondrial MembranesMitochondrial ProteinsMolecular Sequence DataMuscle ProteinsNeoplasm ProteinsNeoplasmsNerve Tissue ProteinsAdenosine TriphosphateAntineoplastic AgentsCHCHD3 protein, humanCHCHD6 protein, humanDISC1 protein, humanIMMT protein, humanMitochondrial ProteinsMuscle ProteinsNeoplasm ProteinsNerve Tissue Proteins

Identifiers

PMID22228767
PMCPMC3293568
OpenAlexW2093226550

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.