Show simple item record

Authordc.contributor.authorCárdenas, César 
Authordc.contributor.authorLiberona Leppe, José es_CL
Authordc.contributor.authorMolgó, Jordi es_CL
Authordc.contributor.authorColasante, Cesare es_CL
Authordc.contributor.authorMignery, Gregory es_CL
Authordc.contributor.authorJaimovich Pérez, Enrique es_CL
Admission datedc.date.accessioned2007-04-18T16:21:48Z
Available datedc.date.available2007-04-18T16:21:48Z
Publication datedc.date.issued2005-07-15
Cita de ítemdc.identifier.citationJOURNAL OF CELL SCIENCE 118 (14): 3131-3140 JUL 15 2005en
Identifierdc.identifier.issn0021-9533
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/127096
Abstractdc.description.abstractSeveral lines of evidence indicate that increases in nuclear Ca2+ have specific biological effects that differ from those of cytosolic Ca2+, suggesting that they occur independently. The mechanisms involved in controlling nuclear Ca2+ signaling are both controversial and still poorly understood. Using hypotonic shock combined with mechanical disruption, we obtained and characterized a fraction of purified nuclei from cultured rat skeletal myotubes. Both immunoblot studies and radiolabeled inositol 1,4,5-trisphosphate [IP3] binding revealed an important concentration Of IP3 receptors in the nuclear fraction. Immunofluorescence and immunoelectron microscopy studies localized type-1 and type-3 IP3 receptors in the nucleus with type-1 receptors preferentially localized in the inner nuclear membrane. Type-2 IP3 receptor was confined to the sareoplasmic reticulum. Isolated nuclei responded to IP3 with rapid and transient Ca2+ concentration elevations, which were inhibited by known blockers Of IP3 signals. Similar results were obtained with isolated nuclei from the 1B5 cell line, which does not express ryanodine receptors but releases nuclear Ca2+ in an IP3-dependent manner. Nuclear Ca2+ increases triggered by IP3 evoked phosphorylation of cAMP response element binding protein with kinetics compatible with sequential activation. These results support the idea that Ca2+ signals, mediated by nuclear IP3 receptors in muscle cells, are part of a distinct Ca2+ release component that originates in the nucleus and probably participates in gene regulation mediated by cAMP response element binding protein.en
Lenguagedc.language.isoenen
Publisherdc.publisherCOMPANY OF BIOLOGISTS LTDen
Keywordsdc.subjectSKELETAL-MUSCLE CELLSen
Títulodc.titleNuclear inositol 1,4,5-trisphosphate receptors regulate local Ca2+ transients and modulate cAMP response element binding protein phosphorylationen
Document typedc.typeArtículo de revista


Files in this item

Icon

This item appears in the following Collection(s)

Show simple item record