A microtubule dependent process through interactions between a short peptide signal, known as the cytoplasmic targeting-retention signal, and the dynein/dynactin motor complex. coupled with the presence of ribosomal clusters. Human genomic P1 artificial chromosome clones spanning the entire CD34 genomic locus, SH3 domain [interactions of the 5 genes then known to cause human LIS1] protein 1 to the bundles suggest their involvement occurred from the anterograde direction, the creation of a mouse model suggesting a role for 14-3-3-epsilon in cortical development these genes in combination may contribute with deletion of LIS1 may contribute to haploinsufficiency of one or more genes. The gl brain showed a diffuse translucent appearance with loss of the normal demarcation between the white and the grey matter, The fact that central nervous system involvement is also present in the gl mouse mutant suggests that he fact that central nervous system involvement is also present in the LIS1 whose products act in two spindle motor pathways that overlap the dynactin complex [Including ribosomal protein S6.], and human LIS-1, required for normal brain development. Is in the same pathway as dynein. The phenotype of a double mutant is similar to that of single mutants, in which the mitotic spindle does not properly partition into the daughter cell. Many cargoes link to a component of the dynactin complex LIS1 interactions , Atpase[ dynein via RPS6, ribosomal protein S6] antigenic reactivity of interactions between dynactin and vesicle-associated spectrin. Thus, the results fulfill the specific criteria [neither S6 proteins inhibited mitochondrial ATPase [?] activity] for the concept and operational definition in focal cortical dysplasia.