凯发一触即发

至今,GenScript的服务及产品已被Cell, Nature, Science, PNAS等1300多家生物医药类杂志引用近万次,处于行业领先水平。NIH、哈佛、耶鲁、斯坦福、普林斯顿、杜克大学等约400家全球著名机构使用GenScript的基因合成、多肽服务、抗体服务和蛋白服务等成功地发表科研成果,再次证明GenScript 有能力帮助业内科学家Make research easy.

Chlamydia pneumoniae Hijacks a Host Autoregulatory IL-1β Loop to Drive Foam Cell Formation and Accelerate Atherosclerosis.

Cell Metab.. 2018; 
Tumurkhuu Gantsetseg,Dagvadorj Jargalsaikhan,Porritt Rebecca A,Crother Timothy R,Shimada Kenichi,Tarling Elizabeth J,Erbay Ebru,Arditi Moshe,Chen Sh
Products/Services Used Details Operation
Catalog Antibody Santa Cruz Cat # SC-47724;RRID:AB_627678 Anti-6xHis Genscript Cat # A00174-40;RRID:AB_914703 Anti-IL Get A Quote

摘要

Pathogen burden accelerates atherosclerosis, but the mechanisms remain unresolved. Activation of the NLRP3 inflammasome is linked to atherogenesis. Here we investigated whether Chlamydia pneumoniae (C.pn) infection engages NLRP3 in promoting atherosclerosis. C.pn potentiated hyperlipidemia-induced inflammasome activity in cultured macrophages and in foam cells in atherosclerotic lesions of Ldlr mice. C.pn-induced acceleration of atherosclerosis was significantly dependent on NLRP3 and caspase-1. We discovered that C.pn-induced extracellular IL-1β triggers a negative feedback loop to inhibit GPR109a and ABCA1 expression and cholesterol efflux, leading to accumulation of intracellular cholesterol and foam ce... More

关键词

ABCA1,C.?pneumoniae,Gpr109a,Nlrp3,aspartate,atherosclerosis,cholesterol efflux,foam cells,interleukin-1 beta,ni