Cathepsin S 蛋白, Human (HEK293, His)

Cathepsin S Protein, Human (HEK293, His) is potent cysteine protease which can promote degradation of damaged or unwanted proteins in the endo-lysosomal pathway.

组织蛋白酶 S 是半胱氨酸组织蛋白酶家族的成员。组织蛋白酶 S 具有特定作用，例如 MHC II 类抗原呈递，在恒定链的降解中发挥重要作用。组织蛋白酶 S 参与多种病理过程，包括关节炎、癌症和心血管疾病，它会被分泌并作用于细胞外底物。组织蛋白酶 S 具有独特的组织表达限制，并且在中性 pH 下更稳定。组织蛋白酶 S 在半胱氨酸组织蛋白酶家族中是独特的，因为其组织表达受到限制，与位于淋巴和脾脏中的抗原呈递细胞以及巨噬细胞等其他免疫细胞相关。组织蛋白酶 S 被认为是一种特别有效的半胱氨酸蛋白酶，可裂解弹性蛋白并产生具有生物活性的弹性蛋白肽，从而促进心血管炎症和钙化。组织蛋白酶 S 也由平滑肌细胞和巨噬细胞释放，作为连续递归反馈循环中炎症的全身反应^[1][2]。

The enzyme activity of this recombinant protein is testing in progress, we cannot offer a guarantee yet.

Human

HEK293

C-His

AAH02642.1 (Q17-I331)

1520  [NCBI]

QLHKDPTLDHHWHLWKKTYGKQYKEKNEEAVRRLIWEKNLKFVMLHNLEHSMGMHSYDLGMNHLGDMTSEEVMSLMSSLRVPSQWQRNITYKSNPNWILPDSVDWREKGCVTEVKYQGSCGACWAFSAVGALEAQLKLKTGKLVSLSAQNLVDCSTEKYGNKGCNGGFMTTAFQYIIDNKGIDSDASYPYKAMDQKCQYDSKYRAATCSKYTELPYGREDVLKEAVANKGPVSVGVDARHPSFFLYRSGVYYEPSCTQNVNHGVLVVGYGDLNGKEYWLVKNSWGHNFGEEGYIRMARNKGNHCGIASFPSYPEI&SNPNWILPDSVDWREKGCVTEVKYQGSCGACWAFSAVGALEAQLKLKTGKLVSLSAQNLVDCSTEKYGNKGCNGGFMTTAFQYIIDNKGIDSDASYPYKAMDQKCQYDSKYRAATCSKYTELPYGREDVLKEAVANKGPVSVGVDARHPSFFLYRSGVYYEPSCTQNVNHGVLVVGYGDLNGKEYWLVKNSWGHNFGEEGYIRMARNKGNHCGIASFPSYPEI&QLHKDPTLDHHWHLWKKTYGKQYKEKNEEAVRRLIWEKNLKFVMLHNLEHSMGMHSYDLGMNHLGDMTSEEVMSLMSSLRVPSQWQRNITYKSHHHHHH

37 kDa

Greater than 90% as determined by reducing SDS-PAGE.

溶液.

Supplied as a 0.2 μm filter solution of 20 mM MES, 150 mM NaCl, 10% Glycerol, pH 5.5.

<1 EU/μg, determined by LAL method.

Stored at -80°C for 1 year. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.

Shipping with dry ice.

• [1]. Richard D A Wilkinson, et al. Cathepsin S: therapeutic, diagnostic, and prognostic potential. Biol Chem. 2015 Aug;396(8):867-82.  [Content Brief]

  [2]. Brena F Sena, et al. Cathepsin S As an Inhibitor of Cardiovascular Inflammation and Calcification in Chronic Kidney Disease. Front Cardiovasc Med. 2018 Jan 5;4:88.  [Content Brief]