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malfunction
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arsenite treatment of human glioblastoma cells induces autophagosome formation and permeabilization of mitochondria, followed by caspase 3/7-mediated apoptosis. Arsenite toxicity involves a complex interplay between autophagy and apoptosis in human glioblastoma cells and is associated with inhibition of CatB, mechanism, overview
malfunction
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BmCatB RNAi treatment results in an arrest of the larval-pupal transformation. RNAi-mediated BmCatB knockdown sustains the expression of BmCatD during the larval-pupal transformation. On the other hand, when BmCatD is inhibited via RNAi, the expression of BmCatB is upregulated
malfunction
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cathepsin B confers protection against cell death in clonogenic assays of CD34+ primary cells from chronic myelogenous leukemia patients
malfunction
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cathepsin B is a major lysosomal protease, its overactivation is involved in muscular dystrophy, bone resorption, pulmonary emphysem, and tumor metastasis
malfunction
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cathepsin B is involved in several cancers
malfunction
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cathepsin B is involved in several cancers
malfunction
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cathepsin B overexpression in glioblastoma is correlated with a short survival of the patient
malfunction
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cathepsin B significantly decreases the number of apoptotic nuclei in both the cumulus cell layer of matured oocytes and blastocysts
malfunction
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cathepsin B-mediated autophagy flux facilitates the anthrax toxin receptor 2-mediated delivery of anthrax lethal factor, LeTx, into the cytoplasm, requiring lysosomal fusion with LeTx-containing endosomes. Anthrax lethal toxin is a virulence factor secreted by Bacillus anthracis and has direct cytotoxic effects on most cells once released into the cytoplasm. Inhibition of cathepsin B blocks MEK1 cleavage induced by anthrax lethal toxin through delaying LeTx release into the cytoplasm
malfunction
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cathespin-B is an important proteolytic enzyme involved in the disease course of invasion in many types of cancer. It correlates with the growth and angiogenesis of tumors, but not with the adhesion induced by CD44v6, in the subcutaneous heteroplastic pancreatic carcinoma model, overview
malfunction
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CtsB inhibition blunts AKT phosphorylation in activated hepatic stellate cells in response to platelet-derived growth factor. CtsB inactivation mitigates CCl4-induced inflammation, hepatic stellate cell activation, and collagen deposition
malfunction
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exposure of GSH-depleted B cells to NO-releasing compounds lowers their capacity to present a reduced and alkylated lysozyme due to inhibition of cathepsin B by NO, overview. Cells with a normal GSH content are protected from this inhibition
malfunction
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extracellular release of the lysosomal proteases, cathepsins, and their inhibitors is associated with the development and progression of several types of cancer
malfunction
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genetic cathepsin B deficiency reduces beta-amyloid in transgenic mice expressing human wild-type amyloid precursor protein
malfunction
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glioblastoma and endothelial cells cross-talk, mediated by SDF-1, enhances tumour invasion and endothelial proliferation by increasing expression of cathepsins B, S, and MMP-9. Enhanced invasiveness correlates with increased expression of MMP-9 in both U87 and HMEC-1 cells, increased expression of cysteine cathepsins B and S and down-regulation of endogenous cell adhesion molecule NCAM in U-87 cells. U-87 tumour cells significantly enhance the proliferation of co-cultured endothelial cells by a mechanism involving cathepsin B, but not cathepsin S, overview. Regulation of invasion of U-87 cells involves cathepsin B, overview
malfunction
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inhibition of cathepsin B impairs lysosomal proteolysis. FYAD, an irreversible inhibitor of cathepsin B, induces apoptosis of neuroblastoma cells but not of other tumor cells. Inhibition of cathepsin D does not rescue cells from FYAD-induced death
malfunction
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lysosomal destabilization contributes for cell death through controlled release of lysosomal enzymes, the prominent among them being cathepsin B. p53-dependent lysosomal destabilization and cathepsin B activation contribute for increased sensitivity of p21-deficient cells to embelin with enhanced caspase 9 and caspase 3 activation, overview
malfunction
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Microglia induce apoptosis of glioma cells via the release of NO and cathepsin B protease. Cathepsin B causes a decrease in cell survival. Cathepsin B plays a critical role in cytotoxicity in the central nervous system
malfunction
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Microglia induce apoptosis of glioma cells via the release of NO and cathepsin B protease. Cathepsin B causes a decrease in cell survival. Cathepsin B plays a critical role in cytotoxicity in the central nervous system
