Autophagy is catabolic cellular degradation process responsible for degrading damaged organelles or unusual protein aggregates, which is activated in the presence of a variety of stimuli18.
Klionsky, D. J. & Emr, S. D. Autophagy as a regulated pathway of cellular degradation.
Peak expression shifted to cellular degradation (CEL3 and 5) and MS2 at the yellow stage and pectin degradation and LRR in the last two stages.
Inflammatory TNFα and downstream cellular degradation process markers for autophagy, lysosome production, and atrophy significantly increased in a pattern corresponding to increased CTMP expression and reduced Akt phosphorylation.
Cellular degradation of ceramide to sphingosine is catalyzed by a family of ceramidases (CDases).
Autophagy is a potent cellular degradation pathway, and its activation needs to be tightly controlled.
Several studies have investigated the cellular mechanisms that are characteristic of denervated skeletal muscle, particularly with regard to metabolic and cellular degradation pathways linked to progressive muscle atrophy30,31.
Autophagy is a tightly regulated cellular degradation pathway by which defective or superfluouscytosolic proteins, organelles and other cellular constituents are sequestered in autophagosomes and delivered to lysosomes for degradation.
Hypoxia-inducible factors (HIF) act as the major protagonist in orchestrating manifold hypoxic responses by escaping cellular degradation mechanisms.
Blood levels of thrombopoietin (TPO) are regulated in part by cellular degradation following its binding to the cell surface receptor c-mpl.
Long-term biologic storage of articular cartilage has proven elusive due to cellular degradation over time or acute damage during attempts at cryopreservation.
