P1584
肽基精氨酸脱亚胺酶 来源于兔骨骼肌
buffered aqueous glycerol solution, ≥200 units/mg protein (Bradford)
别名:
蛋白质精氨酸亚氨基水解酶
一般描述
肽基精氨酸脱亚胺酶是将精氨酸转化为瓜氨酸的酶。
应用
肽基精氨酸脱亚胺酶已被用于一项评估了有前途的新型生物标志物，用于类风湿性关节炎的早期诊断的研究。 也有研究用于探讨牙周炎和类风湿关节炎的自身致病相关性。
生化/生理作用
在体外，钙是肽酰精氨酸脱亚胺酶活性所必需的。
外形
溶液溶于 20 mM Tris-HCl，pH 7.4，含 10 mM 2-巯基乙醇、1 mM EDTA 和 10% 甘油
其他说明
一个单位将在55°C，pH 7.2下每小时从BAEE产生 1μN-α 摩尔苯甲酰瓜氨酸乙酯。
警示用语：
Danger
危险声明
预防措施声明
危险分类
Resp. Sens. 1
储存分类代码
10 - Combustible liquids
WGK
WGK 2
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
动植物源性产品
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
John G Routsias et al.
Rheumatology (Oxford, England), 50(7), 1189-1193 (2011-02-24)
Recently, a number of studies have pointed to a potential relationship between periodontitis (PO) and RA and vice versa. Both diseases are characterized by chronic inflammation, osseous destruction, damage of the supporting soft tissues, similar cellular immune responses and common
Murat Bozdag et al.
Bioorganic & medicinal chemistry letters, 23(3), 715-719 (2012-12-26)
Protein arginin deaminase 4 (PAD4) is a calcium dependent enzyme which catalyses the conversion of peptidyl-arginine into peptidyl-citrulline and is implicated in several diseases such as rheumatoid arthritis (RA) and cancer. Herein we report the discovery of novel small-molecule, non
Leendert A Trouw et al.
Autoimmunity reviews, 12(2), 318-322 (2012-06-06)
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation and damage of the joints affecting about 0.5% of the general population. Early treatment in RA is important as it can prevent disease progression and irreversible damage of the
M Fujisaki et al.
Journal of biochemistry, 89(1), 257-263 (1981-01-01)
An enzyme which catalyzes the coversion of arginyl residues to citrullyl residues in protein was obtained from the extract of the epidermis of newborn rats. The enzyme required Ca2+ for its activity. The enzyme activity was enhanced in the presence
Jason S Knight et al.
Circulation research, 114(6), 947-956 (2014-01-16)
Neutrophil extracellular trap (NET) formation promotes vascular damage, thrombosis, and activation of interferon-α-producing plasmacytoid dendritic cells in diseased arteries. Peptidylarginine deiminase inhibition is a strategy that can decrease in vivo NET formation. To test whether peptidylarginine deiminase inhibition, a novel
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