Author

Junjun Jiang

Guangxi Medical UniversityORCID 0000-0003-4905-9348Unclaimed ORCID profile · follow to get notified of new preprints

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Junjun Jiang1 paper

Biology Disciplines

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Bioinformatics· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Assay:bulk RNA-seq· 2 Approach:statistical model· 2 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Approach:machine learning (classical)· 1 Assay:proteomics· 1 Assay:scRNA-seq· 1

Frequent Co-Authors

Sanqi AniD· 3 shared Yao LiniD· 3 shared Hao LiangiD· 2 shared Jiemei ChuiD· 2 shared Jinming SuiD· 2 shared Wenxing LiiD· 2 shared Anqi XuiD· 1 shared Chen XiuiD· 1 shared

Activity by Year

2022-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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3 shared papersBioinformatics

Sanqi AnORCID

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3 papers

Recent·Most cited

ImmunologybioRxivPreprintNov 13, 2025

METTL3-mediated SOCS3 m6A Modification in Preserving CD4+ T Cell Homeostasis in HIV Infected Long-term Non-progressors

Jinming Su, Rongfeng Chen, Xing Tao…·Junjun Jiang

This study identifies a novel m6A-METTL3-SOCS3 regulatory axis that preserves CD4+ T cell homeostasis in HIV-infected long-term non-progressors by modulating JAK2/STAT4 signaling.

DOI 10.1101/2025.11.13.688240

humanbulk RNA-seq

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BioinformaticsGenomics Proteomics & BioinformaticsPeer-reviewedJun 7, 2024

Scm6A: A fast and low-cost method for quantifying m6A modifications at the single-cell level

Yue-Qi Li, Jingyi Li, Wenxing Li…·Sanqi An

Scm6A is a machine learning method for single-cell m6A quantification, validated against m6A-seq and showing strong correlation in T-cells and disease samples.

13 citations

humanmachine learning (classical)

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BioinformaticsbioRxivPreprintJul 23, 2022

Multi-omics integrated analysis reveals a specific phenotype of CD8+ T cell may contribute to immunothromosis via Th17 response in severe and critical COVID-19

Wenxing Li, Sanqi An, Shao‐Xing Dai…·Cheng Zhou

The paper identifies a specific CD8+ T cell phenotype in severe COVID-19 linked to Th17 response and immunothrombosis using multi-omics data.

1 citation

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