CCL

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1.

001-es BibID:BIBFORM042386
Első szerző:De Luca, Luigi M.
Cím:Vitamin A in epithelial differentiation and skin carcinogenesis / De Luca L. M., Darwiche N., Celli G., Kosa K., Jones C., Ross S., Chen L. C.
Dátum:1994
ISSN:0029-6643
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Nutrition Reviews 52 : 2 Pt2 (1994), p. S45-S52. -
További szerzők:Darwiche, Nadine Celli, Giulia Kósa Karolina (1962-) (népegészségügyi szakember) Jones, Carol Ross, Sharon Chen, Li-Chuan
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

001-es BibID:BIBFORM042358
Első szerző:De Luca, Luigi M.
Cím:The role of vitamin A in differentiation and skin carcinogenesis / De Luca Luigi M., Kósa Karolina, Andreola Fausto
Dátum:1997
Megjegyzések:The field of vitamin A research has witnessed a remarkable surge in interest since the late 1980's, when the retinoid receptors were discovered and their genes cloned. Heterodimeric interactions between the retinoid X receptors (RXRs α, β, and γ), which bind 9-cis-retinoic acid, and other hormone receptors, including the retinoic acid receptors (RARs α, β, and γ), the thyroid hormone receptor (TR), the vitamin D receptor (VDR), the peroxisomal proliferator activated receptor (PPAR), and others make hormone action dependent on retinoid homeostasis. Retinoid response elements (RAREs) are present in the promoter and/or enhancer regions of several genes, including some of the homeobox genes, which control development and differentiation. The interaction between hormones and retinoids is added additional orders of complexity by the diversity of the RAREs including the spacer length, their 5' or 3' position, and their coexistence in composite sequences with other hormone response elements (e.g., an estrogen response element in the lactablbumin gene promoter, see Table 2). Control of normal epithelial differentiation is a fundamental function of retinoids. The histogenesis of squamous metaplasia caused by vitamin A deficiency is a stepwise process, which permits the gradual transition of phenotypes from simple-columnar, typical of the endocervical epithelium, to pseudostratified, to stratified-squamous and, eventually, to keratinizing. Conversely, the maintenance of the squamous keratinizing differentiation in the ectocervix and vagina requires estrogen. In the absence of this hormone, the squamous stratified ectocervical epithelium retrogrades to a simpler, two or three cell layer morphology, with the topmost layer expressing keratin K8, typical of the endocervical epithelium and mucous cells. Retinoid and estrogen receptor transcript expression is governed by dietary retinoid status and by estrogen availability, with squamous cells mostly expressing RARγ and estrogen receptor transcripts, and columnar cells mostly expressing RARβ. RXR transcripts appear mostly expressed in proliferating cells. The relevance of the retinoid receptors to carcinogenesis is highlighted in the work on acute promyelocytic leukemia. This work has demonstrated that the fusion gene PML-RARα, resulting from the t(15;17) chromosomal translocation, is etiologically connected with the disease and with complete remission after oral retinoid administration. Developments in retinoid metabolism, including the cloning of the cytochrome P450RAI and the connection between RA metabolism and cell growth inhibition, have recently taken place. Recent work has also shown that pharmacological dietary retinoic acid specifically inhibits malignant conversion in the mouse two-stage carcinogenesis system. Because RA upregulates retinoid receptor expression, it seems that retinoid receptors function as tumor suppressors. p]This field should serve as a paradigm for things to come for other essential nutrients, and spells out the notion that nutritional sciences are indeed fundamentally important, because they can contribute significantly to our understanding of different diseases and provide effective therapeutic approaches.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
retinoic acid
estrogen
nuclear receptors
differentiation
carcinogenesis
epithelium
Megjelenés:Journal of Nutritional Biochemistry. - 8 : 8 (1997), p. 426-437. -
További szerzők:Kósa Karolina (1962-) (népegészségügyi szakember) Andreola, Fausto
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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3.

