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Comparison of transcriptional programs between undifferentiated (0 hr) and differentiated N2A-A5 (96 hr) cells

GSE335602 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/20 Platform GPL19057
Summary
Kinesins are molecular motor proteins essential for organizing and remodeling the cytoskeleton during neuronal development and maintenance. One key regulator is kinesin family binding protein (KIFBP), which inhibits a subset of kinesins by blocking motor-microtubule interactions. Homozygous nonsense mutations in KIFBP cause Goldberg-Shprintzen Syndrome (GOSHS), a neurodevelopmental disorder characterized by intellectual disability, microcephaly, and axonal neuropathy. Although loss of KIFBP has been linked to reduced neurite length and microtubule disorganization, the specific kinesins underlying these phenotypes remain unclear. This work uses a variety of approaches, including transcriptomics, to establish Neuro-2a cells as a model for studying KIFBP function and provide new insight into the regulation of kinesin activity and cytoskeletal dynamics in neurons.
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Also filed as BioProject PRJNA1478971 and SRA study SRP710037. Searching any of these in the dataset finder brings you back here.

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