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CTSB — TNF

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CTSB → TNF (increases) Lemaire et al., Br J Rheumatol 1997*
  Evidence: The addition of recombinant TNF-alpha to the cultured medium led to increased secretion of cathepsin B. The stimulating effect of TNF-alpha on the secretion of Cathepsin B by synovial fibroblast like cells appeared maximum at a concentration of 2ng/ml. TNF-alpha induced a 5 fold increase in cathepsin B secretion.
• OpenBEL Selventa BEL large corpus: CTSB → TNF (increases, TNF Translocation) Lemaire et al., Br J Rheumatol 1997*
  Evidence: Treatment of synovial fibroblast-like cells with TNF-alpha or PDGF resulted in a marked increase in cathepsin B secretion.

Text-mined interactions from Literome

Foghsgaard et al., J Cell Biol 2001 (Fibrosarcoma) : In WEHI-S fibrosarcoma cells, tumor necrosis factor (TNF) induced an increase in cytosolic cathepsin B activity followed by death with apoptotic features
Foghsgaard et al., J Biol Chem 2002 (Breast Neoplasms...) : Furthermore, TNF induced cathepsin B-dependent AA release could be dissociated from the cathepsin B-independent cell death in MCF-7S1 cells, whereas both events required cathepsin B activity in other cell lines tested
Nakayama et al., Cell Biol Int 2004 (Osteosarcoma) : We used RT-PCR to examine the effects of TNF-alpha on bone sialoprotein ( BSP ), core binding factor a1 (Cbfa1), osterix, alpha 1 ( I ) collagen, cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), cathepsin B , cathepsin L and tissue inhibitors of metalloproteinase-1 ( TIMP-1 )
Dai et al., Sci China Life Sci 2011 (Fibrosarcoma) : It was found for the first time that TNF-a released from PEG-vcTNF-a was specifically dependent on the presence of cathepsin B
Dai et al., Sci China Life Sci 2013 (Neoplasms, Experimental) : Release of TNF-a from rPEG-TNF-a in vitro was dependent on the presence of cathepsin B and was inhibited by a cathepsin B inhibitor
Bíró et al., Eur J Clin Invest 1998 (Acute-Phase Reaction...) : These findings indicate that, except for regulation of the negative APPs by TNF-alpha , the mechanism of APP regulation is different under the conditions of the short-term and the chronic, long lasting ` acute-phase reaction '