Cystatin-B

2020 ◽  
Author(s):  
Keyword(s):  
Cystatin B

scholarly journals Cystatin B-deficiency triggers ectopic histone H3 tail cleavage during neurogenesis

2021 ◽  
pp. 105418
Author(s):  
Eduard Daura ◽  
Saara Tegelberg ◽  
Masahito Yoshihara ◽  
Christopher Jackson ◽  
Francesca Simonetti ◽  
...  
Keyword(s):  
Histone H3 ◽  
Cystatin B

scholarly journals Nuclear Cathepsin F Regulates Activation Markers in Rat Hepatic Stellate Cells

2008 ◽  
Vol 19 (10) ◽  
pp. 4238-4248 ◽  
Author(s):  
Gunter Maubach ◽  
Michelle Chin Chia Lim ◽  
Lang Zhuo
Keyword(s):  
Hepatic Stellate Cells ◽  
Cell Activation ◽  
Stellate Cell ◽  
Stellate Cells ◽  
Activation Process ◽  
Type I ◽  
Activation Markers ◽  
Nuclear Activity ◽  
Cystatin B ◽  
Cathepsin F

Activation of hepatic stellate cells during liver fibrosis is a major event facilitating an increase in extracellular matrix deposition. The up-regulation of smooth muscle α-actin and collagen type I is indicative of the activation process. The involvement of cysteine cathepsins, a class of lysosomal cysteine proteases, has not been studied in conjunction with the activation process of hepatic stellate cells. Here we report a nuclear cysteine protease activity partially attributed to cathepsin F, which co-localizes with nuclear speckles. This activity can be regulated by treatment with retinol/palmitic acid, known to reduce the hepatic stellate cell activation. The treatment for 48 h leads to a decrease in activity, which is coupled to an increase in cystatin B and C transcripts. Cystatin B knockdown experiments during the same treatment confirm the regulation of the nuclear activity by cystatin B. We demonstrate further that the inhibition of the nuclear activity by E-64d, a cysteine protease inhibitor, results in a differential regulation of smooth muscle α-actin and collagen type I transcripts. On the other hand, cathepsin F small interfering RNA transfection leads to a decrease in nuclear activity and a transcriptional down-regulation of both activation markers. These findings indicate a possible link between nuclear cathepsin F activity and the transcriptional regulation of hepatic stellate cell activation markers.

Unverricht-Lundborg disease with cystatin B gene abnormalities

2002 ◽  
Vol 26 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Kuriko Kagitani-Shimono ◽  
Katsumi Imai ◽  
Nobuhiko Okamoto ◽  
Jiro Ono ◽  
Shintaro Okada
Keyword(s):  
Cystatin B

scholarly journals High affinity copper binding by stefin B (cystatin B) and its role in the inhibition of amyloid fibrillation

FEBS Journal ◽  
2006 ◽  
Vol 273 (18) ◽  
pp. 4250-4263 ◽  
Author(s):  
Eva Žerovnik ◽  
Katja Škerget ◽  
Magda Tušek-Žnidarič ◽  
Corina Loeschner ◽  
Marcus W. Brazier ◽  
...  
Keyword(s):  
Copper Binding ◽  
Cystatin B ◽  
High Affinity ◽  
Amyloid Fibrillation

scholarly journals No evidence of a role for cystatin B gene in juvenile myoclonic epilepsy

Epilepsia ◽  
2015 ◽  
Vol 56 (4) ◽  
pp. e40-e43 ◽  
Author(s):  
Laura Mumoli ◽  
Patrizia Tarantino ◽  
Roberto Michelucci ◽  
Amedeo Bianchi ◽  
Angelo Labate ◽  
...  
Keyword(s):  
Juvenile Myoclonic Epilepsy ◽  
Myoclonic Epilepsy ◽  
Cystatin B

scholarly journals Seizures, Ataxia, and Neuronal Loss in Cystatin B Heterozygous Mice

Epilepsia ◽  
2007 ◽  
Vol 48 (4) ◽  
pp. 752-757 ◽  
Author(s):  
Allen Kaasik ◽  
Malle Kuum ◽  
Anu Aonurm ◽  
Anti Kalda ◽  
Annika Vaarmann ◽  
...  
Keyword(s):  
Neuronal Loss ◽  
Cystatin B

Effects of low-dose meloxicam in cats with chronic kidney disease

2020 ◽  
pp. 1098612X2093575
Author(s):  
Kate KuKanich ◽  
Christopher George ◽  
James K Roush ◽  
Sherry Sharp ◽  
Giosi Farace ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Adverse Effects ◽  
Transforming Growth Factor Beta ◽  
Low Dose ◽  
Transforming Growth Factor ◽  
Joint Disease ◽  
Cystatin B

Objectives Meloxicam therapy may benefit cats with degenerative joint disease, and retrospective studies suggest it could slow kidney disease progression and increase survival. This study aimed to prospectively evaluate the renal effects of low-dose meloxicam treatment (0.02 mg/kg/day) over 6 months in cats with chronic kidney disease (CKD). Methods Twenty-one cats with stable International Renal Interest Society stage 2 or 3 CKD were recruited and randomized to placebo or meloxicam groups. Cats were evaluated at baseline and at 1, 3 and 6 months, including blood pressure, chemistry, symmetric dimethylarginine (SDMA), glomerular filtration rate (GFR), urinalysis, urine protein:creatinine ratio (UPC), urine transforming growth factor-beta (ß):creatinine ratio, urine clusterin, urine cystatin B and serum inosine. Results No statistical difference was observed in systolic blood pressure, blood urea nitrogen, creatinine, SDMA, GFR, urine transforming growth factor-ß:creatinine ratio, urine clusterin, urine cystatin B or serum inosine in cats receiving meloxicam vs placebo. Mean UPC was greater in the meloxicam group (0.33) than the placebo group (0.1) at 6 months ( P = 0.006). Four cats had meloxicam discontinued owing to potential (mainly gastrointestinal) adverse effects. Conclusions and relevance No decline in renal excretory function was observed when meloxicam was administered to cats with CKD. However, gastrointestinal adverse effects were observed, and cats that received meloxicam had greater proteinuria at 6 months than cats that received placebo. As proteinuria is associated with negative outcomes (progression of azotemia and hypertension) in cats with CKD, this finding suggests that meloxicam should be used with caution in cats with CKD and UPC monitored. Until further research is available, clinicians should weigh the risk of potential increased proteinuria against quality of life benefits when considering meloxicam for analgesia in cats with renal disease.

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