Monday, May 6, 2013


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Crystallographic structure of the third reelin repeat domain.[1]
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols RELN; LIS2; PRO1598; RL
External IDs OMIM600514 MGI103022 HomoloGene3699 GeneCards: RELN Gene
EC number 3.4.21.-
RNA expression pattern
PBB GE RELN 205923 at tn.png
More reference expression data
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]
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.[10]WIKIPEDIA

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