1992
DOI: 10.1016/s0021-9258(18)42513-6
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Molecular cloning and expression of human alveolar macrophage cathepsin S, an elastinolytic cysteine protease.

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Cited by 296 publications
(50 citation statements)
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“…The effects of cathepsins on ECM expression therefore influence post-MI LV remodelling, while their participation in ECM catabolism may be less important than in other diseases, such as cancers or arterial diseases, including atherosclerosis and abdominal aortic aneurysms. 8,25 Proinflammatory macrophages and T-cells express high levels of cathepsins, 11,37 and these cells increased in the hearts of E64d-treated mice (Figure 3A and Supplementary material online, Figure S5), suggesting that the reduced cardiac cathepsin expression and activities did not result solely from increased infiltration of proinflammatory cells. Cardiomyocytes and fibroblasts in the infarcted myocardium also express CatS (Supplementary material online, Figure S1).…”
Section: Discussionmentioning
confidence: 98%
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“…The effects of cathepsins on ECM expression therefore influence post-MI LV remodelling, while their participation in ECM catabolism may be less important than in other diseases, such as cancers or arterial diseases, including atherosclerosis and abdominal aortic aneurysms. 8,25 Proinflammatory macrophages and T-cells express high levels of cathepsins, 11,37 and these cells increased in the hearts of E64d-treated mice (Figure 3A and Supplementary material online, Figure S5), suggesting that the reduced cardiac cathepsin expression and activities did not result solely from increased infiltration of proinflammatory cells. Cardiomyocytes and fibroblasts in the infarcted myocardium also express CatS (Supplementary material online, Figure S1).…”
Section: Discussionmentioning
confidence: 98%
“…The remaining JPM-binding material in Ctss -/mouse infarct regions likely represents CatK, which has the same molecular weight as CatS. 11,27 Areas remote from the MI did not contain CatS activity as detected by JPM binding (data not shown). Similar to that in E64d-treated mice at 28 days post-MI (Figure 3D), the collagen type I/III ratio fell significantly in Ctss -/mice due to the significantly increased collagen type III deposition in infarct areas, although the absence of CatS did not affect collagen type I deposition (Figure 7B).…”
Section: Cats Deficiency and Post-mi Cardiac Matrix Protein Expression And Myofibroblast Trans-differentiationmentioning
confidence: 91%
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“…This step forms the MHCII compartment (MIIC), which also carries HLA-DR, HLA-DM, LAMP-1 and the antigen (Cobb et al 2004). Acidification activates proteases within the MIIC, which processes the ZPS and cleaves the li leaving the CLIP peptide (cleaved form of li) in the binding groove of MHCII (Shi et al 1992(Shi et al , 1999. The acidic environment allows HLA-DM to catalyze the exchange of CLIP for antigenic peptides (Busch et al 1998).…”
Section: Processing and Presentation Of Zpssmentioning
confidence: 99%
“…Η καθεψίνη S (Εικ. 16) η οποία είναι μία πρωτεάση κυστεΐνης που αρχικά κλωνοποιήθηκε από ανθρώπινα κυψελιδικά μακροφάγα, εκφράζεται έντονα στο σπλήνα και σε κύτταρα όπως τα Β λεμφοκυττάρα, τα μακροφάγα, και άλλα τάξης II-θετικά κύτταρα ( Shi et al, 1992, Shi et al, 1994. Η καθεψίνη S είναι αναγκαία στα κύτταρα Β για την αποτελεσματική πρωτεόλυση της αλυσίδας II (Riese et al, 1996).…”
Section: καθεψίνη κunclassified