ReviewBiochemistry2017
Metalloproteases of the Inner Mitochondrial Membrane.
Review in Biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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.
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.
Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Mitochondrial homeostasis: the central hub governing the progression of atherosclerosis.Precision clinical medicine · 2026Review
- The role of mitochondrial proteases in inflammation and immunity.Frontiers in immunology · 2026Review
- Mitochondrial proteases and their roles in mitophagy in plants, animals, and yeast.Plant & cell physiology · 2025Review
- Solvent-Dependent Emissions Properties of a Model Aurone Enable Use in Biological Applications.Journal of fluorescence · 2025Article
- Targeting mitochondrial metabolism by the mitotoxin bromoxib in leukemia and lymphoma cells.Cell communication and signaling : CCS · 2024Article
- Multifaceted Roles of AFG3L2, a Mitochondrial ATPase in Relation to Neurological Disorders.Molecular neurobiology · 2024Review
- An OMA1 redox site controls mitochondrial homeostasis, sarcoma growth, and immunogenicity.Life science alliance · 2023Article
- Molecular Determinants of Mitochondrial Shape and Function and Their Role in Glaucoma.Antioxidants & redox signaling · 2023Review
- Adaptation of Proteome and Metabolism in Different Haplotypes ofMicroorganisms · 2023Article
- Prohibitin 1 regulates mtDNA release and downstream inflammatory responses.The EMBO journal · 2022Article
- Regulation of mitochondrial proteostasis by the proton gradient.The EMBO journal · 2022Article
- The mystery of mitochondrial plasticity: TMBIM5 integrates metabolic state and proteostasis.The EMBO journal · 2022Article
- Yme2, a putative RNA recognition motif and AAA+ domain containing protein, genetically interacts with the mitochondrial protein export machinery.Biological chemistry · 2022Article
- Protein Processing in Plant Mitochondria Compared to Yeast and Mammals.Frontiers in plant science · 2022Review
- FTSH4 and OMA1 mitochondrial proteases reduce moderate heat stress-induced protein aggregation.Plant physiology · 2021Article
- Mitochondrial ATP-Dependent Proteases-Biological Function and Potential Anti-Cancer Targets.Cancers · 2021Review
- Protease OMA1 modulates mitochondrial bioenergetics and ultrastructure through dynamic association with MICOS complex.iScience · 2021Article
- OMA1-An integral membrane protease?Biochimica et biophysica acta. Proteins and proteomics · 2021Review
- Mitochondrial OMA1 and OPA1 as Gatekeepers of Organellar Structure/Function and Cellular Stress Response.Frontiers in cell and developmental biology · 2021Review
- Targeting Mitochondrial Protein Expression as a Future Approach for Cancer Therapy.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The inner mitochondrial membrane (IM) is among the most protein-rich cellular compartments. The metastable IM subproteome where the concentration of proteins is approaching oversaturation creates a challenging protein folding environment with a high probability of protein malfunction or aggregation. Failure to maintain protein homeostasis in such a setting can impair the functional integrity of the mitochondria and drive clinical manifestations. The IM is equipped with a series of highly conserved, proteolytic complexes dedicated to the maintenance of normal protein homeostasis within this mitochondrial subcompartment. Particularly important is a group of membrane-anchored metallopeptidases commonly known as m-AAA and i-AAA proteases, and the ATP-independent Oma1 protease. Herein, we will summarize the current biochemical knowledge of these proteolytic machines and discuss recent advances in our understanding of mechanistic aspects of their functioning.
Indexed as
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What OpenQuestion holds
Registered trials
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.