Evidence map›Paper›PMID 35634489›Full record

ArticleFrontiers in endocrinology2022

Quantitative Ubiquitinomics Revealed Abnormal Ubiquitinated ATP7A Involved in Down-Regulation of ACTH in Silent Corticotroph Adenomas.

Sida Zhao, Yue He, Hongyun Wang, Dan Li, Lei Gong, Yazhuo Zhang, Chuzhong Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

7 authors at 2 institutions in 1 country.

Sida ZhaoBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Yue HeBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Hongyun WangBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Dan LiBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Lei GongBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Yazhuo ZhangBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Chuzhong LiBeijing Tiantan Hospital, Capital Medical University, Beijing, China.
Beijing Institute of Neurosurgery · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitination is reported to be a critical biological event on ACTH secretion in corticotroph adenomas. However, the effect of ubiquitylation on ACTH secretion in silent corticotroph adenomas (SCAs) remains unclear. The aim of our study was to explore the mechanism of decreased secretion of ACTH in SCAs with ubiquitinomics. The differently expressed ubiquitinated proteins between SCAs and functioning corticotroph adenomas (FCAs) were identified by 4D label-free mass spectrometer, followed by bioinformatics analysis. The function of the candidate ubiquitinated protein ATP7A (K333) was validated in AtT20 cells. A total of 111 ubiquitinated sites corresponding to 94 ubiquitinated proteins were typically different between SCAs and FCAs. Among all the ubiquitinated sites, 102 showed decreased ubiquitination in SCAs, which mapped to 85 ubiquitinated proteins. Pathway enrichment analysis revealed that ubiquitinated proteins were mainly enriched in vesicle pathway and protein secretion pathway. ATP7A (K333) was one of the proteins enriched in vesicle pathway and protein secretion pathway with decreased ubiquitination level in SCAs.

Indexed as

ACTH-Secreting Pituitary AdenomaAdenomaAdrenocorticotropic HormoneCopper-Transporting ATPasesDown-RegulationHumansPeptide FragmentsUbiquitinated ProteinsAdrenocorticotropic HormoneATP7A protein, humanATP7A protein, human (2-79)Copper-Transporting ATPasesPeptide FragmentsUbiquitinated ProteinsACTHATP7Amass spectrumsilent corticotroph adenomasubiquitination

Identifiers

PMID35634489
PMCPMC9130458
OpenAlexW4280584413

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.