Skip to main content
. 2020 Aug 28;19(10):e13221. doi: 10.1111/acel.13221

FIGURE 6.

FIGURE 6

Protein misregulations in Sgo1−/+ in human AD‐relevant proteins (i.e., antioxidant proteins, mitochondrial energy metabolism proteins, and β‐oxidation and peroxisome proteins). (a) Examples of proteins indicating an Sgo1−/+‐specific increase in 24‐month‐old brains. Hspd1 (Heat Shock Protein Family D [Hsp60] Member 1) is a mitochondrial chaperone. Gpi (Glucose‐6‐phosphate isomerase) and Fh1 (Fumarate Hydratase) are involved in energy generation. (b) Examples of proteins indicating both an Sgo1−/+‐specific increase at 24 months and age‐dependent increase in Sgo1−/+ (12 months vs. 24 months). Idh1 (Isocitrate Dehydrogenase [NADP(+)] 1, Cytosolic), and Idh2 (Isocitrate Dehydrogenase [NADP(+)] 2, Mitochondrial) are involved in energy generation. Aco2 (aconitase 2, mitochondrial) localizes in mitochondria and is a part of the TCA cycle. (c) Prohibitin (Phb) and Phosphoinositide‐dependent protein kinase 1(Pdk1) uniquely indicated increases in middle‐aged (12‐month‐old) Sgo1−/+ mice, preceding amyloid‐β accumulation at 24 months. Phb and Pdk1 are also progressively decreased in human olfactory bulb‐AD proteomic analysis (see text). (d) The majority of misregulations were increases at old age, while Phb2 (Prohibitin2), Fabp3 (Fatty Acid‐binding Protein 3), and nnt (Nicotinamide Nucleotide Transhydrogenase) showed decreases. Many of these proteins are also misregulated in human AD (see text)