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外周血淋巴细胞中过氧化氢刺激后p72syk的激活、酪氨酸磷酸化以及钙动员。

Activation and tyrosine phosphorylation of p72syk as well as calcium mobilization after hydrogen peroxide stimulation in peripheral blood lymphocytes.

作者信息

Qin S, Inazu T, Yamamura H

机构信息

Department of Biochemistry, Fukui Medical School, Japan.

出版信息

Biochem J. 1995 May 15;308 ( Pt 1)(Pt 1):347-52. doi: 10.1042/bj3080347.

DOI:10.1042/bj3080347
PMID:7538757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1136883/
Abstract

To determine the regulatory role of p72syk in lymphocyte activation, peripheral blood lymphocytes were treated with 10 mM hydrogen peroxide. Hydrogen peroxide induced a rapid elevation of p72syk activity (4-6-fold) and a dramatic increase in tyrosine phosphorylation of a number of cellular proteins, including phospholipase C gamma 1 (PLC gamma 1) and p72syk. Monoclonal antibodies to PLC gamma 1 co-precipitated p72syk from hydrogen peroxide-stimulated cell lysates, but not from unstimulated cell lysates. Furthermore, we observed a rise in intracellular Ca2+, corresponding to the combination of extracellular Ca2+ influx and the release from intracellular Ca2+ stores. Extracellular Ca2+ influx was necessary for the sustenance of p72syk activity, but not for the initiation of p72syk activation induced by hydrogen peroxide. Taken together, these data suggested that one possible role of p72syk was to activate PLC gamma 1, at least in part through tyrosine phosphorylation, and then to trigger calcium mobilization in pig peripheral blood lymphocytes in response to hydrogen peroxide stimulation.

摘要

为了确定p72syk在淋巴细胞激活中的调节作用,外周血淋巴细胞用10 mM过氧化氢处理。过氧化氢诱导p72syk活性迅速升高(4 - 6倍),并使包括磷脂酶Cγ1(PLCγ1)和p72syk在内的许多细胞蛋白的酪氨酸磷酸化显著增加。针对PLCγ1的单克隆抗体能从过氧化氢刺激的细胞裂解物中共沉淀p72syk,但不能从未刺激的细胞裂解物中沉淀。此外,我们观察到细胞内Ca2+升高,这与细胞外Ca2+内流和细胞内Ca2+储存释放的联合作用相对应。细胞外Ca2+内流对于维持p72syk活性是必要的,但对于过氧化氢诱导的p72syk激活的起始不是必需的。综上所述,这些数据表明p72syk的一个可能作用是至少部分通过酪氨酸磷酸化激活PLCγ1,然后在猪外周血淋巴细胞中响应过氧化氢刺激触发钙动员。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/302d3f7f3069/biochemj00063-0338-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/c2ecdd8bcf27/biochemj00063-0336-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/dd23b30b1100/biochemj00063-0337-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/08e2f96a4962/biochemj00063-0337-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/3f8191154fda/biochemj00063-0338-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/39ecc2d3c712/biochemj00063-0338-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/302d3f7f3069/biochemj00063-0338-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/c2ecdd8bcf27/biochemj00063-0336-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/dd23b30b1100/biochemj00063-0337-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/08e2f96a4962/biochemj00063-0337-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/3f8191154fda/biochemj00063-0338-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/39ecc2d3c712/biochemj00063-0338-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eec2/1136883/302d3f7f3069/biochemj00063-0338-c.jpg

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Reactive oxygen intermediates activate NF-kappa B in a tyrosine kinase-dependent mechanism and in combination with vanadate activate the p56lck and p59fyn tyrosine kinases in human lymphocytes.
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Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) phosphorylation by protein kinase Cδ (PKCδ) inhibits mitochondria elimination by lysosomal-like structures following ischemia and reoxygenation-induced injury.甘油醛-3-磷酸脱氢酶(GAPDH)被蛋白激酶 Cδ(PKCδ)磷酸化,可抑制缺血再灌注损伤后溶酶体样结构引发的线粒体消除。
J Biol Chem. 2013 Jun 28;288(26):18947-60. doi: 10.1074/jbc.M113.466870. Epub 2013 May 7.
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