ArticleBiophysical journal1998
Transglutaminase-induced cross-linking between subdomain 2 of G-actin and the 636-642 lysine-rich loop of myosin subfragment 1.
Article in Biophysical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- The Biological and Biomechanical Role of Transglutaminase-2 in the Tumour Microenvironment.Cancers · 2021Review
- Biological functionalities of transglutaminase 2 and the possibility of its compensation by other members of the transglutaminase family.TheScientificWorldJournal · 2014Review
- Regulation of Pollen Tube Growth by Transglutaminase.Plants (Basel, Switzerland) · 2013Review
- Beta-actin is a target for transglutaminase activity at synaptic endings in chicken telencephalic cell cultures.Journal of molecular neuroscience : MN · 2012Article
- Transglutaminases: nature's biological glues.The Biochemical journal · 2002Review
- Effect of intramolecular cross-linking between glutamine-41 and lysine-50 on actin structure and function.Journal of muscle research and cell motility · 2000Article
- Divalent cation-, nucleotide-, and polymerization-dependent changes in the conformation of subdomain 2 of actin.Biophysical journal · 1999Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G-actin was covalently cross-linked with S1 in a bacterial transglutaminase-catalyzed reaction. The cross-linking sites were identified with the help of fluorescent probes and limited proteolysis as the Gln-41 on the DNase I binding loop of subdomain 2 in G-actin and a lysine-rich loop (residues 636-642) on the S1 heavy chain. The same lysine-rich loop was cross-linked to another region of G-actin in a former study (Combeau, C., D. Didry, and M-F. Carlier. 1992. J. Biol. Chem. 267:14038-14046). This indicates the existence of more than one G-actin-S1 complex. In contrast to G-actin, no cross-linking was induced between F-actin and S1 by the transglutaminase reaction. This shows that in F-actin the inner part of the DNase I binding loop, where Gln-41 is located, is not accessible for S1. The cross-linked G-actin-S1 polymerized upon addition of 2 mM MgCl2 as indicated by electron microscopy and sedimentation experiments. The filaments obtained from the polymerization of cross-linked actin and S1 were much shorter than the control actin filaments. The ATPase activity of the cross-linked S1 was not activated by actin, whereas the K+ (EDTA)-activated ATPase activity of S1 was unaffected by the cross-linking. The cross-linking between G-actin and S1 was not influenced by the exchange of the tightly bound calcium to magnesium; however, it was inhibited by the exchange of the actin-bound ATP to ADP. This finding supports the view that the structure of the DNase binding loop in ADP-G-actin is somewhere between the structures of ATP-G-actin and F-actin.
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