Fig 1: The possible mechanism of YNJ-medicated serum on the regulation of autophagy in INS-1 cells. 1: treatment of INS-1 cells cultured under HG/HF conditions with YNJ-medicated serum. 2: there were some damaged organelles and proteins in INS-1 cells. 3: damaged organelles or proteins binding to p62. 4: p62 binding to LC3/GABARAP with the involvement of ATG3 \ATG7. 5: LC3 binding to PE to form LC3-II;. 6: LC3-II; and ATG2-WIPI2 were localized in PAS. 7: with the extension of the membrane, autophagosomes were formed. 8: autophagosomes fused with lysosomes to form autolysosomes where the sequestered contents were degraded. 9: After the clearance of damaged substances, INS-1 cells were protected from HG/HF-induced apoptosis by YNJ-medicated serum.
Fig 2: SIRT4 inhibits BLCA growth through autophagy inhibition. A RFP-GFP-tagged LC3 adenovirus was utilized to infect stably transfected T24 cell strains using SIRT4 overexpression and interference and negative control cells. Green dots indicate autophagosomes, yellow dots (marked in green and red) depict autophagic lysosomes without fusion with the lysosomes, and RFP signals without GFP relate to the fusion of autophagosomes with lysosomes. The yellow fluorescent particles within the cells were observed under the fluorescence microscope. B After 100 nmol/L bafilomycin treatment for 2 h, the changes in autophagy-related proteins LC3, SQSTM1, BECN1, GABARAP, and GABARAPL2 in T24 cells with SIRT4 overexpression and interference were detected (Uncropped gel in supply Fig. 3). C The inhibition effect on T24 cells with SIRT4 overexpression in the presence or absence of 100 nmol/L bafilomycins was detected using CCK-8. D Western blot analysis shows the interference effect of the shATG5 interference sequence on the ATG5 protein in T24 cells (Uncropped gel in supply Fig. 4). E In the presence or absence of shATG5, the inhibition effect on T24 cells with SIRT4 interference was detected by CCK-8
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