Evidence map›Paper›PMID 39428430›Full record

ArticleScience China. Life sciences2025

DTD1 modulates synaptic efficacy by maintaining D-serine and D-aspartate homeostasis.

Xiao Liu, Chaojuan Yang, Zhuoran Lin, Jianing Li, Bin Yin, Xuepei Lei, Wei Han, Boqin Qiang, Pengcheng Shu, Chen Zhang and 1 more

Abstract read
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In one paragraph

Article in Science China. Life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
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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

11 authors.

Xiao Liu *State Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
Chaojuan Yang *School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, Beijing, 100069, China.
Zhuoran Lin *State Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
Jianing Li *State Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
Bin YinState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
Xuepei LeiInstitute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100021, China.
Wei HanState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
Boqin QiangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
Pengcheng ShuState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China. pengcheng_shu@ibms.pumc.edu.cn.
Chen ZhangSchool of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, Beijing, 100069, China. czhang@ccmu.edu.cn.
Xiaozhong PengState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry & Molecular Biology, Medical Primate Research Center, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China. pengxiaozhong@pumc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

D-serine and D-aspartate are involved in N-methyl-D-aspartate receptor (NMDAR)-related physiological and pathological processes. D-aminoacyl-tRNA deacylase 1 (DTD1) may biochemically contribute to D-serine or D-aspartate production. However, it is unclear thus far whether DTD1 regulates D-serine or D-aspartate content in neurobiological processes. In the present research, we found that DTD1 was essential to maintain the D-serine or D-aspartate homeostasis, which was consistent with the phenomenon that DTD1-deficiency resulted in changes in the quantity changes of functional NMDAR subunits in postsynaptic compartments. Moreover, DTD1 played a considerable role in regulating dendritic morphology and synaptic structure. As a consequence, DTD1 affected neurobiological events, including the synaptic strength of the CA3-to-CA1 circuit, dendritic spine density of hippocampal pyramidal neurons, and behavioral performance of mice in the Morris water maze. These findings highlight the important role of DTD1 in synaptic transmission, neuronal morphology, and spatial learning and memory and suggest an undisclosed mechanism of DTD1 that participates the regulation of D-serine or D-aspartate homeostasis in hippocampal neurons.

Indexed as

AminoacyltransferasesAspartic AcidSerineSynapsesAnimalsDendritesDNA-Binding ProteinsHippocampusHomeostasisMemoryMiceMice, Inbred C57BLMice, KnockoutNeuronsReceptors, N-Methyl-D-AspartateSpatial LearningAminoacyltransferasesAspartic AcidDNA-Binding ProteinsReceptors, N-Methyl-D-AspartateSerineD-aminoacyl-tRNA deacylase 1D-aspartateD-serineneuronal morphologyspatial learning and memorysynaptic transmission

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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.