ArticleJournal of medicinal chemistry2009
Identification and optimization of a novel inhibitor of mitochondrial calpain 10.
Article in Journal of medicinal chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 14 citations in OpenAlex.
- Modeling the Effects of Calcium Overload on Mitochondrial Ultrastructural Remodeling.Applied sciences (Basel, Switzerland) · 2021Article
- Calcium phosphate precipitation inhibits mitochondrial energy metabolism.PLoS computational biology · 2019Article
- Calpain-10 Activity Underlies Angiotensin II-Induced Aldosterone Production in an Adrenal Glomerulosa Cell Model.Endocrinology · 2015Article
- Calpains, mitochondria, and apoptosis.Cardiovascular research · 2012Review
- Calpain 10 homology modeling with CYGAK and increased lipophilicity leads to greater potency and efficacy in cells.ACS chemical biology · 2012Article
- Mitochondrial calpain 10 is degraded by Lon protease after oxidant injury.Archives of biochemistry and biophysics · 2012Article
- Activation of mitochondrial μ-calpain increases AIF cleavage in cardiac mitochondria during ischemia-reperfusion.Biochemical and biophysical research communications · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Calpain 10 has been localized to the mitochondria and is a key mediator of Ca(2+) induced mitochondrial dysfunction. A peptide screen followed by a series of modifications identified the homodisulfide form of CYGAK (CYGAK)(2) as an inhibitor of calpain 10 while showing no inhibitory activity against calpain 1. Methylation or truncation of the N-terminal cysteine significantly reduced the inhibitory activity of (CYGAK)(2) and inhibition was reversed by reducing agents, suggesting that CYGAK forms a disulfide with a cysteine near the active site. Data suggests CYGAK may be a P' calpain inhibitor and may achieve its specificity through this mechanism. CYGAK inhibited calpain activity in intact mitochondria, renal cells, and hepatocytes, prevented Ca(2+) induced cleavage of NDUFV2, and blocked Ca(2+) induced state III dysfunction. (CYGAK)(2) is the first P' specific calpain inhibitor and will be a valuable tool to prevent Ca(2+) induced mitochondrial dysfunction and explore the function of calpain 10.
Indexed as
Identifiers
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.