Biofactors - Volume 15, issue 2-4

Authors: Robino, Gaia | Zamara, Elena | Novo, Erica | Dianzani, Mario Umberto | Parola, Maurizio

Article Type: Research Article

Citation: BioFactors, vol. 15, no. 2-4, pp. 103-106, 2001

Authors: Yodoi, Junji | Masutani, Hiroshi | Nakamura, Hajime

Article Type: Research Article

Citation: BioFactors, vol. 15, no. 2-4, pp. 107-111, 2001

Authors: Pineda-Molina, Estela | Lamas, Santiago

Article Type: Research Article

Abstract: Both oxidative and nitrosative stresses may result in the inactivation of the binding to DNA of redox-sensitive transcription factors. The underlying biochemical mechanisms may involve oxidation or nitrosylation of critical thiols within the DNA binding domains of these proteins. However, S-glutahionylation, the formation of a mixed disulfide between glutathione and the redox-sensitive cysteine residues, has been shown to occur under NO exposure and pro-oxidative conditions in c-Jun, one of the AP-1 constituents …[1,2]. This modification may be functionally important as it is reversible and has been detected in other transcription factors, such as NF-κB, by using covalent chromatography with a modified S-nitrosoglutathione sepharose [3]. Show more

Citation: BioFactors, vol. 15, no. 2-4, pp. 113-115, 2001

Authors: Leonarduzzi, Gabriella | Sevanian, Alex | Poli, Giuseppe

Article Type: Research Article

Abstract: Oxidatively modified low density lipoproteins (oxLDL) are known to affect various cellular processes by modulating molecolar transduction pathways and signaling nuclear transcription [1,2]. In particular, the proinflammatory and proatherosclerotic effects of oxLDL are increasingly supported by a multitude of independent but consistent experimental studies. LDL oxidation might be a sequencial process where their lipid moieties are progressively but discretely oxidized, preceding the oxidation/modification of the apolipoprotein domain, an effect that can ultimately …result in the uncontrolled uptake of these particles by cells, such as macrophages, and conversion of them to foam cells which is a hallmark of early atherogenesis [3]. These lipoproteins appear to trigger a variety of events which are strongly implicated in the atherogenesis, the pathological process underlying vascular disease. Show more

Citation: BioFactors, vol. 15, no. 2-4, pp. 117-119, 2001

Authors: Jackson, Malcolm J. | Spiers, Susan | McArdle, Anne

Article Type: Research Article

Citation: BioFactors, vol. 15, no. 2-4, pp. 121-122, 2001

Authors: Suzuki, Hisanori | Colasanti, Marco

Article Type: Research Article

Citation: BioFactors, vol. 15, no. 2-4, pp. 123-125, 2001