Evidence map›Paper›PMID 37210387›Full record

ArticleCell death & disease2023

CD317 maintains proteostasis and cell survival in response to proteasome inhibitors by targeting calnexin for RACK1-mediated autophagic degradation.

Jian Cheng, Guizhong Zhang, Tian Deng, Zhao Liu, Mengqi Zhang, Pengchao Zhang, Funmilayo O Adeshakin, Xiangyun Niu, Dehong Yan, Xiaochun Wan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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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 at 3 institutions in 1 country.

Jian ChengDepartment of Immunology, Jinzhou Medical University, Jinzhou, Liaoning, China.
Guizhong ZhangCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China. gz.zhang@siat.ac.cn.ORCID 0000-0001-8930-5262
Tian DengCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China.
Zhao LiuCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China.
Mengqi ZhangCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China.
Pengchao ZhangCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China.
Funmilayo O AdeshakinCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China.
Xiangyun NiuCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China.
Dehong YanCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China.
Xiaochun WanCenter for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, Shenzhen, People's Republic of China. xc.wan@siat.ac.cn.ORCID 0000-0003-3745-1860
Guang YuDepartment of Immunology, Jinzhou Medical University, Jinzhou, Liaoning, China. yuguang@jzmu.edu.cn.ORCID 0000-0002-7872-0978
Chinese Academy of Sciences · CNJinzhou Medical University · CNShenzhen Institutes of Advanced Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unbalanced protein homeostasis (proteostasis) networks are frequently linked to tumorigenesis, making cancer cells more susceptible to treatments that target proteostasis regulators. Proteasome inhibition is the first licensed proteostasis-targeting therapeutic strategy, and has been proven effective in hematological malignancy patients. However, drug resistance almost inevitably develops, pressing for a better understanding of the mechanisms that preserve proteostasis in tumor cells. Here we report that CD317, a tumor-targeting antigen with a unique topology, was upregulated in hematological malignancies and preserved proteostasis and cell viability in response to proteasome inhibitors (PIs). Knocking down CD317 lowered Ca

Indexed as

Bone Marrow Stromal Antigen 2Proteasome InhibitorsProteostasisCalnexinCell SurvivalHumansMolecular ChaperonesNeoplasm ProteinsReceptors for Activated C KinaseBone Marrow Stromal Antigen 2BST2 protein, humanCalnexinMolecular ChaperonesNeoplasm ProteinsProteasome InhibitorsRACK1 protein, humanReceptors for Activated C Kinase

Identifiers

PMID37210387
PMCPMC10199885
OpenAlexW4377137730

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.