Non-genotoxic carcinogens: early effects on gap junctions, cell proliferation and apoptosis in the rat
- 25 September 2002
- journal article
- Published by Elsevier BV in Toxicology
- Vol. 180 (3), 233-248
- https://doi.org/10.1016/s0300-483x(02)00393-1
Abstract
No abstract availableKeywords
This publication has 44 references indexed in Scilit:
- Inhibition of apoptosis in rat hepatocytes treated with 'non-dioxin-like' polychlorinated biphenyls.Carcinogenesis: Integrative Cancer Research, 2001
- Carbon tetrachloride reduces connexin 32 expression in rat liver in vivo only in association with hepatotoxicityToxicology, 2000
- The cellular internet: On‐line with connexinsBioEssays, 1996
- Connections with Connexins: the Molecular Basis of Direct Intercellular SignalingJBIC Journal of Biological Inorganic Chemistry, 1996
- Inhibition of gap junctional intercellular communication by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rat hepatocytesCarcinogenesis: Integrative Cancer Research, 1995
- Suppression of liver cell apoptosis in vitro by the non-genotoxic hepatocarcinogen and peroxisome proliferator nafenopin.The Journal of cell biology, 1994
- The involvement of primary and secondary metabolism in the covalent binding of 1,2- and 1,4-dichlorobenzenesChemico-Biological Interactions, 1992
- Antisera directed against connexin43 peptides react with a 43-kD protein localized to gap junctions in myocardium and other tissues.The Journal of cell biology, 1989
- Induction of light hydrocarbon nephropathy by p-dichlorobenzeneArchives of Toxicology, 1988
- Major loss of the 28-kD protein of gap junction in proliferating hepatocytes.The Journal of cell biology, 1987