malfunction
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specific blocking cathepsin B expression suppresses apoptosis but does not affect autophagy, which suggests that cathepsin B is a molecular link between autophagy and apoptosis. Cathepsin B inhibition decreases the SPARC-induced release of cytochrome c
malfunction
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the activity of CatB, but not of CatL or CatS, is relevant to glioblastoma invasion, role of cathepsin B in glioma invasion by in vitro 3D spheroids migration modelling of in vivo glioma growth and invasion, overview
malfunction
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the cathepsin family of endosomal proteases is required for proteolytic processing of several viruses during entry into host cells, cathepsins contribute to reovirus tropism, spread, and disease outcome. Mammalian reoviruses utilize cathepsins B, L, and S for disassembly of the virus outer capsid and activation of the membrane penetration machinery. The survival rate of Ctsb-/- mice infected with reovirus is enhanced in comparison to that of wild-type mice, viremia in wild-type and cathepsin-deficient mice following peroral inoculation, overview
malfunction
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both caspase 3 activation and PARP cleavage are significantly reduced in cells lacking cathepsin B. Mitochondrial membrane permeabilization as well as the release of cytochrome C and AIF from mitochondria into cytosol induced by doxorubicin are significantly diminished in cathepsin B suppressed cells. Cell viability following doxorubicin is significantly elevated in cells with cathepsin B silencing
malfunction
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inhibition of cathepsin B has no inhibitory effect on Notch processing
malfunction
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blocking CTSB expression using CTSB siRNA suppresses inflammatory response but does not affect apoptosis markedly
malfunction
Cathepsin B silencing by RNAi in human colorectal cancer (CRC) cells inhibits their growth in soft agar, as well as their invasion capacity, tumoral expansion, and metastatic spread in immunodeficient mice
malfunction
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CysC deletion in knockout mice leads to an enhanced CatB activity
malfunction
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enhancing CatB activity by CysC deletion significantly lowers total amyloid-betaand amyloid-beta42 levels in human amyloid precursor protein wild-type mice, whereas CatB deletion increases amyloidbeta levels
malfunction
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female Ctsb knockout mice, but not males, display a decrease of 31% in cholesterol absorption
malfunction
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fine-mapping studies along with gene expression efforts and studies in knockout animals identified Ctsb as a gender-dependent modifier of cholesterol absorption from the intestine
malfunction
higher levels of the cell cycle inhibitor p27Kip1 are observed in cathepsin B-deficient tumors as well as an increase in cyclin B1
malfunction
reduced cathepsin B expression using RNA interference mimicks pharmacological inhibition of the enzyme and confirms the contribution of cathepsin B to apoptotic events induced by Dengue virus in HepG2 cells
malfunction
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transgenic mice are generated overexpressing CatB under the control of a neuron-specific enolase promoter: Enhancing neuronal CatB activity in human amyloid precursor protein wild-type mice significantly lowers amyloidbeta42 levels
malfunction
silencing of cathepsin B significantly depresses coelomocytes apoptosis rate by 0.16fold
malfunction
silencing of cathepsin B significantly inhibits the development and hatching of Radopholus similis and greatly reduces its pathogenicity
malfunction
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the cathepsin family of endosomal proteases is required for proteolytic processing of several viruses during entry into host cells, cathepsins contribute to reovirus tropism, spread, and disease outcome. Mammalian reoviruses utilize cathepsins B, L, and S for disassembly of the virus outer capsid and activation of the membrane penetration machinery. The survival rate of Ctsb-/- mice infected with reovirus is enhanced in comparison to that of wild-type mice, viremia in wild-type and cathepsin-deficient mice following peroral inoculation, overview
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malfunction
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exposure of GSH-depleted B cells to NO-releasing compounds lowers their capacity to present a reduced and alkylated lysozyme due to inhibition of cathepsin B by NO, overview. Cells with a normal GSH content are protected from this inhibition
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malfunction
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genetic cathepsin B deficiency reduces beta-amyloid in transgenic mice expressing human wild-type amyloid precursor protein
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malfunction
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CtsB inhibition blunts AKT phosphorylation in activated hepatic stellate cells in response to platelet-derived growth factor. CtsB inactivation mitigates CCl4-induced inflammation, hepatic stellate cell activation, and collagen deposition
