Evidence map›Paper›PMID 38592586›Full record

ArticleMolecular neurobiology2024

Limb-Clasping Response in NMDA Receptor Palmitoylation-Deficient Mice.

Nami Suzuki, Akiko Oota-Ishigaki, Toshie Kaizuka, Masayuki Itoh, Maya Yamazaki, Rie Natsume, Manabu Abe, Kenji Sakimura, Masayoshi Mishina, Takashi Hayashi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Nami SuzukiBiomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Central 6 (6-10), 1-1-1 Higashi, Tsukuba, Ibaraki, 305-8566, Japan.
Akiko Oota-IshigakiBiomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Central 6 (6-10), 1-1-1 Higashi, Tsukuba, Ibaraki, 305-8566, Japan.
Toshie KaizukaNational Center of Neurology and Psychiatry (NCNP), National Institute of Neuroscience, Kodaira, Tokyo, 187-8502, Japan.
Masayuki ItohNational Center of Neurology and Psychiatry (NCNP), National Institute of Neuroscience, Kodaira, Tokyo, 187-8502, Japan.
Maya YamazakiDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.
Rie NatsumeDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.
Manabu AbeDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.
Kenji SakimuraDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.
Masayoshi MishinaDepartment of Molecular Neurobiology and Pharmacology, Graduate School of Medicine, University of Tokyo, Tokyo, 113-0033, Japan.
Takashi HayashiBiomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Central 6 (6-10), 1-1-1 Higashi, Tsukuba, Ibaraki, 305-8566, Japan. takashi.hayashi@aist.go.jp.ORCID http://orcid.org/0000-0003-3591-2109

Funding

Japan Agency for Medical Research and Development JP18gm5910009Japan Agency for Medical Research and Development JP20gm4010004Japan Society for the Promotion of Science 16H04676Japan Society for the Promotion of Science 16K07078Japan Society for the Promotion of Science 21249012Japan Society for the Promotion of Science 21300118Japan Society for the Promotion of Science 22123008Japan Society for the Promotion of Science 22680029Japan Society for the Promotion of Science 23650187Japan Society for the Promotion of Science 24111512Japan Society for the Promotion of Science 24249014Japan Society for the Promotion of Science 24650195Japan Society for the Promotion of Science 24700321Japan Society for the Promotion of Science 26350979
6 · The paper itself

Abstract

Proper regulation of N-methyl-D-aspartate-type glutamate receptor (NMDA receptor) expression is responsible for excitatory synaptic functions in the mammalian brain. NMDA receptor dysfunction can cause various neuropsychiatric disorders and neurodegenerative diseases. Posttranslational protein S-palmitoylation, the covalent attachment of palmitic acid to intracellular cysteine residues via thioester bonds, occurs in the carboxyl terminus of GluN2B, which is the major regulatory NMDA receptor subunit. Mutations of three palmitoylatable cysteine residues in the membrane-proximal cluster of GluN2B to non-palmitoylatable serine (3CS) lead to the dephosphorylation of GluN2B Tyr1472 in the hippocampus and cerebral cortex, inducing a reduction in the surface expression of GluN2B-containig NMDA receptors. Furthermore, adult GluN2B 3CS homozygous mice demonstrated a definite clasping response without abnormalities in the gross brain structure, other neurological reflexes, or expression levels of synaptic proteins in the cerebrum. This behavioral disorder, observed in the GluN2B 3CS knock-in mice, indicated that complex higher brain functions are coordinated through the palmitoylation-dependent regulation of NMDA receptors in excitatory synapses.

Indexed as

LipoylationReceptors, N-Methyl-D-AspartateAnimalsMiceNR2B NMDA receptorReceptors, N-Methyl-D-AspartateClasping responseExcitatory synapsesGluN2BNMDA receptorPalmitoylationTyrosine phosphorylation

Identifiers

PMID38592586
PMCPMC11496324

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Registered trials

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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.