981 resultados para Aa2024-t3
Resumo:
En el artículo se presenta un modelo continuo y determinista de la actividad proliferativa celular. Sobre dicho modelo básico se aplican sucesivos refinamientos que tienen por objeto mejorar el ajuste a datos experimentales existentes. La base experimental del método son los ensayos realizados sobre el pez Cauratus aclimatado a 25 grados con un fotoperiodo de 12 horas durante un mes. Se analizó la actividad proliferativa en las células intestinales observando que aquélla es parcialmente sincronizada. Las medidas efectuadas y su contraste con el método propuesto sugieren que el modelo determinista y contínuo es una aproximación adecuada a la interpretación del ciclo evolutivo. Los resultados numéricos sugieren un comportamiento circadiano también para los tiempos de tránsito en las fases. Las amplitudes se ajustan observando los mínimos de las curvas y la fase se induce mediante análisis armónico de la tendencia general.
Resumo:
Peroxisome proliferators cause rapid and coordinated transcriptional activation of genes encoding peroxisomal beta-oxidation system enzymes by activating peroxisome proliferator-activated receptor (PPAR) isoform(s). Since the thyroid hormone (T3; 3,3',5-triiodothyronine) receptor (TR), another member of the nuclear hormone receptor superfamily, regulates a subset of fatty acid metabolism genes shared with PPAR, we examined the possibility of interplay between peroxisome proliferator and T3 signaling pathways. T3 inhibited ciprofibrate-induced luciferase activity as well as the endogenous peroxisomal beta-oxidation enzymes in transgenic mice carrying a 3.2-kb 5'-flanking region of the rat peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase gene fused to the coding region of luciferase. Transfection assays in hepatoma H4-II-E-C3 and CV-1 cells indicated that this inhibition is mediated by TR in a ligand-dependent fashion. Gel shift assays revealed that modulation of PPAR action by TR occurs through titration of limiting amounts of retinoid X receptor (RXR) required for PPAR activation. Increasing amounts of RXR partially reversed the inhibition in a reciprocal manner; PPAR also inhibited TR activation. Results with heterodimerization-deficient TR and PPAR mutants further confirmed that interaction between PPAR and TR signaling systems is indirect. These results suggest that a convergence of the peroxisome proliferator and T3 signaling pathways occurs through their common interaction with the heterodimeric partner RXR.
