Transcriptome-Wide Analysis Reveals Modulation of Human Macrophage Inflammatory Phenotype Through Alternative Splicing | Zendy

Jennie Lin | Zendy; Yu Hu | Zendy; Sara Núñez | Zendy; Andrea S. Foulkes | Zendy; Benjamin Cieply | Zendy; Chenyi Xue | Zendy; Mark Gerelus | Zendy; Wenjun Li | Zendy; Hanrui Zhang | Zendy; Daniel J. Rader | Zendy; Kiran Musunuru | Zendy; Mingyao Li | Zendy; Muredach P. Reilly | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Transcriptome-Wide Analysis Reveals Modulation of Human Macrophage Inflammatory Phenotype Through Alternative Splicing

Author(s) -

Jennie Lin,

Yu Hu,

Sara Núñez,

Andrea S. Foulkes,

Benjamin Cieply,

Chenyi Xue,

Mark Gerelus,

Wenjun Li,

Hanrui Zhang,

Daniel J. Rader,

Kiran Musunuru,

Mingyao Li,

Muredach P. Reilly

Publication year - 2016

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.116.307573

Subject(s) - biology , phenotype , transcriptome , alternative splicing , rna splicing , gene knockdown , macrophage , microbiology and biotechnology , genetics , gene , gene expression , rna , gene isoform , in vitro

Human macrophages can shift phenotype across the inflammatory M1 and reparative M2 spectrum in response to environmental challenges, but the mechanisms promoting inflammatory and cardiometabolic disease-associated M1 phenotypes remain incompletely understood. Alternative splicing (AS) is emerging as an important regulator of cellular function, yet its role in macrophage activation is largely unknown. We investigated the extent to which AS occurs in M1 activation within the cardiometabolic disease context and validated a functional genomic cell model for studying human macrophage-related AS events.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research