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Human Monoclonal CSTB Primary Antibody pour IHC, WB - ABIN223204
Penna, Cerciello, Chambery, Russo, Cernilogar, Pedone, Perrone-Capano, Cappello, Di Giaimo, Crispino: Cystatin B Involvement in Synapse Physiology of Rodent Brains and Human Cerebral Organoids. dans Frontiers in molecular neuroscience 2019
CSTB was overexpressed and miR1433p was downregulated in ovarian malignant tumors. Mature miR1433p directly bound CSTB 3'UTR, leading to a decrease in CSTB expression in OC cells, which was regulated by TGFbeta1.
While novel diagnostic tumour markers are urgently needed, the examined potential tumour markers, with the exception of PIVKAII seem to be inadequate for diagnosing HCC in ALC
cystatin B expression was significantly and inversely correlated with lung tumor stage and tumor grade
The results demonstrate that cystatin B interferes with the STAT-1 signaling and IFN-beta-antiviral responses perpetuating HIV in macrophage reservoirs.
apoptosis is accompanied by degradation of the cysteine cathepsin inhibitor stefin B (StfB). CatD 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 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 and ANXA4 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.
glutamate dehydrogenase is a euchromatin-associated enzyme, and its H3 clipping activity is regulated by chromatin structure, histone modifications and an in vivo inhibitor.
detected a homozygous expansion of dodecamer repeats in the CSTB gene in four patients with clinical diagnosis of ULD.
The increased CSTB expression in ovarian tissue represents tumor progression and is dysregulated by the TGF-beta signaling pathway.
A reciprocal influence of CSTB and SOD1 at the gene expression level and for a direct interaction of the two proteins, is reported.
The present study was performed on two more missense mutants of human stefin B, G50E and Q71P, and they similarly showed numerous aggregates upon overexpression.
High levels of bioactive recombinant stefins A and B can be produced by fermentation in P. pastoris.
The data of this study show that CXCL13 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-STAT pathway signaling
Deletion of the encoding Cstb gene in Npc1-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), 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 in response to TLR4 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 region is not playing a major role in locomotor and cognitive deficits found in mice model of Down syndrome.
Data show that cystatin C effectively rescues cystatin B loss-of-function mutation, facilitating the reversal of pathophysiological changes and suggesting a novel therapeutic intervention for patients with neurodegenerative disorders.
Stefin B interacts with histones and cathepsin L in the nucleus
These findings indicate that neuronal atrophy is an important consequence of cystatin-B deficiency independent of seizure events, suggesting a physiological role for this protein in the maintenance of normal neuronal structure.
greater degree of neuronal damage was observed in CSTB-deficient than in WT mice after seizures of identical grade, indicating increased susceptibility to seizure-induced cell death
Increased cleavage of MARCKS in brain and macrophages, but not in liver and kidney extracts of stefin B-deficient mice compared to wild-type mice, was observed.
This study identifies a novel function for Cystatin B in defending cerebellar granule neurons from oxidative stress.
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