Evidence map›Paper›PMID 35165513›Full record

ArticleInternational journal of medical sciences2022

ZFP91 promotes cell proliferation and inhibits cell apoptosis in AML via inhibiting the proteasome-dependent degradation of RIP1.

Zhonghui Zhang, Liang Zhong, Wenran Dan, Xuan Chu, Chen Liu, Xu Luo, Peng Wan, Zhenyan Liu, Yang Lu, Xiao Wang and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of medical sciences, 2022. 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
0.3field-weighted citation impact, top 50% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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 1 institution in 1 country.

Zhonghui ZhangCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Liang ZhongKey Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China.
Wenran DanCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Xuan ChuCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Chen LiuKey Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China.
Xu LuoCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Peng WanCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Zhenyan LiuCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Yang LuCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Xiao WangCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Beizhong LiuCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a quickly progressive and devastated hematological malignancy with large rate of relapse and the appearance of chemotherapy resistance. Therefore, the identification of new therapeutic targets is urgent. ZFP91 is a hidden oncogene. Nevertheless, how ZFP91 takes part in regulating AML is less clear. Our research aims at investigating the molecular mechanisms and uncovering the effects of ZFP91 on AML. This research demonstrates that ZFP91 boosts AML cell proliferation and stops AML cell apoptosis. Mechanistically, experimental results showed the interaction between ZFP91 and RIP1 and inhibitory effect of ZFP91 on the K48-linked ubiquitination of endogenous RIP1, which is an important molecule in AML. Taken together, our results provide the evidence that targeted inhibition of ZFP91 could be a hopeful measure to treat AML.

Indexed as

ApoptosisCell Line, TumorCell ProliferationHumansLeukemia, Myeloid, AcuteNuclear Pore Complex ProteinsProteasome Endopeptidase ComplexRNA-Binding ProteinsUbiquitinationUbiquitin-Protein LigasesAGFG1 protein, humanNuclear Pore Complex ProteinsProteasome Endopeptidase ComplexRNA-Binding ProteinsUbiquitin-Protein LigasesZFP91 protein, humanAMLE3 ligaseProteasome degradationRIP1UbiquitinationZFP91

Identifiers

PMID35165513
PMCPMC8795797
OpenAlexW4205573396

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.