An <scp>LXR</scp> – <scp>NCOA</scp> 5 gene regulatory complex directs inflammatory crosstalk‐dependent repression of macrophage cholesterol efflux

Mark A. Gillespie; Elizabeth S. Gold; Stephen A. Ramsey; Irina Podolsky; Alan Aderem; Jeffrey A. Ranish

doi:10.15252/embj.201489819

ScienceGate Book Chapters

JOURNAL ARTICLE

An LXR – NCOA 5 gene regulatory complex directs inflammatory crosstalk‐dependent repression of macrophage cholesterol efflux

Mark A. Gillespie Elizabeth S. Gold Stephen A. Ramsey Irina Podolsky Alan Aderem Jeffrey A. Ranish

Year: 2015 Journal: The EMBO Journal Vol: 34 (9)Pages: 1244-1258 Publisher: Springer Nature

DOI: 10.15252/embj.201489819

Get Full-Text PDF Get Analytical Report

Keywords:

Biology Crosstalk Efflux Psychological repression Cell biology Liver X receptor Cholesterol Molecular biology Biochemistry Gene Gene expression Nuclear receptor Transcription factor

Metrics

Cited By

5.99

FWCI (Field Weighted Citation Impact)

Refs

0.95

Citation Normalized Percentile

Is in top 1%

Is in top 10%

Citation History

Topics

Cholesterol and Lipid Metabolism

Health Sciences → Medicine → Surgery

Lipid metabolism and biosynthesis

Life Sciences → Biochemistry, Genetics and Molecular Biology → Biochemistry

Peroxisome Proliferator-Activated Receptors

Life Sciences → Biochemistry, Genetics and Molecular Biology → Molecular Biology

An LXR – NCOA 5 gene regulatory complex directs inflammatory crosstalk‐dependent repression of macrophage cholesterol efflux

Metrics

Citation History

Topics

Related Documents

Paraoxonase 1‐treated oxLDL promotes cholesterol efflux from macrophages by stimulating the PPARγ–LXRα–ABCA1 pathway

Simvastatin promotes NPC1‐mediated free cholesterol efflux from lysosomes through CYP7A1/LXRα signalling pathway in oxLDL‐loaded macrophages

SIRT6 reduces macrophage foam cell formation by inducing autophagy and cholesterol efflux under ox‐LDL condition

The CaSR/TRPV4 coupling mediates pro‐inflammatory macrophage function

JNK ‐dependent gene regulatory circuitry governs mesenchymal fate