Evidence map›Paper›PMID 31829413›Full record

ArticleBioscience reports2020

Ubiquitin fold modifier 1 activates NF-κB pathway by down-regulating LZAP expression in the macrophage of diabetic mouse model.

Xiaolei Hu, Hengyan Zhang, Yuan Song, Langen Zhuang, Qingqing Yang, Minglin Pan, Fengling Chen

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Epigenome-wide Association Study Analysis of Calorie Restriction in Humans, CALERIETM Trial Analysis.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
    Trial
  2. Review
  3. Review
  4. Review
  5. KIF11 UFMylation Maintains Photoreceptor Cilium Integrity and Retinal Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. 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

7 authors at 3 institutions in 1 country.

Xiaolei HuDepartment of Endocrinology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
Hengyan ZhangDepartment of Endocrinology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
Yuan SongDepartment of Endocrinology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
Langen ZhuangDepartment of Endocrinology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
Qingqing YangDepartment of Endocrinology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
Minglin PanDepartment of Endocrinology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210011, China.
Fengling ChenDepartment of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
First Affiliated Hospital of Bengbu Medical College · CNSecond Affiliated Hospital of Nanjing Medical University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory response is closely related with the development of many serious health problems worldwide including diabetes mellitus (DM). Ubiquitin-fold modifer 1 (Ufm1) is a newly discovered ubiquitin-like protein, while its function remains poorly investigated, especially in inflammatory response and DM. In the present study, we analyzed the role of Ufm1 on inflammatory response in DM, and found that the proinflammatory cytokine levels (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β) and Ufm1 expression were highly increased both in the peritoneal macrophages of db/db mice and Raw264.7 cells induced by lipopolysaccharide (LPS). Western blot and luciferase reporter assay showed that NF-κB pathway was obviously activated in macrophages and the expression of LZAP, an inhibitor of NF-κB pathway, was down-regulated. With the LZAP knockdown plasmid and activation plasmid, we demonstrated that NF-κB/p65 activation was inhibited by LZAP in macrophages. The interaction of Ufm1 and LZAP was further proved with co-immunoprecipitation assay in HEK293 and Raw264.7 cells. The LZAP expression was also related with the presence of Ufm1 demonstrated by Ufm1 knockdown plasmid and activation plasmid. Besides that, we finally proved that the expression and activation of Ufm1 induced by LPS were regulated by JNK/ATF2 and JNK/c-Jun pathway with the use of SP600125. In conclusion, the present study demonstrated that Ufm 1 could activate NF-κB pathway by down-regulating LZAP in macrophage of diabetes, and its expression and activation were regulated by JNK/ATF2 and c-Jun pathway.

Indexed as

AnimalsCell Cycle ProteinsCell LineDiabetes MellitusDisease Models, AnimalDown-RegulationHEK293 CellsHumansInterleukin-6Macrophages, PeritonealMaleMiceMice, Inbred C57BLMice, Inbred NODNF-kappa BProteinsCell Cycle ProteinsInterleukin-6NF-kappa BProteinsTranscription Factor RelATumor Necrosis Factor-alphaUbiquitinsUfm1 protein, mouseDiabetes mellitusLZAPNF-κBUbiquitin-fold modifer 1

Identifiers

PMID31829413
PMCPMC6944655
OpenAlexW2996660032

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.