CoChat
Sign Up
Cited by 209Mitochondrial Function and PathologyCell death mechanisms and regulationATP Synthase and ATPases Research

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.

SPG7 Is an Essential and Conserved Component of the Mitochondrial Permeability Transition Pore

Open access
Shanmughapriya, Santhanam, Rajan, Sudarsan, Hoffman, Nicholas E., Higgins, Andrew M., Tomar, Dhanendra, Nemani, Neeharika, Hines, Kevin J., Smith, Dylan J., Eguchi, Akito, Vallem, Sandhya, Shaikh, Farah, Cheung, Maggie, Leonard, Nicole J., Stolakis, Ryan S., Wolfers, Matthew P., Ibetti, Jessica, Chuprun, J. Kurt, Jog, Neelakshi R., Houser, Steven R., Koch, Walter J., Elrod, John W., Madesh, Muniswamy·2015·Molecular Cell
DOI 10.1016/j.molcel.2015.08.009PMC PMC4592475
Open this paper in CoChat — free account

Abstract

Mitochondrial permeability transition is a phenomenon in which the mitochondrial permeability transition pore (PTP) abruptly opens, resulting in mitochondrial membrane potential (ΔΨm) dissipation, loss of ATP production, and cell death. Several genetic candidates have been proposed to form the PTP complex, however, the core component is unknown. We identified a necessary and conserved role for spastic paraplegia 7 (SPG7) in Ca(2+)- and ROS-induced PTP opening using RNAi-based screening. Loss of SPG7 resulted in higher mitochondrial Ca(2+) retention, similar to cyclophilin D (CypD, PPIF) knockdown with sustained ΔΨm during both Ca(2+) and ROS stress. Biochemical analyses revealed that the PTP is a heterooligomeric complex composed of VDAC, SPG7, and CypD. Silencing or disruption of SPG7-CypD binding prevented Ca(2+)- and ROS-induced ΔΨm depolarization and cell death. This study identifies an ubiquitously expressed IMM integral protein, SPG7, as a core component of the PTP at the OMM and IMM contact site.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.molcel.2015.08.009

Cites

49 of 49 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 49 references

Cited by

Sorted by citations

Items 201–209 of 209

Related

See all

Metadata

Authors
Shanmughapriya, S., Rajan, S., Hoffman, N. E., Higgins, A. M., Tomar, D., Nemani, N., Hines, K. J., Smith, D. J., Eguchi, A., Vallem, S., Shaikh, F., Cheung, M., Leonard, N. J., Stolakis, R. S., Wolfers, M. P., Ibetti, J., Chuprun, J. K., Jog, N. R., Houser, S. R., Koch, W. J., Elrod, J. W., & Madesh, M.
Affiliations
Temple University (US)
Corresponding author
Madesh, Muniswamy
ORCID
Venue
Molecular Cell
Publisher
Elsevier BV
Published
2015-10
Volume
60
Issue
1
Pages
47-62
ISSN
1097-2765 (ISSN-L)
DOI
10.1016/j.molcel.2015.08.009
PMC
PMC4592475
OpenAlex
W1895235630
Cited by
209
References
49
Citations by year
2026: 12 · 2025: 15 · 2024: 10 · 2023: 17 · 2022: 20 · 2021: 13 · 2020: 25 · 2019: 23 · 2018: 26 · 2017: 22 · 2016: 24 · 2015: 1
FWCI
10.56
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Cell (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institutes of Health (1S10RR027327, R01GM109882, R01HL086699, R01HL119306)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
Keywords
SPG7, mitochondrial permeability transition pore, mitochondrial permeability transition, cyclophilin D, voltage-dependent anion channel, mitochondrial membrane potential, reactive oxygen species, mitochondrial depolarization, cell death, inner membrane, outer membrane, RNAi screening
MeSH terms
ATPases Associated with Diverse Cellular Activities, Peptidyl-Prolyl Isomerase D, Binding Sites, Calcium, HeLa Cells, Humans, Metalloendopeptidases, Mitochondria, Cell Death, Reactive Oxygen Species, Cyclophilins, RNA Interference, Voltage-Dependent Anion Channel 1, Mitochondrial Membranes, Membrane Potential, Mitochondrial, HEK293 Cells

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review