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Reelin's name comes from the abnormal reeling gait of reeler mice, [17] 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 Disabled-1 (Dab1) gene encodes a key regulator of Reelin signaling. Reelin is a large glycoprotein secreted by neurons of the developing brain, particularly Cajal-Retzius cells. DAB1 functions downstream of Reln in a signaling pathway that controls cell positioning in the developing brain and during adult neurogenesis.
The product of the reeler gene in mouse is reelin, a large extracellular protein secreted by pioneer neurons that coordinates cell positioning during neurodevelopment. [1] F-spondin and mindin are a family of matrix-attached adhesion molecules that share structural similarities and overlapping domains of expression. Both F-spondin and mindin ...
The examples include: Double knockout of VLDLR and ApoER2 receptors; [5] Double knockout of Src and Fyn kinases. [6] Cre-loxP recombination mice model that lacks Crk and CrkL in most neurons. [7] Was used to show that Crk/CrkL lie downstream of DAB1] in the reelin signaling pathway. Scrambler mouse; Brain slices of wildtype and reeler mice
The 5’ end of reelin was further analyzed using 125 multiple-incidence families. There was no significant difference between the length of repeats found between affected and controls however, family based association test found that larger reelin alleles were transmitted more frequently than expected to affected children [11].
A chart created with data from a Microsoft Excel spreadsheet that only saves the chart. To save the chart and spreadsheet save as .XLS. XLC is not supported in Excel 2007 or in any newer versions of Excel. Dialog .xld: Used in older versions of Excel. Archive .xlk: A backup of an Excel Spreadsheet Add-in (DLL) .xll
Through interactions with one of its ligands, reelin, ApoER2 plays an important role in embryonic neuronal migration and postnatal long-term potentiation. Another LDL family receptor, VLDLR, also interacts with reelin, and together these two receptors influence brain development and function. Decreased expression of ApoER2 is associated with ...
It was found later that the mutation causing these disorders was located in the RELN gene which codes for reelin, a glycoprotein secreted by Cajal–Retzius cells in the developing brain. This protein seems to act as a stop signal for migrating neurons, controlling the positioning and orientation of neurons in their layers, according to the ...