产品介绍 评论(0)
物种
Human分子别名
Cathepsin F,CTSFAccession
Q9UBX1表达序列
Ala20-Asp484 with His Tag at the C-Terminus
表达宿主
HEK293分子量
60-75kDa (Reducing)
纯度
>95% by SDS-PAGE活性
The specific activity is >10 pmol/min/μg, as measured under the described conditions.标记
Unconjugated标签
His Tag性状
Lyophilized Powder缓冲体系
PBS, PH7.4, 5% trehalose
溶解方法
Reconstitute at 0.1-1 mg/ml according to the size in ultrapure water after rapid centrifugation.
储存条件
· 12 months from date of receipt, lyophilized powder stored at -20 to -80℃.
· 3 months, -20 to -80℃ under sterile conditions after reconstitution.
· 1 week, 2 to 8℃ under sterile conditions after reconstitution.
· Please avoid repeated freeze-thaw cycles.文献引用
1.Wang X, Zhu Z. Unraveling the causal relationship and underlying mechanisms between cathepsins on liver cancer: findings from mendelian randomization and bioinformatics analysis. Discov Oncol. 2025 Mar 7;16(1):277.
2.Mohan S, Sampognaro PJ, Argouarch AR, Maynard JC, Welch M, Patwardhan A, Courtney EC, Zhang J, Mason A, Li KH, Huang EJ, Seeley WW, Miller BL, Burlingame A, Jacobson MP, Kao AW. Processing of progranulin into granulins involves multiple lysosomal proteases and is affected in frontotemporal lobar degeneration. Mol Neurodegener.
CTSF (Cathepsin F) is a cysteine protease primarily localized in lysosomes. Its protein structure contains a typical catalytic domain of cysteine proteases, which specifically cleaves peptide bonds through its active site. Within the cell, it is responsible for degrading abnormal or damaged proteins and participates in antigen processing and presentation, thereby regulating immune responses. Clinically, aberrant expression or dysfunction of CTSF is closely associated with various diseases: its overexpression may promote tumor invasion and metastasis, while in autoimmune diseases, it may lead to immune imbalance due to disrupted antigen processing. Consequently, CTSF has emerged as a potential disease biomarker and therapeutic target.
电泳
2μg (R: reducing condition, N:non-reducing condition).







评论(0)