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Autophagic Punctum

Polyamines reverse immune senescence via the translational control of autophagy

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Pages 181-182 | Received 13 Oct 2019, Accepted 29 Oct 2019, Published online: 06 Nov 2019

Figures & data

Figure 1. Anabolism and catabolism are upregulated in activated B cells in a coordinated manner. MTOR integrates growth and nutrient signals to promote translation and cellular growth. Despite the high MTOR activity, autophagy is also upregulated in activated B cells via MTOR-independent signaling pathways. High autophagic flux relies on efficient protein synthesis. Specifically, spermidine sustains optimal translation via hypusinating EIF5A, which is required for maintaining high TFEB protein levels. Autophagy may in turn provide nutrients and degrade damaged organelles to assist the high growth rate and antibody production of activated B cells.

Figure 1. Anabolism and catabolism are upregulated in activated B cells in a coordinated manner. MTOR integrates growth and nutrient signals to promote translation and cellular growth. Despite the high MTOR activity, autophagy is also upregulated in activated B cells via MTOR-independent signaling pathways. High autophagic flux relies on efficient protein synthesis. Specifically, spermidine sustains optimal translation via hypusinating EIF5A, which is required for maintaining high TFEB protein levels. Autophagy may in turn provide nutrients and degrade damaged organelles to assist the high growth rate and antibody production of activated B cells.

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