Evidence map›Paper›PMID 35941338›Full record

ArticleClinical rheumatology2022

Proteomics analysis of lysine crotonylation and 2-hydroxyisobutyrylation reveals significant features of systemic lupus erythematosus.

Ting Xie, Jingjing Dong, Xianqing Zhou, Donge Tang, Dandan Li, Jiejing Chen, Yumei Chen, Huixuan Xu, Wen Xue, Dongzhou Liu and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical rheumatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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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

14 authors at 4 institutions in 1 country.

Ting XieInstitute of Nephrology and Blood Purification, the First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China.
Jingjing DongInstitute of Nephrology and Blood Purification, the First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China.
Xianqing ZhouDepartment of Pathology, Guangxi Key Laboratory of Metabolic Diseases Research, No.924 Hospital of PLA Joint Logistic Support Force, Guilin, 541002, Guangxi, China.
Donge TangClinical Medical Research Center, the Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, 518020, Guangdong, China.
Dandan LiInstitute of Nephrology and Blood Purification, the First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China.
Jiejing ChenDepartment of Pathology, Guangxi Key Laboratory of Metabolic Diseases Research, No.924 Hospital of PLA Joint Logistic Support Force, Guilin, 541002, Guangxi, China.
Yumei ChenClinical Medical Research Center, the Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, 518020, Guangdong, China.
Huixuan XuClinical Medical Research Center, the Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, 518020, Guangdong, China.
Wen XueDepartment of Pathology, Guangxi Key Laboratory of Metabolic Diseases Research, No.924 Hospital of PLA Joint Logistic Support Force, Guilin, 541002, Guangxi, China.
Dongzhou LiuClinical Medical Research Center, the Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, 518020, Guangdong, China.
Xiaoping HongClinical Medical Research Center, the Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, 518020, Guangdong, China.
Fang TangDepartment of Pathology, Guangxi Key Laboratory of Metabolic Diseases Research, No.924 Hospital of PLA Joint Logistic Support Force, Guilin, 541002, Guangxi, China. fangtang@163.com.
Lianghong YinInstitute of Nephrology and Blood Purification, the First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China. yin-yun@126.com.
Yong DaiClinical Medical Research Center, the Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, 518020, Guangdong, China. daiyong22@aliyun.com.ORCID http://orcid.org/0000-0002-6840-9158
Jinan University · CN181st Hospital of Chinese People's Liberation Army · CNFirst Affiliated Hospital of Jinan University · CN81th Hospital of PLA · CN

Funding

Guangdong Provincial Key Laboratory of Prevention and Control for Severe Clinical Animal Diseases No.20-065-76
6 · The paper itself

Abstract

INTRODUCTION/

objectivesTo seek significant features of systemic lupus erythematosus (SLE) by utilizing bioinformatics analysis.

methodLiquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to quantify lysine crotonylation (Kcr) and lysine 2-hydroxyisobutyrylation (Khib) in peripheral blood mononuclear cells (PBMCs) of systemic lupus erythematosus (SLE) patients and normal controls.

resultsSeventy-six differentially modified proteins (DMPs) dually modified by Kcr and Khib were identified between SLE patients and healthy people. GO enrichment analysis prompted significant enrichment of seventy-six DMPs in MHC class II protein complex binding and leukocyte migration. KEGG pathways were enriched in antigen processing and presentation pathway and leukocyte transendothelial migration pathway. Six DMPs (CLTC, HSPA1B, HSPA8, HSP90AB1, HSPD1, and PDIA3) were identified in antigen processing and presentation pathway, of which HSPA8 was the core protein. Significant changes of Kcr and Khib in HSPA8 may increase ATP hydrolysis and promote antigen binding to MHC II molecule. In leukocyte transendothelial migration pathway, 7 DMPs (ACTN1, ACTN4, EZR, MSN, RAC1, RHOA, and VCL) were identified. MSN was the protein with the most modification sites in this pathway. In amino terminal ferm region of MSN, Kcr and Khib expression change may lead to the adhesion between leukocytes and endothelial cells, which was an important step of leukocyte migration.

conclusionKcr and Khib may promote the antigen presentation and jointly regulate the tissue damage mediated by leukocyte migration in SLE patients, which may play key roles in the pathogenesis of SLE probably. Key Points • Antigen processing and presentation and leukocyte transendothelial migration may play key roles in the pathogenesis of SLE.

Indexed as

Lupus Erythematosus, SystemicLysineChromatography, LiquidEndothelial CellsHumansLeukocytes, MononuclearProtein Processing, Post-TranslationalProteomicsTandem Mass SpectrometryLysine2-HydroxyisobutyrylationCrotonylationProtein post-translational modificationSystemic lupus erythematosus

Identifiers

PMID35941338
PMCPMC9652266
OpenAlexW4290721372

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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.