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Trypsin-3 / PRSS3 抗体, 兔单抗

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Human PRSS3 抗体产品信息
免疫原:Recombinant Human Trypsin-3 / PRSS3 protein (Catalog#11866-H08H)
克隆号:001
Ig 类型:Rabbit IgG
浓度:
内毒素:
缓冲液:0.2 μm filtered solution in PBS with 5% trehalose
抗体制备方法:This antibody was obtained from a rabbit immunized with purified, recombinant Human Trypsin-3 / PRSS3 (rh Trypsin-3 / PRSS3; Catalog#11866-H08H; P35030-3; Met1-Ser247).
Human PRSS3 抗体使用指导
特异性:Human Trypsin-3 / PRSS3
推荐应用:ELISA

ELISA: 0.1-0.2 μg/mL

This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human PRSS3. The detection limit for Human PRSS3 is approximately 0.00245 ng/well.

储存方法:This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Other PRSS3 抗体 Products
Trypsin-3/PRSS3 研究背景

Trypsin-3, also known as Trypsin III, brain trypsinogen, Serine protease 3 and PRSS3, is a secreted protein which belongs to the peptidase S1 family. Trypsin-3 / PRSS3 is expressed is in pancreas and brain. It contains one peptidase S1 domain. Trypsin-3 / PRSS3 can degrade intrapancreatic trypsin inhibitors that protect against CP. Genetic variants that cause higher mesotrypsin activity might increase the risk for chronic pancreatitis (CP). A sustained imbalance of pancreatic proteases and their inhibitors seems to be important for the development of CP. The trypsin inhibitor-degrading activity qualified PRSS3 as a candidate for a novel CP susceptibility gene. Trypsin-3 / PRSS3 has been implicated as a putative tumor suppressor gene due to its loss of expression, which is correlated with promoter hypermethylation, in esophageal squamous cell carcinoma and gastric adenocarcinoma.

Human Trypsin-3/PRSS3 参考资料
  • Venter JC. et al., 2001, Science 291:1304-51.
  • Marsit,CJ. et al., 2005, Mol Carcinog 44 (2):146-50.
  • Rowen, L. et al., 2005, Mol Biol Evol. 22 (8):1712-20.
  • Rosendahl, J. et al., 2010, Pancreatology. 10 (2-3):243-9
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