Author

Xin Tian

Yale UniversityORCID 0009-0003-1616-9097Unclaimed ORCID profile · follow to get notified of new preprints

Additional preprints under this name without ORCID

Xin Tian1 paper · The Affiliated Yongchuan Hospital of Chongqing Medical University

Biology Disciplines

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Genetics· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 3 Organism:mouse· 3 Research Focus:differential expression· 2 Approach:statistical model· 2 Assay:ATAC-seq· 1 Approach:experimental assay· 1 Research Focus:host-pathogen & immune response· 1 Assay:scRNA-seq· 1

Frequent Co-Authors

Stefan SomloiD· 3 shared Hongyu ZhaoiD· 2 shared Jianlei GuiD· 2 shared Ke DongiD· 2 shared Zemeng WeiiD· 2 shared Adrián CordidoiD· 1 shared Anand Chellappan ReghuvaraniD· 1 shared Ashwani Kumar· 1 shared

Activity by Year

2025-2025 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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3 shared papersGenetics

Stefan SomloORCID

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3 papers

Recent·Most cited

GeneticsJournal of the American Society of NephrologyPeer-reviewedDec 16, 2025

Glis3 is a modifier of cyst progression in autosomal dominant polycystic kidney disease

Zemeng Wei, Jianlei Gu, Xin Tian…·Stefan Somlo

This study investigates Glis3's role in ADPKD, finding that its dual inactivation with Pkd1 worsens kidney disease, affecting metabolism and circadian function.

2 citations

mousebulk RNA-seq

𝕏 PostBluesky

GeneticsJournal of the American Society of NephrologyPeer-reviewedOct 1, 2025

Anks3 mediates cilia dependent polycystin signaling and is essential for adult kidney homeostasis

Zemeng Wei, Michael Rehman, Jianlei Gu…·Stefan Somlo

This study identifies Anks3 as a key regulator of cilia-dependent polycystin signaling and shows its essential role in kidney homeostasis.

4 citations

mousebulk RNA-seq

𝕏 PostBluesky

ImmunologyAmerican Journal of TransplantationPeer-reviewedAug 1, 2025

A T-cell Intrinsic Role for APOL1 Risk Alleles in Allograft Rejection

John F. Pell, E. M. Tanvir, Zhengliang Sun…·Madhav C. Menon

This study identifies a T-cell intrinsic mechanism by which APOL1 risk alleles contribute to kidney rejection through altered calcium signaling and T-cell activation.

DOI 10.1016/j.ajt.2025.07.188

mousebulk RNA-seq

𝕏 PostBluesky