Evidence map›Paper›PMID 39858578›Full record

ArticleGenes2024

Systematic Analysis of UFMylation Family Genes in Tissues of Mice with Metabolic Dysfunction-Associated Steatotic Liver Disease.

Mingdi Jiang, Chenlu Zhang, Zhengyao Zhang, Yingying Duan, Shuaiyong Qi, Qingyu Zeng, Jiabao Wang, Jiawen Zhang, Yu Jiang, Ying Wang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

12 authors.

Mingdi JiangZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Chenlu ZhangZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Zhengyao ZhangZhejiang Key Laboratory of Medical Epigenetics, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Yingying DuanZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Shuaiyong QiZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Qingyu ZengZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Jiabao WangZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Jiawen ZhangZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Yu JiangZhejiang Key Laboratory of Medical Epigenetics, Department of Human Anatomy and Histoembryology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Ying WangZhejiang Key Laboratory of Medical Epigenetics, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Yi ChenZhejiang Key Laboratory of Medical Epigenetics, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Jiang LiuZhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.ORCID 0000-0002-9192-3622

Funding

National Natural Science Foundation of China 32270751, 82371571Natural Science Foundation of Zhejiang Province of China LQ24C070003, LY24H250002the health commission of Zhejiang Province of China 2024KY239
6 · The paper itself

Abstract

BACKGROUND/

objectivesUFMylation, a newly identified ubiquitin-like modification, modulates a variety of physiological processes, including endoplasmic reticulum homeostasis maintenance, DNA damage response, embryonic development, and tumor progression. Recent reports showed that UFMylation plays a protective role in preventing liver steatosis and fibrosis, serving as a defender of liver homeostasis in the development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the regulation of UFMylation in MASLD remains unclear. This study aimed to determine the expressed patterns of UFMylation components in multiple tissues of leptin-deficient

methodsThe

resultsThe protein levels of UBA5, UFC1 and UFL1 were down-regulated in liver, brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT), whereas the messenger RNA (mRNA) levels of

conclusionsOur findings established the expressed profiles of UFMylaiton in multiple tissues of mice mimicking MASLD, indicating an important regulation for UFMylation in these tissues' homeostasis maintenance.

Indexed as

Fatty LiverUbiquitinsAnimalsDiet, High-FatLiverMaleMiceMice, Inbred C57BLMice, ObeseUbiquitinationUbiquitinshigh-fat diet-fed miceMASLDobesityob/ob miceUFMylation

Identifiers

PMID39858578
PMCPMC11765366

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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.