Fig. 2From: TMEM106B deficiency impairs cerebellar myelination and synaptic integrity with Purkinje cell lossALS/FTLD related pathological changes in the cerebellum of aged Tmem106b−/− mice. a–d Western blot analysis of p62, ubiquitin (Ub), TDP‐43, and p‐TDP-43 in RIPA—(a, b) and urea—(c, d) soluble fractions from the cerebellum of 16‐month‐old WT and Tmem106b−/− mice. Protein levels were quantified and normalized to GAPDH. n = 5, *, p < 0.05; **, p < 0.01, ***, p < 0.001, ****, p < 0.0001, unpaired t-test. e–g Western blot analysis of p62, ubiquitin (Ub), and TDP‐43 in RIPA—(e, g) and urea—(f, g) soluble fractions from the cerebellum of 2-month‐old WT and Tmem106b−/− mice. Protein levels were quantified and normalized to GAPDH. n = 5, *, p < 0.05, unpaired t-test. h Immunostaining of TDP‐43 and p‐TDP-43 in the cerebellar sections from 16‐month‐old WT and Tmem106b−/− mice. Representative images from the Purkinje cell layer and deep cerebellar nuclei (DCN) are shown. i, j Immunostaining of p62 and ubiquitin (Ub) in the cerebellar sections from 16‐month‐old WT and Tmem106b−/− mice. The number of p62 or Ub positive puncta was quantified in (j). n = 4. ****, p < 0.0001, unpaired t-testBack to article page