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apoptosis is accompanied by degradation of the cysteine cathepsin inhibitor stefin B (StfB). CatD (zeige CTSD Antikörper) did not exhibit a crucial role in this step. However, this degradation was partially prevented through pre-incubation with the antioxidant N-acetyl cysteine
Homozygous for a c.218dupT (p.His75Serfs*2) mutation in exon 3 of CSTB causes neurodegeneration, progressive cerebral volume loss and diffuse hypomyelination.
CSTB downregulation may promote the development of gastric cancer.
It was shown that decreased expression of (zeige NPC1 Antikörper)cystatin B enhances cathepsin activity in Niemann-Pick C cerebellar degeneration patient fibroblasts.
High expression of stefin B may be an important factor contributing to the development and metastasis of Hepatocellular Carcinoma.
CSTB null mutation associated with microcephaly, early developmental delay, and severe dyskinesia.
Data shows that CYTB (zeige MT-CYB Antikörper) and ANXA4 (zeige ANXA4 Antikörper) overexpression may be involved in carcinogenesis and histopathological differentiation of ovarian clear cell carcinoma and suggest they may serve as a potential diagnostic biomarkers.
A role for disease-causing mutations in cystatin B gene in patients with juvenile myoclonic epilepsy was not supported.
Even though the majority of EPM1 patients have a uniform genetic mutation, the actual size of the longer CSTB expansion mutation allele is likely to have a modulating effect on the age at disease onset, myoclonus severity, and cortical neurophysiology.
The study shows detection of stefin B dimers in HEK293 cells and the importance of their residual activity.
The data of this study show that CXCL13 (zeige CXCL13 Antikörper) expression is a hallmark of microglial activation in Cstb (-/-) mice and that the brain inflammation is linked to peripheral inflammatory changes, which might contribute to the disease pathology of progressive myoclonus epilepsy..
CSTB has a role in chemotaxis, antigen-presentation, and in immune- and defense response-associated processes by altering JAK (zeige JAK3 Antikörper)-STAT (zeige STAT1 Antikörper) pathway signaling
Deletion of the encoding Cstb gene in Npc1 (zeige NPC1 Antikörper)-deficient mice resulted in striking deleterious effects, particularly within the cerebellum where diffuse loss of Purkinje cells was observed in young mice. This may be a consequence of damage to lysosomal membranes by reactive oxygen species (ROS (zeige ROS1 Antikörper)), leading to the leakage of lysosomal contents that culminates in apoptosis.
Results suggest a role for CSTB in regulating microglial activation: data link CSTB deficiency to early activation and altered functional properties of microglia, imply presence of both enhanced and suppressed immune response-related microglial functions
the LPS-induced sepsis in StB KO mice is dependent on caspase-11 and mitochondrial reactive oxygen species but is not associated with the lysosomal destabilization and increased cathepsin activity in the cytosol
These results indicate an in vivo role for Stfb in protecting cancer cells by promoting their resistance to oxidative stress and to apoptosis induced through the lysosomal pathway.
Sefin B influences the expression of anti-inflammatory IL-10 (zeige IL10 Antikörper) in response to TLR4 (zeige TLR4 Antikörper) agonists.
An increase in Cstb does not induce any spontaneous epileptic activity.
Pathologic events in the CSTB-deficient brain highlight the potential role of glial activation at the initial stages of progressive myoclonic epilepsy type 1.
this study suggesting that the Cstb-Prmt2 (zeige PRMT2 Antikörper) region is not playing a major role in locomotor and cognitive deficits found in mice model of Down syndrome.
The interaction between AtCYSb and AtCaN2 AtCYSb regulates nucleic acid degradation in cells
Data suggests that AtCYS6 expression is enhanced by the germination inhibitory phytohormone ABA and that it participates in the control of germination rate and seedling growth by inhibiting the activity of stored cysteine proteinases. [AtCYS6]
The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors, while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and kininogens. This gene encodes a stefin that functions as an intracellular thiol protease inhibitor. The protein is able to form a dimer stabilized by noncovalent forces, inhibiting papain and cathepsins l, h and b. The protein is thought to play a role in protecting against the proteases leaking from lysosomes. Evidence indicates that mutations in this gene are responsible for the primary defects in patients with progressive myoclonic epilepsy (EPM1).
, liver thiol proteinase inhibitor
, cystatin B protein
, cystatin B (stefin B)
, cystatin beta
, stefin B
, stefin C
, cystatin B
, Leukocyte cysteine proteinase inhibitor 1