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. 2017 Oct 10;159(1):323–340. doi: 10.1210/en.2017-00738

Figure 2.

Figure 2.

Loss of essential protein components of the cytosolic quality control mechanisms, mitochondrial dynamics, mitochondrial biogenesis, uncoupling mechanisms, endoplasmic reticulum, and apoptosis in DKO mice. (a) Representative Western blots from iBAT showing different regulators of cytosolic quality control mechanism, mitochondrial dynamics and biogenesis, and brown fat functionality between 3-month-old WT and DKO mice. (b) Western blot quantification of BCL2, HSL, and PGC1-α (WT, n = 3; DKO, n = 3); p-Drp1/Drp1, OPA-1 (WT, n = 4; DKO, n = 4); LC3B (WT, n = 6; DKO, n = 5); UCP1, MFN2, and PARKIN (WT, n = 6; DKO, n = 6); PINK1 (WT, n = 6; DKO, n = 7); P62 (WT, n = 7; DKO, n = 6); and BIP (WT, n = 8; DKO, n = 7) and VDAC (WT, n = 8; DKO, n = 8). (c) Plot indicating fold-increased mRNA levels of Dio2 (WT, n = 6; DKO, n = 3); Ppargc1a, Tfam, and Ucp1 (WT, n = 7; DKO, n = 3) and Adrb3 (WT, n = 9; DKO, n = 3) genes in iBAT from 3-month-old mice. All results are presented as mean ± standard error of the mean. Statistical significance assessed by two-tailed Student t test. WT vs DKO groups: *P < 0.05; **P < 0.01; ***P < 0.001. Statistical significance of OPA-1 was assessed by one-way analysis of variance followed by the Tukey test. $P < 0.05 L-OPA-1 between WT and DKO groups. PINK1, phosphatase and tensin homolog–induced putative kinase 1.