Interaction of Calmodulin with TRPM: An Initiator of Channel Modulation
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, přehledy
Grantová podpora
RVO: 61388963
Czech Academy of Sciences, Institute of Organic Chemistry and Biochemistry
PubMed
37894842
PubMed Central
PMC10607381
DOI
10.3390/ijms242015162
PII: ijms242015162
Knihovny.cz E-zdroje
- Klíčová slova
- TRPM channels, calcium homeostasis, calmodulin, calmodulin binding site, regulation,
- MeSH
- kalmodulin * metabolismus MeSH
- kationtové kanály TRPM * metabolismus MeSH
- proteiny vázající vápník metabolismus MeSH
- vápník metabolismus MeSH
- vápníková signalizace MeSH
- vazba proteinů MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- kalmodulin * MeSH
- kationtové kanály TRPM * MeSH
- proteiny vázající vápník MeSH
- vápník MeSH
Transient receptor potential melastatin (TRPM) channels, a subfamily of the TRP superfamily, constitute a diverse group of ion channels involved in mediating crucial cellular processes like calcium homeostasis. These channels exhibit complex regulation, and one of the key regulatory mechanisms involves their interaction with calmodulin (CaM), a cytosol ubiquitous calcium-binding protein. The association between TRPM channels and CaM relies on the presence of specific CaM-binding domains in the channel structure. Upon CaM binding, the channel undergoes direct and/or allosteric structural changes and triggers down- or up-stream signaling pathways. According to current knowledge, ion channel members TRPM2, TRPM3, TRPM4, and TRPM6 are directly modulated by CaM, resulting in their activation or inhibition. This review specifically focuses on the interplay between TRPM channels and CaM and summarizes the current known effects of CaM interactions and modulations on TRPM channels in cellular physiology.
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