001-es BibID:BIBFORM042369
Első szerző:Kósa Karolina (népegészségügyi szakember)
Cím:Transformation of NIH3T3 cells with ras oncogenes abrogates the retinoic acid induction of tissue transglutaminase / Kósa K., Meyers K., De Luca L. M.
Dátum:1993
ISSN:0006-291X
Megjegyzések:Retinoic acid greatly increases enzyme activity and mRNA expression of the tissue-type transglutaminase enzyme in NIH3T3 cells. This response is blocked in cells transformed with activated H-ras, K-ras or N-ras oncogenes, but not in pSVneo vector transfected cells. Lack of induction by RA of the tissue-type TGase in these ras-transformed fibroblasts suggests intersecting pathways between retinoid action and the ras oncogene.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biochemical and Biophysical Research Communications. - 196 : 3 (1993), p. 1025-1033. -
További szerzők:Meyers, Kim De Luca, Luigi M.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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4.

001-es BibID:BIBFORM006415
Első szerző:Kósa Karolina (népegészségügyi szakember)
Cím:TPA induces transglutaminase C and inhibits cell growth in the colon carcinoma cell line SW620 / Kosa, K., Rosenberg, M. I., Chiantore, M. V., De Luca, L. M.
Dátum:1997
ISSN:0006-291X (Print)
Megjegyzések:In contrast to most other systems, TPA induced TGc activity and protein in SW620 human colon carcinoma cells. This induction was accompanied by cell growth inhibition and increased apoptosis. The general protein kinase-C inhibitor GF-109203X blocked the induction of TGc by TPA, whereas the specific inhibitor of the PKC alpha isoform, the indocarbazole Go6976, reduced it by 40%. These PKC inhibitors had similar inhibitory effects on TPA increased apoptosis and inhibition of cell growth, suggesting that the observed actions of TPA are mediated by PKC, and a close connection between TGc activity, increased apoptosis and cell growth inhibition. We conclude that TPA may offer new approaches in the management of colon cancer cell growth.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Apoptosis/drug effects
Cell Division/ drug effects
Colonic Neoplasms/ drug therapy/ enzymology/pathology
Dose-Response Relationship, Drug
Enzyme Activation/drug effects
Enzyme Induction/drug effects
Humans
Protein Kinase C/metabolism
Tetradecanoylphorbol Acetate/administration & dosage/ pharmacology
Thymidine/metabolism
Transglutaminases/ biosynthesis
Tumor Cells, Cultured
Megjelenés:Biochemical and Biophysical Research Communications. - 232 : 3 (1997), p. 737-741. -
További szerzők:Rosenberg, M. I. Chiantore, M. V. De Luca, Luigi M.
Internet cím:elektronikus változat
elektronikus változat
DOI
Borító:

5.

001-es BibID:BIBFORM006413
Első szerző:Kósa Karolina (népegészségügyi szakember)
Cím:The H-ras oncogene interferes with retinoic acid signaling and metabolism in NIH3T3 cells / Kosa, K., Jones, C. S., De Luca, L. M.
Dátum:1995
ISSN:0008-5472 (Print)
Megjegyzések:We have previously shown that retinoic acid (RA) fails to induce transglutaminase C in H-ras transformed NIH-3T3 cells. Therefore, we investigated the effect of the H-ras oncogene on the metabolism of RA and on the expression of the cellular RA-binding protein I mRNA. HPLC analysis of the media and cell extracts demonstrated that H-ras-transformed cells metabolize RA to a much lesser extent than control cells, resulting in a higher concentration of RA in H-ras cells. Although inactive in endogenous transglutaminase induction, H-ras cell-associated RA was shown to be biologically available to induce activation of a reporter construct containing a retinoid response element and in stimulating transglutaminase activity in nontransfected cells. Cellular RA-binding protein I mRNA, supposedly involved in RA storage, was significantly increased in the H-ras-transformed cells. These data demonstrate that, even though H-ras-transformed cells accumulate up to 20 fold the concentration of RA as NIH-3T3 cells, they fail to show transglutaminase induction, suggesting that H-ras interferes with signal transduction by RA.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
3T3 Cells/drug effects/physiology
Animals
Base Sequence
Chromatography, High Pressure Liquid
Culture Media
Gene Expression Regulation/drug effects
Genes, Reporter
Genes, ras/drug effects/ physiology
Mice
Molecular Sequence Data
RNA, Messenger/genetics
Receptors, Retinoic Acid/genetics
Signal Transduction/drug effects/ physiology
Transfection
Tretinoin/ metabolism/ pharmacology
Tritium
Megjelenés:Cancer Research. - 55 : 21 (1995), p. 4850-4854. -
További szerzők:Jones, C. S. De Luca, Luigi M.
Internet cím:elektronikus változat
elektronikus változat
Borító:
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