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Last update 23 Jan 2025

FARS2

Last update 23 Jan 2025

Basic Info

Synonyms

dJ236A3.1, FARS1, FARS2

+ [5]

Introduction

Is responsible for the charging of tRNA(Phe) with phenylalanine in mitochondrial translation. To a lesser extent, also catalyzes direct attachment of m-Tyr (an oxidized version of Phe) to tRNA(Phe), thereby opening the way for delivery of the misacylated tRNA to the ribosome and incorporation of ROS-damaged amino acid into proteins.

Drugs associated with FARS2

BRD-5018

Target

FARS2

Mechanism

FARS2 inhibitors

Active Org.

Eisai, Inc. [+1]

Originator Org.

The Broad Institute, Inc. [+1]

Active Indication

Malaria

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with FARS2

100 Translational Medicine associated with FARS2

0 Patents (Medical) associated with FARS2

713

Literatures (Medical) associated with FARS2

01 Jan 2025·Journal of Affective Disorders

Causal association between mitochondrial function and psychiatric disorders: Insights from a bidirectional two-sample Mendelian randomization study

Article

Author: Wang, Ying-Wei ; Yao, Tao ; Lu, Jia-Hao ; Wu, Yu-Qing ; Qian, Xin-Ge ; Zheng, Cheng ; Lin, Jia-Feng ; Chen, Yan-Min ; Liu, Jing-Chen ; Lin, Yun-Lu ; Wu, Chun-Hui ; Fang, Luo-Xiang

BACKGROUNDPrevious observational studies have suggested that there appears to be a close association between mitochondrial function and psychiatric disorders, but whether a causal role exists remains unclear.METHODSWe extracted genetic instruments for 67 mitochondrial-related proteins and 10 psychiatric disorders from publicly available genome-wide association studies, and employed five distinct MR methods and false discovery rate correction to detect causal associations between them. Additionally, we conducted a series of sensitivity tests and additional model analysis to ensure the robustness of the results. For potential causal associations, we further performed reverse MR analyses to assess the impact of reverse causality.RESULTSWe identified a total of 2 significant causal associations and 24 suggestive causal associations. Specifically, Phenylalanine-tRNA ligase was found to increase the risk of Alzheimer's disease, while Mitochondrial glutamate carrier 2 decreased the risk of autism spectrum disorder. Furthermore, there was no evidence of significant pleiotropy, heterogeneity, or reverse causality.LIMITATIONSThis study was limited to individuals of European ancestry, and the conclusions drawn are merely revelatory.CONCLUSIONThis study provides novel insights into the relationship between mitochondria and psychiatric disorders, as well as the pathogenesis and treatment strategies for psychiatric disorders.

31 Dec 2024·Fly

Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2

Article

Author: Brunßen, Dominique ; Suter, Beat

Amino acyl-tRNA synthetases perform diverse non-canonical functions aside from their essential role in charging tRNAs with their cognate amino acid. The phenylalanyl-tRNA synthetase (PheRS/FARS) is an α₂β₂ tetramer that is needed for charging the tRNA^Phe for its translation activity. Fragments of the α-subunit have been shown to display an additional, translation-independent, function that activates growth and proliferation and counteracts Notch signalling. Here we show in Drosophila that overexpressing the β-subunit in the context of the complete PheRS leads to larval roaming, food avoidance, slow growth, and a developmental delay that can last several days and even prevents pupation. These behavioural and developmental phenotypes are induced by PheRS expression in CCHa2⁺ and Pros⁺ cells. Simultaneous expression of β-PheRS, α-PheRS, and the appetite-inducing CCHa2 peptide rescued these phenotypes, linking this β-PheRS activity to the appetite-controlling pathway. The fragmentation dynamic of the excessive β-PheRS points to β-PheRS fragments as possible candidate inducers of these phenotypes. Because fragmentation of human FARS has also been observed in human cells and mutations in human β-PheRS (FARSB) can lead to problems in gaining weight, Drosophila β-PheRS can also serve as a model for the human phenotype and possibly also for obesity.

01 Nov 2024·Annals of Clinical and Translational Neurology

A pseudo‐homozygous missense variant and Alu‐mediated exon 5 deletion in FARS2 causing spastic paraplegia 77

Article

Author: Wang, Ning ; Yan, Xin‐Yu ; Lin, Shu‐Huai ; Hong, Chao‐Yin ; Xie, Jun‐Hao ; Jiang, Jun‐Yi ; Chen, Wan‐Jin ; Lin, Xiang

AbstractFARS2‐associated hereditary spastic paraplegia, later onset spastic paraplegia type 77, is a rarely neurodegenerative disease. Here, we reported two affected siblings in an autosomal recessive spastic paraplegia family with a pseudo‐homozygous missense variant and Alu‐mediated exon 5 deletion in FARS2. Both patients gradually developed altered gaits and weakness in both lower limbs. In our literature review, spastic paraplegia type 77 shows high heterogeneity in clinical manifestations. Our study broadens the scope of pathogenic mechanisms of SPG77 resulting from compound heterozygous mutations in FARS2 and provides strong evidence that deletion in FARS2 due to recombination event mediated by Alu element.

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FARS2

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