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The calpain system.

Darrell E Goll¹, ValeryY F Thompson, Hongqi Li

¹Muscle Biology Group, University of Arizona, Tucson, AZ 85721, USA. darrel.goll@arizona.edu

Physiological Reviews

|July 5, 2003

Summary

The calpain system involves calcium-dependent proteases (calpains) and their inhibitor (calpastatin). Dysregulation of calpain activity, particularly after calcium imbalance, leads to significant tissue damage in conditions like stroke and trauma.

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Area of Science:

Biochemistry
Molecular Biology
Cell Biology

Background:

The calpain system comprises calcium-dependent proteases (mu-calpain and m-calpain) and their inhibitor, calpastatin.
Calpains are heterodimers with shared subunits, and m-calpain's 80-kDa subunit has a defined domain structure, including active sites and a penta EF-hand-like domain.
Calpastatin, derived from a single gene, produces multiple isoforms with varying sizes, all capable of inhibiting calpains through calcium-dependent binding.

Purpose of the Study:

To elucidate the structural and functional aspects of the calpain system.
To understand the regulation and cellular roles of calpains and calpastatins.
To explore the implications of deregulated calpain activity in cellular processes and disease.

Main Methods:

Structural analysis of m-calpain using crystallography.
Analysis of calpastatin gene expression and protein isoforms.
Review of cDNA cloning data for calpain-like molecules in mammals and other organisms.

Main Results:

The 80-kDa subunit of m-calpain possesses six distinct domains, including active site domains (IIa, IIb) and a penta EF-hand-like domain (IV).
A single calpastatin gene generates multiple inhibitory polypeptides through alternative splicing and promoter usage.
Numerous calpain-like mRNAs have been identified, suggesting a broader family of proteases, though their properties remain largely uncharacterized.

Conclusions:

Calpain activity is tightly regulated and implicated in crucial cellular functions like cytoskeletal remodeling, signal transduction, and apoptosis.
Loss of calcium homeostasis disrupts calpain regulation, resulting in tissue damage observed in myocardial infarction, stroke, and brain trauma.
Further research is needed to fully characterize the newly identified calpain-like molecules and their regulatory mechanisms.

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