Parkinsonism‐pyramidal syndrome (PPS) is a mind boggling development problem that may introduce in youth related with complex genetic spastic paraplegia (SPG), young‐onset parkinsonism, neurodegeneration with cerebrum iron collection (NBIA) messes, and innate mistakes of metabolism.1 FBXO7 inadequacy (PARK15; MIM 260300) is an uncommon reason for PPS with 26 known patients since 2008.2-9 Most of these patients create spastic paraparesia and additionally levodopa‐responsive youthful beginning parkinsonism with ordinary mind attractive reverberation imaging (MRI) and diminished dopamine take-up on DaTSCAN.2-9 The F‐box just protein7 (FBXO7) quality encodes for a protein engaged with ubiquitin–proteasome framework (UPS) action and mitophagy. FBXO7 protein is a subunit of a complex answerable for the phosphorylation‐dependent ubiquitination, the SKP1/cullin‐1/F‐box protein (SCF) E3 ubiquitin ligase complex. FBXO7 goes about as a substrate enrollment specialist in this complex and has an administrative job in proteasome through the immediate collaboration with the center proteasome subunit PSMA2, a basic protein needed for a completely useful proteasome. Another part of FBXO7 protein is to give a viable enrollment of parkin to harmed mitochondria and start mitophagy.
Reference link- https://onlinelibrary.wiley.com/doi/10.1002/acn3.51095
