Exploring the Roles of Pseudophosphatase MK-STYX in Autophagy

Exploring the Roles of Pseudophosphatase MK-STYX in Autophagy

 

Cells carry out an incredible variety of processes to keep themselves and the greater organism they comprise functioning efficiently and healthily. As with most complex systems, cells possess a means of eliminating unwanted components and reusing or recycling the individual parts of these superfluous components into important constituent parts like amino acids and nucleic acids. This cellular recycling system is known as autophagy, and it permits organisms and their various cell types to remove redundant biomolecules [1]. In addition, autophagy allows cells to sustain themselves in times of starvation or stress by breaking down complex organelles and proteins into energy and basic biological building blocks. Unsurprisingly, autophagy is highly relevant to both healthy and diseased states, because a baseline level of autophagy is essential to an organism’s physical wellbeing. Conversely, a grossly dysregulated autophagic process affects and mediates pathogenesis and progression of cancers, neurodegenerative diseases, and metabolic disorders [2]. The pseudophosphatase MK-STYX and its roles in cellular processes represent the primary research focus of the Hinton Lab.  As a pseudophosphatase, MK-STYX lacks the catalytic ability to remove a phosphate group from proteins, but can bind targets with its pseudophosphatase domain and protein-interacting CH2 domain.  The importance of pseudophospahtases has only recently been accepted, thus MK-STYX and the other proteins in this group populate an exciting forefront of scientific inquiry.  Previous findings from our research lab have demonstrated that MK-STYX activity helps clear stress granules (made of translationally halted mRNA and associated proteins) from cells [3].  The two pathways that clear stress granules are the autophagy and ubiquitin protease pathways.  Based on recent studies conducted by our lab that showed MK-STYX altering the activity and expression levels of autophagy proteins, I decided to focus my research efforts on further characterizing MK-STYX’s roles in this critical intracellular homeostatic process.

 

Citations

  1. Glick, Danielle, Sandra Barth, and Kay F. Macleod. “Autophagy: Cellular and Molecular Mechanisms.” The Journal of pathology 221.1 (2010): 3–12. PMC. Web. 21 Apr. 2018.
  2. Levine, Beth, and Guido Kroemer. “Autophagy in the Pathogenesis of Disease.” Cell 132.1 (2008):27–42. PMC. Web. 21 Apr. 2018.
  3. Banks, Dallas A. et al. “MK-STYX Alters the Morphology of Primary Neurons, and Outgrowths in MKSTYX Overexpressing PC-12 Cells Develop a Neuronal Phenotype.” Frontiers in Molecular Biosciences 4 (2017): 76. PMC. Web. 21 Apr. 2018.

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