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.

NOS1-derived nitric oxide promotes NF-κB transcriptional activity through inhibition of suppressor of cytokine signaling-1.

J. Exp. Med.. 2015; 
BaigMirza Saqib,ZaichickSofia V,MaoMao,de AbreuAndre L,BakhshiFarnaz R,HartPeter C,SaqibUzma,DengJing,ChatterjeeSaurabh,BlockMichelle L,VogelStephen M,MalikAsrar B,ConsolaroMarcia E L,ChristmanJohn W,MinshallRichard D,GantnerBenjamin N,BoniniMarce
Products/Services Used Details Operation
ORF cDNA Clones/MolecularCloud Cysteine mutations (C147S, C179S, C43S, C78S and C112S) were introduced in SOCS1 ORF (GenScript USA Inc.). Get A Quote

摘要

The NF-κB pathway is central to the regulation of inflammation. Here, we demonstrate that the low-output nitric oxide (NO) synthase 1 (NOS1 or nNOS) plays a critical role in the inflammatory response by promoting the activity of NF-κB. Specifically, NOS1-derived NO production in macrophages leads to proteolysis of suppressor of cytokine signaling 1 (SOCS1), alleviating its repression of NF-κB transcriptional activity. As a result, NOS1(-/-) mice demonstrate reduced cytokine production, lung injury, and mortality when subjected to two different models of sepsis. Isolated NOS1(-/-) macrophages demonstrate similar defects in proinflammatory transcription on challenge with Gram-negative bacterial LPS... More

关键词