Figure 3.

A₁R controls the maturation of SREBPs via PKAc

(A) Relative hepatic protein expression of flSREBP1c and nSREBP1c from LKO mice and A₁R^{Liver OE} mice on HFD and CD-HFD.

(B) Hepatic PKAc protein expression in LKO and A₁R^{Liver OE} mice.

(C) PKAc protein expression in AML-12 cells treated with CPA (A₁R activator, 1 μM) and DPCPX (A₁R inhibitor, 1 μM) for 48 h. GAPDH or tubulin was used as total protein control, and lamin B1 was used as nuclear protein control.

(D) AML-12 cells were treated with CPA (1 μM, 48 h), DbcAMP (PKA activator, 200 μM, 12 h), or co-treated with CPA and DbcAMP, respectively. Fluorescent staining of SREBP1c or SREBP2 (red) in each group was performed. The nuclei were stained by Hoechst (blue).

(E) Overview of A₁R intracellular signaling pathways. Activated A₁R decreases adenylate cyclase (AC) activity to suppress the activity of cAMP/PKAc in cytoplasm, resulting in modulation of the intracellular signaling molecules. However, the exact modulation on SREBPs by PKAc remains unclear. Image created using BioRender. Results are representative of one biological replicate. Data are depicted as mean ± SEM. Student’s unpaired t test; ∗p < 0.05, ∗∗p < 0.01.