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dc.contributor.authorPennypacker, K.es
dc.date.accessioned2011-02-22T10:42:46Z-
dc.date.available2011-02-22T10:42:46Z-
dc.date.issued1997-
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/19017-
dc.description.abstractAfter brain injury, neuronal genes are regulated to adjust to an altered environment; however, if neurons are damaged then genes related apoptosis are activated. Glial cells, astrocytes and microglia, respond to neuronal death by transcribing genes to enhance the survival of remaining neurons and for regeneration and repair. AP-1 transcription factors are induced in the neuronal response to injury. Depending on the AP-1 dimer combination, neuronal genes related to either apoptosis or survival are transcribed. A 35 kDa Fosrelated antigen:JunD dimer is present in neurons that survive injury. Jun and JunD exists in neurons prior to undergoing apoptosis. Neuronal death activates gene expression in astrocytes and microglia. NFkB transcription factors are induced in astrocytes reacting to neuronal injury. In the microglial response, STATs appear to be activated to regulate gene transcription. These transcription factors that modulate the genes involved in the cellular processes of brain injury are examined in this review.es
dc.formatapplication/pdfes
dc.format.extent9es
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectNeuronal apoptosises
dc.subjectMicrogliaes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::615 - Farmacología. Terapéutica. Toxicología. Radiologíaes
dc.titleTranscription factors in brain injuryes
dc.typeinfo:eu-repo/semantics/articlees
Aparece en las colecciones:Vol.12, nº 4 (1997)

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