Evidence map›Paper›PMID 42351183›Full record

ArticleCell communication and signaling : CCS2026

Amino-acids-mTORC1-driven DDA1 phosphorylation promotes DNA repair and glioblastoma progression.

Xing Chen, Zhixing Wang, An Yan, Yunpeng Liu, Ruimin Zhu, Li Li, Doudou Xu, Ruixue Liu, Xiangwen Zhan, Bin Yin and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Xing ChenState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, China.
Zhixing WangState 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, 5 Dongdan SAN Tiao, Beijing, 100005, China.
An YanState 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, 5 Dongdan SAN Tiao, Beijing, 100005, China.
Yunpeng LiuState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, China.
Ruimin ZhuState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, China.
Li LiState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, China.
Doudou XuState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, China.
Ruixue LiuState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, China.
Xiangwen ZhanState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, 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, 5 Dongdan SAN Tiao, Beijing, 100005, 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, 5 Dongdan SAN Tiao, Beijing, 100005, China.
Xiaozhong PengState Key Laboratory of Respiratory Health and Multimorbidity, National Center of Technology Innovation for Animal Model, Institute of Laboratory Animal Science, Beijing, 100021, China. pengxiaozhong@pumc.edu.cn.ORCID http://orcid.org/0000-0002-9592-9554

Funding

Beijing Natural Science Foundation 7244374Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences 2023-I2M-2-001National Postdoctoral Program for Innovative Talents GZC20230307State Key Laboratory Special Fund 2060204
6 · The paper itself

Abstract

backgroundDDA1 is a protein involved in protein degradation, cell cycle regulation, and DNA damage repair. Although its expression varies across tumor types, the precise role of DDA1 in gliomagenesis remains unclear.

methodsWe investigated the function of DDA1 in multiple glioblastoma cell models using biochemical assays, phosphorylation analysis, subcellular localization studies, and integrated genomic and transcriptomic profiling to determine its signaling interactions and downstream effects.

resultsWe identified a physical association between cytoplasmic DDA1 and Raptor, a core component of lysosome-associated mTORC1. Amino acid stimulation triggered phosphorylation of DDA1 at serine 33 promoting its nuclear translocation and involvement in DNA damage repair. Integrated transcriptomic analyses revealed that the mTORC1-DDA1

conclusionOur findings identify DDA1 as a previously unrecognized phosphorylation target downstream of mTORC1 and a critical mediator of the mTORC1 driven DNA damage response. Through its involvement in DNA repair and metabolic gene regulation, DDA1 appears to support glioblastoma progression, providing mechanistic insight into mTORC1 related gliomagenesis and suggesting potential therapeutic relevance.

Indexed as

Amino AcidsBrain NeoplasmsDisease ProgressionDNA RepairGlioblastomaMechanistic Target of Rapamycin Complex 1Cell Line, TumorHumansPhosphorylationAmino AcidsMechanistic Target of Rapamycin Complex 1DDA1 phosphorylationDNA repairGlioblastoma progressionmTORC1

Identifiers

PMID42351183
PMCPMC13556064

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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.