The authors studied the effect of conditionally deleting Atxn2l in adult frontal cortex neurons expressing CamK2a‑CreERT2. Deletion of Atxn2l did not induce neuronal death but significantly reduced spontaneous mobility. Proteomic profiling revealed disrupted alternative splicing and RNA-binding protein regulation.
Conditional Atxn2l deletion caused hypoactivity without cell loss and altered expression of splicing-related proteins, supporting a role for ATXN2L in RNA regulation in mature neurons
Atxn2l^flox/flox conditional Knockout mouse, crossed with CamK2a‑CreERT2 — genOway-developed
RNA-binding protein function, neurodegeneration modeling, adult neuron targeting, alternative splicing dysfunction
Floxed exons 10–17 of Atxn2l, CreERT2 under CamK2a promoter, tamoxifen injection in adult mice, open field test for mobility, label-free proteomics, GO-term analysis for RNA and splicing pathways
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