Nuclear cathepsin L activity is required for cell cycle progression of colorectal carcinoma cells
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- 作者：Tripti Tamhanea ; triptimani@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Rukshala lllukkumburaa ; 1 ; illukkum@embl.de" class="auth_mail" title="E-mail the corresponding author ; Shiying Lua ; 1 ; shiying.lu@embl.de" class="auth_mail" title="E-mail the corresponding author ; Gunhild M. Maelandsmob ; Gunhild.Mari.Malandsmo@rr-research.no" class="auth_mail" title="E-mail the corresponding author ; Mads H. Haugena ; b ; Mads.Haugland.Haugen@rr-research.no" class="auth_mail" title="E-mail the corresponding author ; Klaudia Brixa ; k.brix@jacobs-university.de" class="auth_mail" title="E-mail the corresponding author
- 关键词：Colorectal carcinoma ; cysteine cathepsins ; Trafficking
- 刊名：Biochimie
- 出版年：2016
- 出版时间：March 2016
- 年：2016
- 卷：122
- 期：Complete
- 页码：208-218
- 全文大小：2638 K
文摘
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Enhanced levels of cysteine cathepsin L but not V in adenocarcinoma vs. normal colon tissue.
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Full-length, active cathepsin L in the nuclei of colorectal carcinoma cells.
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Absence of the cathepsin L-selective endogenous inhibitor stefin B from the nuclei of colorectal carcinoma cells.
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Cathepsin L activity is essential for cell cycle progression of HCT116 cells.
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Mistrafficking of cathepsins plays significant roles in promoting colorectal cancer.