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PRTN3 — TNF

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: PRTN3 — TNF (in vivo) Coeshott et al., Proc Natl Acad Sci U S A 1999*
• IRef Ophid Interaction: PRTN3 — TNF (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: PRTN3 — TNF (aggregation, confirmational text mining) Coeshott et al., Proc Natl Acad Sci U S A 1999*

Text-mined interactions from Literome

Yard et al., Clin Exp Immunol 2002 (Wegener Granulomatosis) : Human proteinase 3 can inhibits LPS mediated TNF-alpha production through CD14 degradation : lack of influence of antineutrophil cytoplasmic antibodies
Ohlsson et al., Clin Exp Immunol 2005 (Lupus Erythematosus, Systemic...) : Stimulation of monocytes with tumour necrosis factor (TNF)-alpha , interferon (IFN)-gamma or LPS did not result in any increase of PR3 or elastase transcription, whereas interleukin (IL)-8 transcription was increased 10-fold
Hsieh et al., Clin Rheumatol 2007 : The spontaneous membrane expression of MPO and PR3 on PMN could be significantly increased by lipopolysaccharide (LPS) and TNF-alpha , but not by IL-8 or GRO-alpha
Ammar et al., Cell Immunol 1993 (HIV Infections) : In addition, p29 could not inhibit the production of IL1 and TNF alpha by normal adherent cells
Mayet et al., Blood 1993 (Wegener Granulomatosis) : We were able to show that tumor necrosis factor-alpha , interleukin-1 alpha/beta, and interferon-gamma led to an increased PR-3 expression in the cytoplasm of endothelial cells by performing polymerase chain reaction analysis, Western blot, cyto-enzyme linked immunosorbent assays, and confocal laser scanning microscopy
Mayet et al., Eur J Clin Invest 1997 : Membrane expressed PR-3 was detected by affinity purified and monoclonal anti-PR-3 Ab. Tumour necrosis factor alpha (TNF-alpha) induced membrane expression of PR-3 could be blocked with the RNA synthesis inhibitor actinomycin D, the protein kinase C ( PKC ) and proteinase A ( PKA ) inhibitor staurosporine, the specific PKA inhibitor calphostin C, the c-AMP dependent PKA inhibitor KT5720 and the tyrosine kinase inhibitor genistein in a dose dependent manner ... This effect, however, could be overridden by TNF-alpha stimulation, i.e. TNF-alpha induced membrane expression of PR-3 was resistant to down-regulation of PKC