Calpain-2 participates in the process of calpain-1 inactivation.


Journal

Bioscience reports
ISSN: 1573-4935
Titre abrégé: Biosci Rep
Pays: England
ID NLM: 8102797

Informations de publication

Date de publication:
27 11 2020
Historique:
received: 29 02 2020
revised: 18 09 2020
accepted: 20 10 2020
pubmed: 21 10 2020
medline: 13 4 2021
entrez: 20 10 2020
Statut: ppublish

Résumé

Calpain-1 and calpain-2 are highly structurally similar isoforms of calpain. The calpains, a family of intracellular cysteine proteases, cleave their substrates at specific sites, thus modifying their properties such as function or activity. These isoforms have long been considered to function in a redundant or complementary manner, as they are both ubiquitously expressed and activated in a Ca2+- dependent manner. However, studies using isoform-specific knockout and knockdown strategies revealed that each calpain species carries out specific functions in vivo. To understand the mechanisms that differentiate calpain-1 and calpain-2, we focused on the efficiency and longevity of each calpain species after activation. Using an in vitro proteolysis assay of troponin T in combination with mass spectrometry, we revealed distinctive aspects of each isoform. Proteolysis mediated by calpain-1 was more sustained, lasting as long as several hours, whereas proteolysis mediated by calpain-2 was quickly blunted. Calpain-1 and calpain-2 also differed from each other in their patterns of autolysis. Calpain-2-specific autolysis sites in its PC1 domain are not cleaved by calpain-1, but calpain-2 cuts calpain-1 at the corresponding position. Moreover, at least in vitro, calpain-1 and calpain-2 do not perform substrate proteolysis in a synergistic manner. On the contrary, calpain-1 activity is suppressed in the presence of calpain-2, possibly because it is cleaved by the latter protein. These results suggest that calpain-2 functions as a down-regulation of calpain-1, a mechanism that may be applicable to other calpain species as well.

Identifiants

pubmed: 33078830
pii: 226716
doi: 10.1042/BSR20200552
pmc: PMC7610153
pii:
doi:

Substances chimiques

Troponin T 0
Calpain EC 3.4.22.-
CAPN1 protein, human EC 3.4.22.52
CAPN2 protein, human EC 3.4.22.53

Types de publication

Comparative Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2020 The Author(s).

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Auteurs

Fumiko Shinkai-Ouchi (F)

Calpain Project, Department of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science (TMiMS), 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156- 8506, Japan.

Mayumi Shindo (M)

Center for Basic Technology Research, Tokyo Metropolitan Institute of Medical Science (TMiMS), 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156- 8506, Japan.

Naoko Doi (N)

Calpain Project, Department of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science (TMiMS), 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156- 8506, Japan.

Shoji Hata (S)

Calpain Project, Department of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science (TMiMS), 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156- 8506, Japan.

Yasuko Ono (Y)

Calpain Project, Department of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science (TMiMS), 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156- 8506, Japan.

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Classifications MeSH