◀ Back to IL6

CTSB — IL6

Text-mined interactions from Literome

Gerber et al., J Interferon Cytokine Res 2001 : The proinflammatory cytokine IL-6 induced an upregulation of cathepsin L, whereas TGF-beta 1 suppressed cathepsin B and L expression
Haeryfar et al., Cell Mol Biol Incl Cyto Enzymol 2001 (Acute-Phase Reaction) : The stimulation of APR activates the hypothalamic-pituitary-adrenal ( HPA ) axis, resulting in the suppression of specific immunity, which might serve to protect the organism from adverse immune reactions ; the immunostimulatory hormones ( e.g., PRL, GH, IGF-1 ) are suppressed, whereas the production of APPs in the liver is stimulated by IL-6 , catecholamines and GCs
Chae et al., Immunopharmacol Immunotoxicol 2007 (Second Messenger Systems) : When added to MG-63 cells, IL-6 stimulated the production of cathepsin B , which was reduced significantly by the addition of SB203580, a specific p38 MAPK inhibitor ... This strongly suggests that p38 MAPK and NF-kappaB are essential to the IL-6 induced activation of cathepsin B or uPA and that these two IL-6 activated pathways can act independently
Dziedzic et al., Frontiers in bioscience : a journal and virtual library 2008 (Acute Disease...) : IL-6 induces synthesis of the acute phase proteins (APPs) in the liver
Yamaguchi et al., J Cell Physiol 2008 (Periodontitis) : IL-6/sIL-6R enhances cathepsin B and L production via caveolin-1 mediated JNK-AP-1 pathway in human gingival fibroblasts ... In this study, we investigated the role of Cav-1 on ( 1 ) the productivity, and ( 2 ) the enzymatic activity of cathepsin B and L in human gingival fibroblasts ( HGFs ) treated with IL-6 in the presence of soluble form of IL-6 receptor ( sIL-6R ) ... Then, cell lysates were collected, and examined the IL-6 induced signaling pathway, cathepsin B and L production, and measurement of cathepsins activity ... We found that IL-6/sIL-6R enhanced significantly both production and activity of cathepsin B and L in HGFs. Interestingly, IL-6 mediated phosphorylation of both p44/42 MAPK and JNK was dramatically suppressed in Cav-1 down-regulated HGFs treated with IL-6/sIL-6R ... Importantly, we demonstrated that JNK inhibition, but not p44/42 MAPK inhibition, significantly diminished IL-6/sIL-6R induced cathepsin B and L production ... Taken together, we concluded that IL-6/sIL-6R enhances cathepsin B and L production via IL-6/sIL-6R mediated Cav-1-JNK-AP-1 pathway in HGFs
Quinton et al., Infect Immun 2009 (Escherichia coli Infections...) : Interleukin-6 (IL-6) deficiency inhibited the activation of STAT3 and the induction of select APPs in the livers of pneumonic mice
Mohamed et al., Cell Physiol Biochem 2010 (Breast Neoplasms) : Our data suggest a role for IL-6 in increased monocyte expression and secretion of CTSB in response to soluble factors secreted by breast cancer cells
Ebisui et al., Clin Sci (Lond) 1995 : Interleukin-6 ( 100 units/ml ) increased the activity of 26S proteasome by 31.5 %, of cathepsin B by 53.5 % and of cathepsin B+L by 21.3 %
Scotté et al., Cytokine 1997 : Moreover, these specific changes of cytokine gene expression seen in the liver following major hepatectomy might reflect a preferential activation of the IL-6 dependent APPs
Li et al., Eur J Pharmacol 1998 (Multiple Sclerosis) : Production of tumor necrosis factor-alpha and the lysosomal cysteine proteinase cathepsin B were markedly inhibited, but production of interleukin-1 increased