Reelin

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Reelin
Crystallographic structure of the third reelin repeat domain.[1]
Available structures PDB Ortholog search: PDBe, RCSB [show]List of PDB id codes
Identifiers
Symbols	RELN; LIS2; PRO1598; RL
External IDs	OMIM: 600514 MGI: 103022 HomoloGene: 3699 GeneCards: RELN Gene
EC number	3.4.21.-
[show]Gene Ontology
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	5649	19699
Ensembl	ENSG00000189056	ENSMUSG00000042453
UniProt	P78509	Q60841
RefSeq (mRNA)	NM_005045	NM_011261
RefSeq (protein)	NP_005036	NP_035391
Location (UCSC)	Chr 7: 103.11 – 103.63 Mb	Chr 5: 21.88 – 22.34 Mb
PubMed search	[1]	[2]
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Reelin is a large secreted extracellular matrix glycoprotein that helps regulate processes of neuronal migration and positioning in the developing brain by controlling cell–cell interactions. Besides this important role in early development, reelin continues to work in the adult brain. It modulates synaptic plasticity by enhancing the induction and maintenance of long-term potentiation.^[2][3] It also stimulates dendrite^[4] and dendritic spine^[5] development and regulates the continuing migration of neuroblasts generated in adult neurogenesis sites like subventricular and subgranular zones. It is found not only in the brain, but also in the spinal cord, blood, and other body organs and tissues.
Reelin has been suggested to be implicated in pathogenesis of several brain diseases. The expression of the protein has been found to be significantly lower in schizophrenia and psychotic bipolar disorder, but the cause of this observation remains uncertain as studies show that psychotropic medication itself affects reelin expression. Moreover, the epigenetic hypothesis aimed at explaining the changed levels^[6] has received some contradictory evidence.^[7][8] Total lack of reelin causes a form of lissencephaly. Reelin may also play a role in Alzheimer's disease, temporal lobe epilepsy and autism.
Reelin's name comes from the abnormal reeling gait of reeler mice,^[9] which were later found to have a deficiency of this brain protein and were homozygous for mutation of the RELN gene. The primary phenotype associated with loss of reelin function is a failure of neuronal positioning throughout the developing central nervous system (CNS). The mice heterozygous for the reelin gene, while having little neuroanatomical defects, display the endophenotypic traits linked to psychotic disorders.<sup>[10]WIKIPEDIA


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