Fig. 5

IL-4 treatment protects STAT6 from autophagy-induced degradation and PARP-1 inhibition abrogates such protection without affecting autophagy. A Splenocytes isolated from WT C57BL/6 J mice were stimulated with IL-4 in the absence or presence of olaparib for the indicated time points. Protein lysates were subjected to immunoblot analysis with antibodies to STAT6 or Actin. B Jurkat cells were exposed to AA starvation media then supplemented with different percentages of AAs in the presence or absence of IL-4 or the PARP inhibitor, olaparib, for 12 h. Protein extracts were then subjected to immunoblot analysis with antibodies to STAT6, p62 or Tubulin. The brackets on the left indicate that the two sets of panels were of same samples but run on two different gels. C Jurkat were cultured in starvation media then supplemented with 25% AAs and treated for 12 h with IL-4, olaparib, calpastatin or combinations of the different agents. Not starved cells were used as control. Protein extracts were then subjected to immunoblot analyses with antibodies to STAT6, STAT4, p62 or actin. D The intensity of the STAT6 bands showed on (B) was quantified using ImageJ-Fiji and results were normalized to respective Actin band intensity