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Cited by 227Neuroscience and Neuropharmacology ResearchProtein Kinase Regulation and GTPase SignalingSignaling Pathways in Disease

Characterization of a calmodulin kinase II inhibitor protein in brain

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Chang, Bill H., Mukherji, Sucheta, Soderling, Thomas R.·1998·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.95.18.10890PMC PMC27991
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Abstract

Ca 2+ /calmodulin-dependent protein kinase II (CaM-KII) regulates numerous physiological functions, including neuronal synaptic plasticity through the phosphorylation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors. To identify proteins that may interact with and modulate CaM-KII function, a yeast two-hybrid screen was performed by using a rat brain cDNA library. This screen identified a unique clone of 1.4 kb, which encoded a 79-aa brain-specific protein that bound the catalytic domain of CaM-KII α and β and potently inhibited kinase activity with an IC 50 of 50 nM. The inhibitory protein (CaM-KIIN), and a 28-residue peptide derived from it (CaM-KIINtide), was highly selective for inhibition of CaM-KII with little effect on CaM-KI, CaM-KIV, CaM-KK, protein kinase A, or protein kinase C. CaM-KIIN interacted only with activated CaM-KII (i.e., in the presence of Ca 2+ /CaM or after autophosphorylation) by using glutathione S -transferase/CaM-KIIN precipitations as well as coimmunoprecipitations from rat brain extracts or from HEK293 cells cotransfected with both constructs. Colocalization of CaM-KIIN with activated CaM-KII was demonstrated in COS-7 cells transfected with green fluorescent protein fused to CaM-KIIN. In COS-7 cells phosphorylation of transfected α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors by CaM-KII, but not by protein kinase C, was blocked upon cotransfection with CaM-KIIN. These results characterize a potent and specific cellular inhibitor of CaM-KII that may have an important role in the physiological regulation of this key protein kinase.

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  • CaMKIIN inhibits CaMKII with nanomolar potency.

    “The second class of peptides is derived from an endogenous protein that inhibits CaMKII with nanomolar potencies (CaMKIIN) (149).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [149]

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Cited by

Sorted by citations

Authors
Chang, B. H., Mukherji, S., & Soderling, T. R.
Affiliations
Oregon Health & Science University (US)
ORCID
Chang, Bill H.
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1998-09
Volume
95
Issue
18
Pages
10890-10895
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.95.18.10890
PMC
PMC27991
OpenAlex
W1976444641
Cited by
227
References
2
Citations by year
2026: 2 · 2025: 7 · 2024: 8 · 2023: 8 · 2022: 9 · 2021: 5 · 2020: 3 · 2019: 9 · 2018: 9 · 2017: 12 · 2016: 6 · 2015: 8 · 2014: 16 · 2013: 14 · 2012: 10
FWCI
0.92
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of General Medical Sciences (GM 41292, R01GM041292)
  • National Institute of Neurological Disorders and Stroke (T32NS007381, NS07381)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
calcium/calmodulin-dependent protein kinase II, protein-protein interaction, synaptic plasticity, AMPA receptor phosphorylation, brain-specific proteins, kinase autophosphorylation, Ca2+/calmodulin signaling, protein kinase specificity
MeSH terms
Amino Acid Sequence, Animals, Base Sequence, Brain, Carrier Proteins, Cell Line, Enzyme Inhibitors, Humans, Male, Molecular Sequence Data, Phosphorylation, Recombinant Fusion Proteins, Calcium-Calmodulin-Dependent Protein Kinases, Intracellular Signaling Peptides and Proteins, Rats

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