THEORETICAL MECHANISMS FOR SYNTHESIS OF CARCINOGEN-INDUCED EMBRYONIC PROTEINS .17. HETEROCHROMATIN MECHANISMS

AudienciaPúblico en generales_ES
CoberturaMéxicoes_ES
Fecha de ingreso2026-10-05T16:32:32Z
Fecha de publicación1987-01-01
ResumenA mechanism for induced embryonic gene expression via a process of deheterochromatization using a model carcinogen has been derived. First ethionine becomes activated to S-adenosyl-L-ethionine which inhibits the methylation of nicotinamide, a resulting product of polyADP-ribose polymerase. This causes hyporibosylated nucleosome core histones which normally would base pair by virtue of the adenine moieties with thymidine-rich regions of DNA, being the precursor of heterochromatin. Thus in the anomalous state a deheterochromatized condition of embryonic genes would be created. Possibly embryonic genes are dispersed in AT-rich regins potentially capable of becoming hyperspiralized by this process. Repressable embryonic genes would not be inactivated. It was also noted that hyomethylated non-histone chromatin proteins cause an extension of the nucleosome chains which would also favor the above situation. This mechanism explains our experimental findings of the relatively rapid reversal of ethionine induced alpha-fetoprotein levels by methionine. The process of heterochromatization is hypothesized to be induced by short (pentanucleotides) moieties of poly(ADP-ribose), formed on core histones, that hydrogen bond to thymidine rich inter Nu body DNA.es_ES
Doihttps://doi.org/10.1016/0306-9877(87)90056-9es_ES
URIhttps://riuat.uat.edu.mx/handle/123456789/4362
Idiomaenes_ES
EditorialELSEVIERes_ES
RelaciónMedical Hypotheseses_ES
URL relacionadohttps://doi.org/10.1016/0306-9877(87)90056-9es_ES
DerechosAcceso restringido / Suscripción (Metadatos de producción científica)es_ES
Licenciahttp://purl.org/coar/access_right/c_16eces_ES
FuenteMedical Hypotheses
TítuloTHEORETICAL MECHANISMS FOR SYNTHESIS OF CARCINOGEN-INDUCED EMBRYONIC PROTEINS .17. HETEROCHROMATIN MECHANISMSes_ES
TipoArtículoes_ES
ArbitradoHa sido Arbitradoes_ES
AutorHANCOCK, RL
AutorHANCOCK, RLes_ES
InstituciónUniversidad Autónoma de Tamaulipas
InstituciónUniversidad Autónoma de Tamaulipases_ES
Número4es_ES
Rango de páginas363-369es_ES
URL relacionadahttps://doi.org/10.1016/0306-9877(87)90056-9
Tipo de artículoIndexado
Tipo de artículoIndexadoes_ES
Volumen23es_ES

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