ArticleThe EMBO journal1995
Human calcium-calmodulin dependent protein kinase I: cDNA cloning, domain structure and activation by phosphorylation at threonine-177 by calcium-calmodulin dependent protein kinase I kinase.
Article in The EMBO journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 180 citations in OpenAlex.
- Research advances on CaMKs-mediated neurodevelopmental injury.Archives of toxicology · 2024Review
- CaMKK2: bridging the gap between Ca2+ signaling and energy-sensing.Essays in biochemistry · 2024Review
- The CaMK Family Differentially Promotes Necroptosis and Mouse Cardiac Graft Injury and Rejection.International journal of molecular sciences · 2024Article
- PINK1 and Parkin regulate IPNature communications · 2023Article
- CaMK1D signalling in AgRP neurons promotes ghrelin-mediated food intake.Nature metabolism · 2023Article
- AI-Assisted chemical probe discovery for the understudied Calcium-Calmodulin Dependent Kinase, PNCK.PLoS computational biology · 2023Article
- Calcium Signalling in Heart and Vessels: Role of Calmodulin and Downstream Calmodulin-Dependent Protein Kinases.International journal of molecular sciences · 2022Review
- Molecular Mechanisms Underlying CaInternational journal of molecular sciences · 2022Review
- Article
- Backbone resonance assignments of the catalytic and regulatory domains of CaBiomolecular NMR assignments · 2020Article
- Cyclin-Dependent Kinase-Like 5 (CDKL5): Possible Cellular Signalling Targets and Involvement in CDKL5 Deficiency Disorder.Neural plasticity · 2020Review
- Article
- The Multi-Functional Calcium/Calmodulin Stimulated Protein Kinase (CaMK) Family: Emerging Targets for Anti-Cancer Therapeutic Intervention.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Insights into the roles of CMK-1 and OGT-1 in interstimulus interval-dependent habituation inProceedings. Biological sciences · 2018Article
- Neuronal pentraxin 2 supports clear cell renal cell carcinoma by activating the AMPA-selective glutamate receptor-4.Cancer research · 2014Article
- Negative feedback regulation of calcineurin-dependent Prz1 transcription factor by the CaMKK-CaMK1 axis in fission yeast.Nucleic acids research · 2014Article
- PTEN-mediated ERK1/2 inhibition and paradoxical cellular proliferation following Pnck overexpression.Cell cycle (Georgetown, Tex.) · 2014Article
- Fbxl12 triggers G1 arrest by mediating degradation of calmodulin kinase I.Cellular signalling · 2013Article
- Ca2+-independent activation of Ca2+/calmodulin-dependent protein kinase II bound to the C-terminal domain of CaV2.1 calcium channels.The Journal of biological chemistry · 2013Article
- A regulatory feedback loop between Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and the androgen receptor in prostate cancer progression.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human Ca(2+)-calmodulin (CaM) dependent protein kinase I (CaMKI) encodes a 370 amino acid protein with a calculated M(r) of 41,337. The 1.5 kb CaMKI mRNA is expressed in many different human tissues and is the product of a single gene located on human chromosome 3. CaMKI 1-306, was unable to bind Ca(2+)-CaM and was completely inactive thereby defining an essential component of the CaM-binding domain to residues C-terminal to 306. CaMKI 1-294 did not bind CaM but was fully active in the absence of Ca(2+)-CaM, indicating that residues 295-306 are sufficient to maintain CaMKI in an auto-inhibited state. CaMKI was phosphorylated on Thr177 and its activity enhanced approximately 25-fold by CaMKI kinase in a Ca(2+)-CaM dependent manner. Replacement of Thr177 with Ala or Asp prevented both phosphorylation and activation by CaMKI kinase and the latter replacement also led to partial activation in the absence of CaMKI kinase. Whereas CaMKI 1-306 was unresponsive to CaMKI kinase, the 1-294 mutant was phosphorylated and activated by CaMKI kinase in both the presence and absence of Ca(2+)-CaM although at a faster rate in its presence. These results indicate that the auto-inhibitory domain in CaMKI gates, in a Ca(2+)-CaM dependent fashion, accessibility of both substrates to the substrate binding cleft and CaMKI kinase to Thr177. Additionally, CaMKI kinase responds directly to Ca(2+)-CaM with increased activity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.