Mechanistic contributions of FBXO7 to Parkinson disease. Issue 2 (11th December 2017)

• Record Type: Journal Article
• Authors: Joseph, Sabitha; Schulz, Jörg Bernhard; Stegmüller, Judith
• Is Part Of: Journal of neurochemistry. Volume 144:Issue 2(2018)
• Page Start: 118
• Page End: 127
• Publication Date: 2017-12-11
• Subjects: FBXO7 -- mitochondria -- parkinsonism -- Parkinson disease -- ubiquitin proteasome system; Neurochemistry -- Periodicals; 616.8042
• DOI: 10.1111/jnc.14253
• Languages: English
• ISSNs: 0022-3042

Abstract

Abstract: Parkinson disease (PD) is, without doubt, a burden on modern society as the prevalence increases significantly with age. Owing to this growing number of PD cases, it is more critical than ever to understand the pathogenic mechanisms underlying PD to identify therapeutic targets. The discovery of genetic mutations associated with PD and parkinsonism paves the way toward this goal. Even though, familial forms of the disease represent the minority of PD cases and some forms are so rare that there are only a few affected families, the research on the associated genes is invaluable. Recent additions to PARK mutations are those in PARK15 that encodes the F‐box protein O‐type 7 (FBXO7). In this review, we highlight the recent research on FBXO7, which advances our knowledge of the etiopathological pathways and fills unexpected gaps therein, justifying the dedicated study of rare variants of PD. Abstract : Understanding the molecular underpinnings of Parkinson disease (PD) is key to tackling the burden associated with this movement disorder. In this review, we report on the latest research on FBXO7, a subunit of the cullin‐1‐based E3 ubiquitin ligase. Although implicated in a rare juvenile form of parkinsonism, FBXO7 plays a surprising role in major pathways implicated in PD.