Evidence map›Paper›PMID 31444354›Full record

ArticleNature communications2019

hCINAP regulates the DNA-damage response and mediates the resistance of acute myelocytic leukemia cells to therapy.

Ruidan Xu, Shuyu Yu, Dan Zhu, Xinping Huang, Yuqi Xu, Yimin Lao, Yonglu Tian, Jinfang Zhang, Zefang Tang, Zemin Zhang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. PKMYT1 kinase ameliorates cisplatin sensitivity in osteosarcoma.Signal transduction and targeted therapy · 2025
    Article
  7. Review
  8. Review
  9. NClinical and translational medicine · 2024
    Article
  10. Review
  11. SUMO and the DNA damage response.Biochemical Society transactions · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. RAD51 Inhibition Shows Antitumor Activity in Hepatocellular Carcinoma.International journal of molecular sciences · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022
    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

13 authors at 2 institutions in 1 country.

Ruidan XuState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0002-3941-4054
Shuyu YuState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0002-7276-1541
Dan ZhuState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0003-2056-1393
Xinping HuangState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0002-3794-9362
Yuqi XuDepartment of Biochemistry and Molecular Biology, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0003-0537-0708
Yimin LaoShanghai Key Laboratory of Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.ORCID http://orcid.org/0000-0002-3269-6001
Yonglu TianPeking-Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0002-1036-767X
Jinfang ZhangState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.
Zefang TangSchool of Life Sciences and BIOPIC, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0002-5264-9560
Zemin ZhangSchool of Life Sciences and BIOPIC, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0003-3789-6536
Jing YiShanghai Key Laboratory of Tumor Microenvironment and Inflammation, Department of Biochemistry and Molecular Cell Biology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Hong-Hu ZhuPeking University People's Hospital, Peking University, Beijing, 100014, China.ORCID http://orcid.org/0000-0003-2343-0436
Xiaofeng ZhengState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China. xiaofengz@pku.edu.cn.ORCID http://orcid.org/0000-0001-6790-0669
Peking University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a genetically heterogeneous malignant disorder of the hematopoietic system, characterized by the accumulation of DNA-damaged immature myeloid precursors. Here, we find that hCINAP is involved in the repair of double-stranded DNA breaks (DSB) and that its expression correlates with AML prognosis. Following DSB, hCINAP is recruited to damage sites where it promotes SENP3-dependent deSUMOylation of NPM1. This in turn results in the dissociation of RAP80 from the damage site and CTIP-dependent DNA resection and homologous recombination. NPM1 SUMOylation is required for recruitment of DNA repair proteins at the early stage of DNA-damage response (DDR), and SUMOylated NPM1 impacts the assembly of the BRCA1 complex. Knockdown of hCINAP also sensitizes a patient-derived xenograft (PDX) mouse model to chemotherapy. In clinical AML samples, low hCINAP expression is associated with a higher overall survival rate in patients. These results provide mechanistic insight into the function of hCINAP during the DNA-damage response and its role in AML resistance to therapy.

Indexed as

Recombinational DNA RepairAdenylate KinaseAdultAgedAged, 80 and overAnimalsAntineoplastic AgentsBRCA1 ProteinCysteine EndopeptidasesDNA Breaks, Double-StrandedDNA End-Joining RepairDrug Resistance, NeoplasmFemaleGene Knockdown TechniquesGene Knockout TechniquesHEK293 CellsAdenylate KinaseAK6 protein, humanAntineoplastic AgentsBRCA1 ProteinBRCA1 protein, humanCysteine EndopeptidasesNPM1 protein, humanNpm1 protein, mouseNuclear ProteinsNucleophosminSENP3 protein, human

Identifiers

PMID31444354
PMCPMC6707248
OpenAlexW2959431180

What OpenQuestion holds

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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.