Evidence map›Paper›PMID 18991950›Full record

ReviewAnnals of the New York Academy of Sciences2008

Protein kinases and addiction.

Anna M Lee, Robert O Messing

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Novel neurotherapeutic targets for substance use disorders: Neuroplasticity, neuroinflammation, gasotransmitters and non-canonical organ systems.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Natural variation in protein kinase D modifies alcohol sensitivity inbioRxiv : the preprint server for biology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The Role of CaMKII and ERK Signaling in Addiction.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Phosphorylation barcode-dependent signal bias of the dopamine D1 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Anna M LeeErnest Gallo Clinic and Research Center, Department of Neurology, University of California at San Francisco, Emeryville, CA 94608, USA.
Robert O Messing
Ernest Gallo Clinic and Research Center · US

Funding

Vector, Transgenic, and Imaging CoreP50AA017072 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2008 to 2017
$13.9M
Regulation of GABAA Receptors by PKC epsilon.R37AA013588 · NIAAA · ERNEST GALLO CLINIC AND RESEARCH CENTER · PI MESSING, ROBERT O. · 2003 to 2011
$3.7M
Regulation of GABAA Receptors by PKC epsilon.R01AA013588 · NIAAA · UNIVERSITY OF TEXAS AT AUSTIN · PI MESSING, ROBERT O. · 2002 to 2016
$1.9M
NIAAA NIH HHS AA013588NIAAA NIH HHS AA017072NIAAA NIH HHS P50 AA017072NIAAA NIH HHS R01 AA013588NIAAA NIH HHS R37 AA013588
6 · The paper itself

Abstract

Although drugs of abuse have different chemical structures and interact with different protein targets, all appear to usurp common neuronal systems that regulate reward and motivation. Addiction is a complex disease that is thought to involve drug-induced changes in synaptic plasticity due to alterations in cell signaling, gene transcription, and protein synthesis. Recent evidence suggests that drugs of abuse interact with and change a common network of signaling pathways that include a subset of specific protein kinases. The best studied of these kinases are reviewed here and include extracellular signal-regulated kinase, cAMP-dependent protein kinase, cyclin-dependent protein kinase 5, protein kinase C, calcium/calmodulin-dependent protein kinase II, and Fyn tyrosine kinase. These kinases have been implicated in various aspects of drug addiction including acute drug effects, drug self-administration, withdrawal, reinforcement, sensitization, and tolerance. Identifying protein kinase substrates and signaling pathways that contribute to the addicted state may provide novel approaches for new pharmacotherapies to treat drug addiction.

Indexed as

AnimalsBehavior, AnimalCentral Nervous System StimulantsConditioning, ClassicalDrug ToleranceEthanolHumansIllicit DrugsMemoryMiceMice, KnockoutNerve Tissue ProteinsNeuronal PlasticityNeurotransmitter AgentsPhosphorylationProtein Kinase InhibitorsCentral Nervous System StimulantsEthanolIllicit DrugsNerve Tissue ProteinsNeurotransmitter AgentsProtein Kinase InhibitorsProtein Kinases

Identifiers

PMID18991950
PMCPMC3050040
OpenAlexW2136026605

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.