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Role of Ca2+/Calmodulin-Dependent Protein Kinase Type II in Mediating Function and Dysfunction at Glutamatergic Synapses

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fnmol.2022.855752

关键词

Ca2+/calmodulin-dependent protein kinase type II (CaMKII); glutamatergic synapse; LTP; LTD; synaptic plasticity; CaMKII genetic models; CaMKII mutations

资金

  1. Rajiv Gandhi Center for Biotechnology (RGCB)
  2. Department of Science and Technology (DST), Government of India [IF150643, IF150638]
  3. Government of India and Science and Engineering Research Board, Government of India [CRG/2018/004528]

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Glutamatergic synapses contain abundant Ca2+/calmodulin-dependent protein kinase type II (CaMKII) with multiple functions, including kinase activity and binding to membrane proteins. The abundance of CaMKII in synapses is similar to scaffolding proteins, but its prominent function is still as a kinase. The multimeric structure of CaMKII enables it to have various functional capabilities, such as Ca2+ signal transduction, memory molecule function, and scaffolding. This article reviews the multiple roles of CaMKII in glutamatergic synapses and how they are affected in disease conditions.
Glutamatergic synapses harbor abundant amounts of the multifunctional Ca2+/calmodulin-dependent protein kinase type II (CaMKII). Both in the postsynaptic density as well as in the cytosolic compartment of postsynaptic terminals, CaMKII plays major roles. In addition to its Ca2+-stimulated kinase activity, it can also bind to a variety of membrane proteins at the synapse and thus exert spatially restricted activity. The abundance of CaMKII in glutamatergic synapse is akin to scaffolding proteins although its prominent function still appears to be that of a kinase. The multimeric structure of CaMKII also confers several functional capabilities on the enzyme. The versatility of the enzyme has prompted hypotheses proposing several roles for the enzyme such as Ca2+ signal transduction, memory molecule function and scaffolding. The article will review the multiple roles played by CaMKII in glutamatergic synapses and how they are affected in disease conditions.

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