Special Issue "Chaperone-Mediated Autophagy"
Deadline for manuscript submissions: 31 August 2019
Chaperone-mediated autophagy (CMA) is a subtype of autophagy whereby the molecular chaperone HSC70/HSPA8 binds protein substrates containing a specific amino acid signature KFERQ (Lys-Phe-Glu-Arg-Gln) and targets them to the lysosome. The direct shuttling of soluble proteins trough the lysosomal membrane also requires the multimerization of LAMP2A, a lysosomal membrane-spanning protein, stabilized by HSP90. Physiological CMA, similar to macroautophagy, contributes to cellular homeostasis by protein quality control and the regulation of particular substrates involved in specific cellular pathways. More and more CMA substrates containing the KFERQ-like amino acid motif are being identified in parallel with the observation that a variety of diseases are affected by altered CMA activity. Of note, CMA may also be linked to cancerous glycolysis, as PKM2 and HK2, two key glycolytic enzymes highly expressed in cancer cells, are CMA substrates.
A better understanding of CMA regulation and function is the basis for proposing new treatment strategies in a variety of diseases and to develop new CMA targeting drugs. In neurodegenerative disease for instance, CMA deficiency—due to either substrate mutation or low LAMP2A expression—leads to an accumulation of protein aggregates that contributes to neuronal demise. In contrast, in a variety of cancers, CMA activity is increased, leading, for example, to the aberrant degradation of tumor suppressor proteins. Thus, on the one hand CMA supports the degradation of pathogenic proteins, on the other hand it promotes tumor cell proliferation. Extensive research remains to be done to understand the context-dependent impact of CMA on human health.
Moreover, CMA is involved in antigen presentation and T-cell signaling. CMA has been identified as a therapeutic target in autoimmune diseases. A first "CMA drug" in clinical trials to treat systemic lupus erythematosus (SLE) is the peptide P140/Lupuzor™, which attenuates CMA activity in lymphocytes.
This Special Issue of Cells is dedicated to all sorts of molecular, cellular and disease-associated aspects of CMA. In contrast to macroautophagy, there are currently fewer data on CMA regulation and function available. Therefore, we are really looking forward to receiving your manuscripts on this exciting topic to start closing this knowledge gap.
Thank you in advance for submitting your contributions for publication in this Special Issue of Cells.
Prof. Mario Tschan
Dr. Magali Humbert
Manuscript Submission Information
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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Chaperone-mediated autophagy