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malfunction
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cathepsin B-mediated autophagy flux facilitates the anthrax toxin receptor 2-mediated delivery of anthrax lethal factor, LeTx, into the cytoplasm, requiring lysosomal fusion with LeTx-containing endosomes. Anthrax lethal toxin is a virulence factor secreted by Bacillus anthracis and has direct cytotoxic effects on most cells once released into the cytoplasm. Inhibition of cathepsin B blocks MEK1 cleavage induced by anthrax lethal toxin through delaying LeTx release into the cytoplasm
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metabolism
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cathepsin B is involved in TNF-alpha-induced signal transduction pathways in lung cells
metabolism
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cathepsin B and proteasome, antagonistically control ER-stress-induced programmed cell death. ER-stress-induced programmed cell death (ERSID) is regulated positively by cathepsin B and negatively by proteasome subunit PBA1. Cathepsin B may execute its function after tonoplast rupture and works in parallel with vacuolar processing enzyme
metabolism
cathepsin B mediates radiation induced bystander effects. The enzyme seems to exert radiation induced bystander effects by acting through the insulin-like growth factor receptor DAF-2
metabolism
increase and leakage of CatB in microglia during aging are responsible for the increased generation of mitochondria-derived reactive oxygen species and proinflammatory mediators, culminating in memory impairment
physiological function
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apoptotic stimuli, e.g. exposure to etoposide, ultraviolet light, FasL or deprivation of interleukin-3, trigger lysosomal membrane permeability, leading to the release of cathepsins, dependent on Bax/Bak and components of the apoptosome, which activate death signaling pathways in the cytosol, overview. Cathepsin B does not contribute to the commitment step of apoptosis, as Bax and Bak do, but enhances the efficiency of apoptosis through an amplification loop
physiological function
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autocatalytic activation of procathepsin B can proceed at neutral pH when bound to heparin and other negatively charged surfaces, which may account for an extracellular physiological role of cathepsins
physiological function
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BmCatB is involved in the programmed cell death of the fat body during metamorphosis, and CatB and CatD contribute to the metamorphosis
physiological function
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CatB is involved in but is not essential for antigen processing
physiological function
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cathepsin B activity is necessary for TAP-HEL, a reduced and alkylated lysozyme, processing, it is essential for generation of the HEL-derived antigenic peptide recognized by B9.1 cells
physiological function
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cathepsin B acts as the main executor of caspase dependent or independent cell death in major organs including the liver, kidney, and lungs
physiological function
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cathepsin B is a molecular link between autophagy and apoptosis. Cathepsin B mediates SPARC-induced apoptosis in primitive neuroectodermal tumor, PNET, cells, overview. SPARC is secreted protein, acidic and rich in cysteine, a matrix-associated glycoprotein. Cathepsin B inhibition decreases the SPARC-induced release of cytochorome c indicating that the release is due to cathepsin B activity
physiological function
cathepsin B is involved in the regulation of apoptosis during serum-starvation in teleost follicles. Cathepsin B may play a role in the activation of the executioner caspase-3
physiological function
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cathepsin B is required for interleukin-1beta maturation, the maturation of pro-IL-1beta in chromogranin A-stimulated microglia is dependent on the enzymatic activities of both cathepsin B and caspase-1
physiological function
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cathepsins B and D drive hepatic stellate cell proliferation and promote their fibrogenic potential
physiological function
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cathepsins B and D drive hepatic stellate cell proliferation and promote their fibrogenic potential, the enzyme is required for transdifferentiation of the cells into myofibroblasts, overview. CtsB modulates the phosphoinositide 3-kinase/AKT pathway in activated mouse hepatic stellate cells, overview
physiological function
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CmCatB has a unique role in insect adaptation to the effect of dietary scN. Cowpea bruchids dramatically induce CmCatB expression when major digestive proteases are inactivated by dietary scN, which is presumably an adaptive strategy that insects use to minimize effects of nutrient deficiency
physiological function
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CTSB is a lysosomal cysteine protease primarily involved in the degradation or processing of lysosomal proteins
physiological function
