Evidence map›Paper›PMID 42844293›Full record

ArticleActa pharmacologica Sinica2026

Loss of Tars induces proteostasis stress and drives HSPC exhaustion through mTORC1 activation.

Ning-Zhe Li, Meng-Ke He, Qiang Wang, Na Liu, Zi-Xuan Wang, Ming-Kang Qi, Yi Chen, Ru-Fang Xiang, Yu-Ting Dai, Fan Zhang

Abstract read
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In one paragraph

Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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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.

Ning-Zhe Li *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China.
Meng-Ke He *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China.
Qiang Wang *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China.
Na Liu *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China.
Zi-Xuan WangShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China.
Ming-Kang QiShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China.
Yi ChenShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China. cy40659@rjh.com.cn.
Ru-Fang XiangShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China. xrf12518@rjh.com.cn.
Yu-Ting DaiShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China. dyt12423@rjh.com.cn.
Fan ZhangShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai, 200025, China. zf13016@rjh.com.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic stem and progenitor cells (HSPCs) rely on tightly regulated proteostasis to preserve their self-renewal and differentiation potential throughout life. However, how proteostasis stress induced by translational dysregulation affects HSPC homeostasis remains poorly understood. Here, we found that knockout of the cytoplasmic threonyl-tRNA synthetase (Tars), which is a component of the translation machinery, caused HSPC exhaustion and definitive, but not primitive, hematopoiesis defects in zebrafish. Similarly, TARS functional deficiency resulted in human CD34

Indexed as

hematopoietic stem and progenitor cellsmTORC1proteostasisthreonyl-tRNA synthetaseZebrafish

Identifiers

PMID42844293

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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.