@article {712,
	title = {Association of caveolin with Chlamydia trachomatis inclusions at early and late stages of infection.},
	journal = {Exp Cell Res},
	volume = {266},
	year = {2001},
	month = {2001 Jun 10},
	pages = {229-38},
	abstract = {The mechanism by which the intracellular bacterial pathogen Chlamydia trachomatis enters eukaryotic cells is poorly understood. There are conflicting reports of entry occurring by clathrin-dependent and clathrin-independent processes. We report here that C. trachomatis serovar K enters HEp-2 and HeLa 229 epithelial cells and J-774A.1 mouse macrophage/monocyte cells via caveolin-containing sphingolipid and cholesterol-enriched raft microdomains in the host cell plasma membranes. First, filipin and nystatin, drugs that specifically disrupt raft function by cholesterol chelation, each impaired entry of C. trachomatis serovar K. In control experiments, filipin did not impair entry of the same organism by an antibody-mediated opsonic process, nor did it impair entry of BSA-coated microspheres. Second, the chlamydia-containing endocytic vesicles specifically reacted with antisera against the caveolae marker protein caveolin. These vesicles are known to become the inclusions in which parasite replication occurs. They avoid fusion with lysosomes and instead traffic to the Golgi region, where they intercept Golgi-derived vesicles that recycle sphingolipids and cholesterol to the plasma membrane. We also report that late-stage C. trachomatis inclusions continue to display high levels of caveolin, which they likely acquire from the exocytic Golgi vesicles. We suggest that the atypical raft-mediated entry process may have important consequences for the host-pathogen interaction well after entry has occurred. These consequences include enabling the chlamydial vesicle to avoid acidification and fusion with lysosomes, to traffic to the Golgi region, and to intercept sphingolipid-containing vesicles from the Golgi.},
	keywords = {Animals, Caveolin 1, Caveolins, Cell Line, Chlamydia trachomatis, Epithelium, Filipin, HeLa Cells, Humans, Inclusion Bodies, Macrophages, Membrane Microdomains, Mice, Nystatin, Phagosomes},
	issn = {0014-4827},
	doi = {10.1006/excr.2001.5202},
	author = {Norkin, L C and Wolfrom, S A and Stuart, E S}
}
@article {705,
	title = {Relationship between expression of epidermal growth factor and simian virus 40 T antigen in a line of transgenic mice.},
	journal = {Transgenic Res},
	volume = {4},
	year = {1995},
	month = {1995 Sep},
	pages = {306-14},
	abstract = {The pattern of expression of the simian virus 40 (SV40) T antigen gene and resultant dysplasia were re-examined in a line of transgenic mice in which the T antigen gene was under the control of the SV40 early promoter. We found that T antigen expression in the kidney, and resulting dysplastic lesions, occurred exclusively in the distal convoluted tubules and the ascending limbs of Henle. Epidermal growth factor (EGF) expression in the kidney of normal mice was similarly immunolocalized. The correlation between high EGF immunoreactivity in normal mouse tissues and T antigen expression in the transgenic counterpart was also seen in the choroid plexus epithelium and in the submandibular glands of male mice. T antigen was not found in the submandibular gland of transgenic females. Similarly, EGF was only rarely detected in the normal female submandibular gland. In contrast to the correlation between T antigen expression in the transgenic mice and EGF expression in the corresponding tissues of the normal mice, within the dysplastic lesions of the transgenic mice EGF expression was severely diminished. Adenocarcinomas of the male submandibular gland from another line of transgenic mice that expresses the Int-1 transgene, showed similarly reduced levels of immunostaining for EGF. Thus, reduced expression of EGF might be a general feature of dysplasia and tumorigenesis in those tissues that normally express EGF.},
	keywords = {Adenocarcinoma, Animals, Antigens, Viral, Tumor, Cattle, Choroid Plexus, Cricetinae, Epidermal Growth Factor, Female, Gene Expression Regulation, Neoplastic, Kidney, Kidney Tubules, Distal, Male, Mice, Mice, Transgenic, Proto-Oncogene Proteins, Simian virus 40, Submandibular Gland, Submandibular Gland Neoplasms, Wnt Proteins, Wnt1 Protein, Zebrafish Proteins},
	issn = {0962-8819},
	author = {Lafond, R E and Giammalvo, J T and Norkin, L C}
}
