Literature DB >> 15788001

Neutrophil serine proteases: potential key regulators of cell signalling during inflammation.

O Wiedow1, U Meyer-Hoffert.   

Abstract

The serine proteases cathepsin G, human leucocyte elastase and proteinase 3 are major contents of neutrophils and are released at sites of inflammation. The common picture of their function was that they do not degrade extracellular proteins specifically. Recent studies provided evidence that these proteases are able to activate specifically pro-inflammatory cytokines and lead to the activation of different receptors. Neutrophil serine proteases might therefore be important regulators of inflammatory processes and are interesting targets for new therapeutic approaches against inflammatory disorders. This review summarizes the current knowledge on the regulation of cell signalling by neutrophil serine proteases.

Entities:  

Mesh:

Substances:

Year:  2005        PMID: 15788001     DOI: 10.1111/j.1365-2796.2005.01476.x

Source DB:  PubMed          Journal:  J Intern Med        ISSN: 0954-6820            Impact factor:   8.989


  53 in total

Review 1.  Neutrophil elastase, proteinase 3, and cathepsin G as therapeutic targets in human diseases.

Authors:  Brice Korkmaz; Marshall S Horwitz; Dieter E Jenne; Francis Gauthier
Journal:  Pharmacol Rev       Date:  2010-12       Impact factor: 25.468

2.  Pro-inflammatory feedback activation cycle evoked by attack of Vibrio cholerae cytolysin on human neutrophil granulocytes.

Authors:  Angela Valeva; Ivan Walev; Silvia Weis; Fatima Boukhallouk; Trudy M Wassenaar; Sucharit Bhakdi
Journal:  Med Microbiol Immunol       Date:  2007-09-20       Impact factor: 3.402

3.  Modulation of neutrophil motility by curcumin: implications for inflammatory bowel disease.

Authors:  C B Larmonier; M T Midura-Kiela; R Ramalingam; D Laubitz; N Janikashvili; N Larmonier; F K Ghishan; P R Kiela
Journal:  Inflamm Bowel Dis       Date:  2011-02       Impact factor: 5.325

4.  Dual inhibition of cathepsin G and chymase reduces myocyte death and improves cardiac remodeling after myocardial ischemia reperfusion injury.

Authors:  Bahman Hooshdaran; Mikhail A Kolpakov; Xinji Guo; Sonni A Miller; Tao Wang; Douglas G Tilley; Khadija Rafiq; Abdelkarim Sabri
Journal:  Basic Res Cardiol       Date:  2017-09-14       Impact factor: 17.165

5.  Localized Cell-Surface Sampling of a Secreted Factor Using Cell-Targeting Beads.

Authors:  Tammi L van Neel; Samuel B Berry; Erwin Berthier; Ashleigh B Theberge
Journal:  Anal Chem       Date:  2020-10-02       Impact factor: 6.986

6.  NETosis Occurs Independently of Neutrophil Serine Proteases.

Authors:  Paulina Kasperkiewicz; Anne Hempel; Tomasz Janiszewski; Sonia Kolt; Scott J Snipas; Marcin Drag; Guy S Salvesen
Journal:  J Biol Chem       Date:  2020-10-15       Impact factor: 5.157

7.  Protective Effects of Chymostatin on Paraquat-Induced Acute Lung Injury in Mice.

Authors:  Chen Yang; Hong-Wei Song; Wei Liu; Xue-Song Dong; Zhi Liu
Journal:  Inflammation       Date:  2018-02       Impact factor: 4.092

8.  c-Cbl ubiquitin ligase regulates focal adhesion protein turnover and myofibril degeneration induced by neutrophil protease cathepsin G.

Authors:  Khadija Rafiq; Jianfen Guo; Liudmila Vlasenko; Xinji Guo; Mikhail A Kolpakov; Archana Sanjay; Steven R Houser; Abdelkarim Sabri
Journal:  J Biol Chem       Date:  2011-12-27       Impact factor: 5.157

9.  Bcr and Abr cooperate in negatively regulating acute inflammatory responses.

Authors:  Jess M Cunnick; Sabine Schmidhuber; Gang Chen; Min Yu; Sun-Ju Yi; Young Jin Cho; Vesa Kaartinen; Parviz Minoo; David Warburton; John Groffen; Nora Heisterkamp
Journal:  Mol Cell Biol       Date:  2009-08-24       Impact factor: 4.272

10.  Cathepsin G, a neutrophil protease, induces compact cell-cell adhesion in MCF-7 human breast cancer cells.

Authors:  Tomoya Kudo; Hideaki Kigoshi; Takashi Hagiwara; Takahisa Takino; Masatoshi Yamazaki; Satoru Yui
Journal:  Mediators Inflamm       Date:  2009-11-10       Impact factor: 4.711

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.