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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 spontaneous autosomal recessive scrambler mutation on chromosome 4 causes a deficiency of DAB1, encoding disabled-1, a protein involved in the signaling of the Reelin protein, lacking in the reeler mutant, [3] Dab1-scm homozygous mutants possess a reeler-like phenotype with respect to cell malpositioning in cerebellar cortex, hippocampus, and neocortex.
It was then demonstrated that the mouse disabled homologue 1 gene is responsible for the phenotypes of these mutant mice, as Dab1 protein was absent (yotari) or only barely detectable (scrambler) in these mutants. [26] Targeted disruption of Dab1 also caused a phenotype similar to that of reeler.
CR cells secrete the extracellular matrix protein reelin, which is critically involved in the control of radial neuronal migration through a signaling pathway, including the very low density lipoprotein receptor (VLDLR), the apolipoprotein E receptor type 2 (ApoER2), and the cytoplasmic adapter protein disabled 1 (Dab1).
The yotari mouse is an autosomal recessive mutant. [1] It has a mutated disabled homolog 1 ( Dab1 ) gene. [ 2 ] This mutant mouse is recognized by unstable gait ("Yota-ru" in Japanese means "unstable gait") and tremor and by early deaths around the time of weaning .
Phil Collins performs on opening night prior to the evening session on Day One of the US Open on Aug. 29, 2016 in the Flushing neighborhood of the Queens borough of New York City.
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DAB2 mRNA is expressed in normal ovarian epithelial cells but is down-regulated or absent from ovarian carcinoma cell lines. The 770-amino acid predicted protein has an overall 83% identity with the mouse p96 protein, a putative mitogen-responsive phosphoprotein; homology is strongest in the amino-terminal end of the protein in a region corresponding to the phosphotyrosine interaction domain.