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000136909 1001_ $$0P:(DE-HGF)0$$aGiesert, Florian$$b0
000136909 245__ $$aExpression analysis of Lrrk1, Lrrk2 and Lrrk2 splice variants in mice.
000136909 260__ $$aSan Francisco, California, US$$bPLOS$$c2013
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000136909 520__ $$aMissense mutations in the leucine-rich repeat kinase 2 gene (LRRK2) are linked to autosomal dominant forms of Parkinson's disease (PD). In order to get insights into the physiological role of Lrrk2, we examined the distribution of Lrrk2 mRNA and different splice variants in the developing murine embryo and the adult brain of Mus musculus. To analyse if the Lrrk2-paralog, Lrrk1, may have redundant functions in PD-development, we also compared Lrrk1 and Lrrk2 expression in the same tissues. Using radioactive in situ hybridization, we found ubiquitous expression of both genes at low level from embryonic stage E9.5 onward, which progressively increased up until birth. The developing central nervous system (CNS) displayed no prominent Lrrk2 mRNA signals at these time-points. However, in the entire postnatal brain Lrrk2 became detectable, showing strongest level in the striatum and the cortex of adult mice; Lrrk1 was only detectable in the mitral cell layer of the olfactory bulb. Thus, due to the non-overlapping expression patterns, a redundant function of Lrrk2 and Lrrk1 in the pathogenesis of PD seems to be unlikely. Quantification of Lrrk2 mRNA and protein level in several brain regions by real-time PCR and Western blot verified the striatum and cortex as hotspots of postnatal Lrrk2 expression. Strong expression of Lrrk2 is mainly found in neurons, specifically in the dopamine receptor 1 (DRD1a) and 2 (DRD2)-positive subpopulations of the striatal medium spiny neurons. Finally, we identified 2 new splice-variants of Lrrk2 in RNA-samples from various adult brain regions and organs: a variant with a skipped exon 5 and a truncated variant terminating in an alternative exon 42a. In order to identify the origin of these two splice variants, we also analysed primary neural cultures independently and found cell-specific expression patterns for these variants in microglia and astrocytes.
000136909 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000136909 542__ $$2Crossref$$i2013-05-10$$uhttp://creativecommons.org/licenses/by/4.0/
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000136909 650_7 $$2NLM Chemicals$$aRNA, Messenger
000136909 650_7 $$0EC 2.7.11.1$$2NLM Chemicals$$aLeucine-Rich Repeat Serine-Threonine Protein Kinase-2
000136909 650_7 $$0EC 2.7.11.1$$2NLM Chemicals$$aLrrk1 protein, mouse
000136909 650_7 $$0EC 2.7.11.1$$2NLM Chemicals$$aLrrk2 protein, mouse
000136909 650_7 $$0EC 2.7.11.1$$2NLM Chemicals$$aProtein-Serine-Threonine Kinases
000136909 650_2 $$2MeSH$$aAlternative Splicing
000136909 650_2 $$2MeSH$$aAnimals
000136909 650_2 $$2MeSH$$aBrain: metabolism
000136909 650_2 $$2MeSH$$aEmbryonic Development: genetics
000136909 650_2 $$2MeSH$$aGene Expression Profiling
000136909 650_2 $$2MeSH$$aGene Expression Regulation, Developmental
000136909 650_2 $$2MeSH$$aGene Order
000136909 650_2 $$2MeSH$$aLeucine-Rich Repeat Serine-Threonine Protein Kinase-2
000136909 650_2 $$2MeSH$$aMice
000136909 650_2 $$2MeSH$$aNeurons: metabolism
000136909 650_2 $$2MeSH$$aProtein-Serine-Threonine Kinases: genetics
000136909 650_2 $$2MeSH$$aProtein-Serine-Threonine Kinases: metabolism
000136909 650_2 $$2MeSH$$aRNA, Messenger: genetics
000136909 650_2 $$2MeSH$$aRNA, Messenger: metabolism
000136909 7001_ $$0P:(DE-HGF)0$$aHofmann, Andreas$$b1
000136909 7001_ $$0P:(DE-HGF)0$$aBürger, Alexander$$b2
000136909 7001_ $$0P:(DE-HGF)0$$aZerle, Julia$$b3
000136909 7001_ $$0P:(DE-HGF)0$$aKloos, Karina$$b4
000136909 7001_ $$0P:(DE-HGF)0$$aHafen, Ulrich$$b5
000136909 7001_ $$0P:(DE-HGF)0$$aErnst, Luise$$b6
000136909 7001_ $$0P:(DE-HGF)0$$aZhang, Jingzhong$$b7
000136909 7001_ $$0P:(DE-HGF)0$$aVogt-Weisenhorn, Daniela Maria$$b8
000136909 7001_ $$0P:(DE-2719)2000028$$aWurst, Wolfgang$$b9$$eLast author
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