Autophagy is generally considered as a process to supply nutrients by self-digestion for cells to survive starvation. However, autophagy, along with the proteasome system, is also involved in the turnover of cellular components under normal conditions.
Autophagy is executed by autophagy-related (Atg) genes. Among these, Atg8, which codes for the LC3 protein, is the most studied. Lipidated LC3 contributes to the closure of autophagosomes and enables the docking of specific cargos and adaptor proteins such as Sequestosome-1/p62. p62 contains an LC3-interacting region and is believed to be a substrate for selective autophagy.
Sequential phosphorylation of p62 phosphorylation sites regulates biological defense mechanisms such as selective autophagy. Impaired selective autophagy is implicated in various diseases. Neurons in familial parkinsonism, for example, fail to clear protein aggregates and depolarized mitochondria, resulting in neuronal damage and compromised brain function. In hepatocarcinoma cells, p62 is constitutively phosphorylated at Ser349, causing continuous activation of Nrf2. Hence, inhibitors of p62 phosphorylation and inhibitors of the interaction between phospho-p62 and Keap1 have the potential to be novel cancer therapeutics.
|Product Code||Product Name||Target||Size||Type|
|CY-7055||CycLex® Total p62 ELISA Kit||Total p62||96 Assay||ELISA Kit|
|CY-7056||CycLex® Phospho-p62 Ser349 ELISA Kit||Phospho-p62 Ser 349||96 Assay||ELISA Kit|
|CY-7057||CycLex® Phospho-p62 Ser403 ELISA Kit||Phospho-p62 Ser403||96 Assay||ELISA Kit|