Cathepsin B and its inhibitor stefin A in brain tumors

2000 ◽  
Vol 439 (7) ◽  
pp. R122-R123 ◽  
Author(s):  
Tadej Strojnik ◽  
Irena Zajc ◽  
Aleš Bervar ◽  
Boris Židanik ◽  
Rastko Golouh ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Cathepsin B ◽  
Stefin A

Cathepsin B and its inhibitor stefin A in brain tumors

2000 ◽  
Vol 439 (S1) ◽  
pp. r122-r123 ◽  
Author(s):  
Tadej Strojnik ◽  
Irena Zajc ◽  
Aleš Bervar ◽  
Boris Židanik ◽  
Rastko Golouh ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Cathepsin B ◽  
Stefin A

scholarly journals Stefin A displaces the occluding loop of cathepsin B only by as much as required to bind to the active site cleft

FEBS Journal ◽  
2010 ◽  
Vol 277 (20) ◽  
pp. 4338-4345 ◽  
Author(s):  
Miha Renko ◽  
Urška Požgan ◽  
Dušana Majera ◽  
Dušan Turk
Keyword(s):  
Active Site ◽  
Cathepsin B ◽  
Active Site Cleft ◽  
Stefin A

Ratio of cathepsin B to stefin A identifies heterogeneity within Gleason histologic scores for human prostate cancer

The Prostate ◽  
2001 ◽  
Vol 48 (4) ◽  
pp. 274-284 ◽  
Author(s):  
Akhouri A. Sinha ◽  
Barry J. Quast ◽  
Michael J. Wilson ◽  
Eduardo T. Fernandes ◽  
Pratap K. Reddy ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cathepsin B ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Stefin A

Prediction of pelvic lymph node metastasis by the ratio of cathepsin B to stefin A in patients with prostate carcinoma

Cancer ◽  
2002 ◽  
Vol 94 (12) ◽  
pp. 3141-3149 ◽  
Author(s):  
Akhouri A. Sinha ◽  
Barry J. Quast ◽  
Michael J. Wilson ◽  
Eduardo T. Fernandes ◽  
Pratap K. Reddy ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Prostate Carcinoma ◽  
Cathepsin B ◽  
Pelvic Lymph Node ◽  
Node Metastasis ◽  
Pelvic Lymph Node Metastasis ◽  
Stefin A

Cathepsin B and middle cerebral artery occlusion in the rat

1997 ◽  
Vol 87 (5) ◽  
pp. 716-723 ◽  
Author(s):  
Donald Seyfried ◽  
Yuxia Han ◽  
Zhang Zheng ◽  
Nancy Day ◽  
Kamiar Moin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cathepsin B ◽  
Infarct Volume ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Inflammatory Cells ◽  
Ischemic Brain ◽  
Mca Occlusion ◽  
Stefin A ◽  
Intraventricular Infusion

✓ Lysosomal proteases, although tightly regulated under physiological conditions, are known to contribute to cell injury after various forms of tissue ischemia have occurred. Because cathepsin B is a prominent lysosomal protease found in brain parenchyma, the authors hypothesized that it may contribute to neuronal cell death after focal cerebral ischemia. The authors measured the expression and spatial distribution of cathepsin B within the ischemic brain in 43 animals by means of immunohistochemical analysis in a rat model of transient middle cerebral artery (MCA) occlusion. Cathepsin B activity was also measured within specific ischemic brain regions by using an in vitro assay (22 animals). In addition, the authors tested the therapeutic effect of preischemic intraventricular administration of stefin A, a cysteine protease inhibitor, on the volume of cerebral infarction after transient MCA occlusion (15 animals). Increased cathepsin B immunoreactivity was detected exclusively within the ischemic neurons after 2 hours of reperfusion following a 2-hour MCA occlusion. Cathepsin B immunolocalization in the ischemic region decreased by 24 hours of reperfusion, but then increased by 48 hours of reperfusion because the infarct was infiltrated by inflammatory cells. Increased immunolocalization of cathepsin B in the inflammatory cells located in the necrotic infarct core continued through 7 days of reperfusion. Cathepsin B enzymatic activity was significantly increased in the ischemic tissue at 2, 8, and 48 hours, but not at 24 hours of reperfusion after 2 hours of MCA occlusion. Continuous intraventricular infusion of stefin A, before 2 hours of MCA occlusion (15 animals), significantly reduced infarct volume compared with control animals (12 animals): the percentage of hemispheric infarct volume was 20 ± 3.9 compared with 33 ± 3.5 (standard error of the mean; p = 0.025). These data indicate that neuronal cathepsin B undergoes increased expression and activation within 2 hours of reperfusion after a 2-hour MCA occlusion and may be a mechanism contributing to neuronal cell death. Intraventricular infusion of stefin A, an inhibitor of cathepsin B, significantly reduces cerebral infarct volume in rats.

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