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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.
5649 19699 Ensembl ENSG00000189056 ENSMUSG00000042453 UniProt P78509 Q60841 RefSeq (mRNA) NM_173054 NM_005045 NM_011261 NM_001310464 RefSeq (protein) NP_005036 NP_774959 NP_001297393 NP_035391 Location (UCSC) Chr 7: 103.47 – 103.99 Mb Chr 5: 22.09 – 22.55 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Reelin, encoded by the RELN gene, is a large secreted extracellular matrix ...
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 .
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).
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The firm was the successor to the firm of Owens, Ebert & Dyer (founded in 1845 by Job E. Owens) which went into receivership in 1876. [1]In 1882, George A. Rentschler, J. C. Hooven, Henry C. Sohn, George H. Helvey, and James E. Campbell merged the firm with the iron works of Sohn and Rentschler, [1] [2] and adopted the name Hooven, Owens, Rentschler Co.