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in case of inflammation of the urethra and cervix after Neisseria gonorrhoeae infection, cathepsin B is an apical controlling step in the downstream activities of NLRP3 including interleukin-1beta production, pyronecrosis, and HMGB1 release. NLRP3 mediates cell death in B-lymphocytes and THP-1 cells
physiological function
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infection with Neisseria gonorrhoeae induces cathepsin B in apical controlling of the downstream activities of NLRP3 including interleukin-1beta production, pyronecrosis, and HMGB1 release. NLRP3 mediates cell death in B-lymphocytes and macrophages, overview
physiological function
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proteases play a major role in the invasion process with correlations between glioma grading, survival and protease expression. Cathepsin B is involved in extracellular matrix degradation in glioblastomas, and in invasion and angiogenesis, overview
physiological function
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the cysteine protease CatB facilitates insects coping with dietary protease inhibitor challenge
physiological function
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the endopeptidase activity of cathepsin B is associated with the degradation of the extracellular matrix proteins, which is a process required for tumor cell invasion and metastasis, the activity can be inhibited by the 2A2 monoclonal antibody
physiological function
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the FhcatB1 protease functions largely as a digestive enzyme in the gut of the parasite. It may be likely important to a vital stage of the parasite's life cycle
physiological function
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the TLR9 ligand CpG DNA inhibits the proliferation of pro-B, but not pre-B, cells by inducing caspase-independent cell death through a pathway that requires the expression of cathepsin B, mechanism, overview
physiological function
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TiO2-induced interleukin-1beta production depends on active cathepsin B and reactive oxygen species production
physiological function
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cathepsin B is involved in cuticle renewal
physiological function
cathepsin B is involved in host immune response during bacterial infection and vaccination
physiological function
cathepsin B is involved in the nutrient digestion of Meretrix meretrix
physiological function
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cathepsin B plays a role in doxorubicin-induced cell death
physiological function
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cathepsin B plays a role in the metabolism of amyloid precursor protein. Cathepsin B is a major CTF- and AICD-degrading enzyme with no effect on alpha- and beta-secretase activities
physiological function
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cathepsin B proteinase plays roles in the early development of Ancylostoma caninum
physiological function
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the enzyme has stimulatory effects on embryonic development, metamorphosis, and larval growth during larval development
physiological function
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Atg7-induced CTSB overexpression contributes to an NLRP3-dependent proinflammatory response and subsequently impairs glucose-stimulated insulin secretion independently of apoptosis
physiological function
cathepsin B activates both caspase-9 and caspase-3
physiological function
cathepsin B is involved in hyperthermic injury-induced cardiomyocyte apoptosis in H9C2 cells and HSP-70 protects these cells from hyperthermic injury-induced cardiomyocyte apoptosis through cathepsin B pathways
physiological function
CsCBs are immune triggers during Clonorchis sinensis infection
physiological function
extracellular cathepsin B is involved in cell invasion whereas intracellular cathepsin B controls tumoral properties of colorectal cancer cells
physiological function
present results implicate cathepsin B activity as one of the possible pathways that are responsible for heat shock-induced apoptosis in bovine cumulus-oocyte complexes
physiological function
sensitivity to mHgIA is linked to an early cathepsin B regulated inflammatory response which is necessary for the subsequent adaptive autoimmune response leading to disease
physiological function
cathepsin B can modulate autophagy processes in adipocytes
physiological function
cathepsin B is essential for the development and pathogenesis of the plant parasitic nematode Radopholus similis
physiological function
exosomal cathepsin B regulates the receptor for advanced glycation end-products (RAGE) in type 1 alveolar cells under conditions of oxidative stress
physiological function
involved in tumour progression
physiological function
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role for maternal Ctsba in dorsoventral patterning and morphogenesis. Ctsba is required in distinct developmental processes to promote epiboly progression through modulation of the YCL cytoskeleton and promotes dorsoventral axial patterning upstream of BMP signaling. The role for Ctsba in morphogenesis is complex because Ctsba has BMP-dependent functions in DV patterning and probably also convergent-extension cell movements, but it also has BMP-independent functions necessary for the cytoskeletal organization underlying epiboly. Ctsba might modulate the ECM, regulate Ints6 or transcription factors such as Pou5f3, which have similar patterning and epiboly defects, or modulate other components to regulate early morphogenesis and epiboly
