Fig. 4: Quantitative analysis of gene- and protein-expression and lipidomes of Cntr and smpd3-/- Golgi complexes. | Cell Death & Disease

Fig. 4: Quantitative analysis of gene- and protein-expression and lipidomes of Cntr and smpd3-/- Golgi complexes.

From: SMPD3 deficiency perturbs neuronal proteostasis and causes progressive cognitive impairment

Fig. 4: Quantitative analysis of gene- and protein-expression and lipidomes of Cntr and smpd3-/- Golgi complexes.

Real-time-PCR of total brain RNA of cohorts (n = 5) of a 6- and b 12-mo-old Cntr and smpd3-/- mice, using neuron-specific markers syntaxin, synapsin, and synaptophysin, of AD-related genes mapt, ttbk1, app, and psen1 and 2; oligodendrocyte-specific markers plp and mbp; and astrocytes-specific markers eaac1 and glast1, mean ± SD. Representative WB of lysates of c–f 6 and gj 12-mo-old total brain using anti -APP, -Aβ, -Tau1, and -pTau, of k–o. Golgi complex using anti –SMPD3, -APP, -Pen2, -Aβ, and -pTau of p, q Golgi DIMs, using anti-APP and -Pen2 antibodies of Cntr and SMPD3-/- mice (n = 3). r HPTLC of Cer and DAG pools of the Golgi lipid extract. Markers: m1 18:0-Cer, m2 1,2-18:1/18:1-DAG s Quantification of Cer species, t “C18-Cer” species (arrow in r), u identical ceramide-species in >20-ceramides. v HPTLC of Golgi lipids. w MS/MS-analysis of SM species. C cholesterol, CMH ceramide monohexoside, PE phosphatidyl ethanolamine, PS phosphatidyl serine, PC phosphatidyl choline, SM sphingomyelin

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