Cell-type-specific and developmental regulation of heterogeneous nuclear ribonucleoprotein K mRNA in the rat nervous system
Department of Psychiatry, Brudnick Neuropsychiatric Research Institute
Medical Subject Headings
Animals; Central Nervous System; Female; Heterogeneous-Nuclear Ribonucleoprotein K; Hippocampus; Immunohistochemistry; Organ Specificity; Peripheral Nervous System; RNA, Messenger; Rats; Rats, Sprague-Dawley; Retina
Life Sciences | Medicine and Health Sciences | Neuroscience and Neurobiology
Heterogeneous nuclear ribonucleoprotein K (hnRNP K) was originally identified as being part of the hnRNP particle. hnRNP K has subsequently been shown to be involved in a number of fundamental biological processes such as RNA transport and processing as well as transcription and translation. In addition, hnRNP K is an integral player in a variety of intracellular signal transduction pathways. Not surprisingly given this broad array of cellular functions, hnRNP K is a highly interactive protein binding directly to both single- and double-stranded nucleic acids as well as numerous signaling proteins. Interestingly, earlier studies demonstrated that hnRNP K protein is not ubiquitously expressed and does not exist in a fixed stoichiometry with other hnRNP proteins. We have extended this earlier work and report here the spatially- and developmentally-regulated expression of hnRNP K mRNA during development of the rat nervous system. In the central nervous system, hnRNP K mRNA expression gradually decreases during development until it is restricted to a very limited number of structures including most notably the hippocampus and the retina. Immunohistochemical data indicate that hnRNP K protein expression closely parallels hnRNP K mRNA expression. In contrast to the central nervous system, hnRNP K in the peripheral nervous system remains high throughout embryonic development with dramatic expression in several peripheral ganglia.
Rights and Permissions
Citation: Gene Expr Patterns. 2006 Aug;6(6):596-606. Epub 2006 Feb 20. Link to article on publisher's site