physiological function
the enzyme could be stable and highly active in the endolysosomal pathway degrading endocytosed peptides predigested by cathepsin L in the gut lumen whereas as a secreted protease it might be short lived but still stimulating an immune response. Due to its exopeptidase activity it could be involved in the regulative processing of other proteins. It is not involved in the immediate infection process
physiological function
the enzyme has critical role as activators of proinflammatory caspases-11 and the regulatory effect in LPS-induced caspases-11-dependent necrosis
physiological function
the enzyme is an important immune factor
physiological function
the enzyme is involved in intracellular proteolysis within lysosomes. Increased activity and expression are strongly associated with many pathological processes, including cancers
physiological function
the enzyme is likely to be involved in the immune reaction
physiological function
the enzyme is upregulated and mediates extracellular matrix degradation in colon adenocarcinoma HT29 cells overexpressing Snail (a key regulator of the extracellular matrix degradation). It is hypothesized that cathepsin B controls extracellular matrix proteolysis related to mesenchymal migration in colon cancer cells at early stages of the epithelial-to-mesenchymal transition
physiological function
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the enzyme might play an important role in defending against the pathogenes infection
physiological function
the main functions are the turnover of cellular proteins, the regulation of angiogenesis, invasion, tumor proliferation and immune resistance, neurogenesis, cellular differentiation and tumor response to hypoxia. Cathepsin B plays a protective role by degrading excessive amounts of misfolded protein inside the cell. In humans, the levels of cathepsin B correlates with hippocampal-dependent memory functions and can be increased by physical exercise. The decrease in the rate of neurogenesis in Alzheimer's disease can be secondary to the accumulation of the critical Alzheimer's disease proteins, which can be induced by inhibition of cathepsin B and the consequent the lysosomal dysfunction. The expression of cathepsin B is elevated in many, but not all, cancers
physiological function
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cathepsin B activity is necessary for TAP-HEL, a reduced and alkylated lysozyme, processing, it is essential for generation of the HEL-derived antigenic peptide recognized by B9.1 cells
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physiological function
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cathepsins B and D drive hepatic stellate cell proliferation and promote their fibrogenic potential, the enzyme is required for transdifferentiation of the cells into myofibroblasts, overview. CtsB modulates the phosphoinositide 3-kinase/AKT pathway in activated mouse hepatic stellate cells, overview
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physiological function
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CTSB is a lysosomal cysteine protease primarily involved in the degradation or processing of lysosomal proteins
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physiological function
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cathepsin B is required for interleukin-1beta maturation, the maturation of pro-IL-1beta in chromogranin A-stimulated microglia is dependent on the enzymatic activities of both cathepsin B and caspase-1
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additional information
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based on the use of proteinase inhibitors, cell death changes from being principally caspase-dependent to being principally cathepsin B-dependent, overview
additional information
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cathepsin B release after imatinib-mediated lysosomal membrane permeabilization triggers tyrosine kinase BCR-ABL cleavage and elimination of chronic myelogenous leukemia cells, overview
additional information
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coordination between transcription factors CmHNF-4 and CmSvp is important in counter-defense gene regulation in insects, overview
additional information
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increased CatB expression in malignant ovarian tumors might be balanced by a corresponding increase in inhibitor CysC, overview
additional information
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relation between cathepsin B activity and the quality of in vitro matured cumulus-oocyte complexes, IVM COCs, and denuded oocytes, overview
additional information
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secreted cathepsin Bs are involved in the pathogenesis of clonorchiasis
additional information
secreted cathepsin Bs are involved in the pathogenesis of clonorchiasis
additional information
secreted cathepsin Bs are involved in the pathogenesis of clonorchiasis
additional information
secreted cathepsin Bs are involved in the pathogenesis of clonorchiasis
additional information
the substrate peptide bond cleaved by cathepsin B (EC 3.4.22.1) and cathepsin L (EC 3.4.22.15) is determined not by the amino acid contributing the carboxyl group to this bond as in the case of serine proteases but rather by the presence of a neighboring amino acid with a large hydrophobic side chain, active center differences between cathepsins L and B in the S1 binding region, overview