更新于：2024-11-01

FARSA

更新于：2024-11-01

基本信息

别名

CML33、FARS、FARSA

+ [6]

简介-

关联

项与 FARSA 相关的药物

BRD-7929

靶点

FARSA

作用机制

FARSA调节剂

在研机构-

原研机构

卫材（中国）药业有限公司 [+4]

在研适应症-

非在研适应症

隐孢子虫病

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 FARSA 相关的临床结果

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100 项与 FARSA 相关的转化医学

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0 项与 FARSA 相关的专利（医药）

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项与 FARSA 相关的文献（医药）

2024-12-31·Fly

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

Article

作者: 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.

2024-10-01·Theriogenology

Impact of the near-physiological temperature on the in vitro maturation of bovine oocytes: A comparative proteomic approach

Article

作者: Quirino, Celia Raquel ; Maretto, Vinicius ; Silveira, Vanildo ; Pinto, Vitor Batista ; Bustamante-Filho, Ivan Cunha ; Ortiz Vega, Wilder Hernando ; Tavares, Winny Caldas Moreno ; Caldas-Bussiere, Maria Clara

In vivo, the temperature inside preovulatory follicles of cows is approximately 1 °C lower than rectal temperature. However, standard bovine oocyte in vitro maturation (IVM) protocols use 38.5 °C based on rectal temperature. This study evaluated the effect of reducing IVM temperature to 37.5 °C on the proteomic profile of oocytes compared to the routine 38.5 °C. Nuclear maturation rate and cumulus cell (CC) expansion (30 COCs per group, 21 replicates) were assessed by observing the first polar body and using a subjective scoring method (0-4). Total nitrite concentrations in the culture medium were measured using the Griess method. Differential proteomics was performed using LC-MS/MS on pooled oocyte samples (500 matured oocytes per group, three replicates), followed by gene ontology enrichment, protein-protein interaction, and putative miRNA target analyses. No significant differences were observed between the groups in nuclear maturation, CC expansion, or nitrite concentration (P > 0.05). A total of 806 proteins were identified, with 7 up-regulated and 12 down-regulated in the treatment group compared to the control. Additionally, 12 proteins were unique to the control group, and 8 were unique to the treatment group. IVM at 37.5 °C resulted in the upregulation of proteins involved in protein folding and GTP binding, and the downregulation of enzymes with oxidoreductase activity and proteins involved in cytoskeletal fiber formation. Furthermore, 43 bovine miRNAs potentially regulating these genes (DES, HMOX2, KRT75, FARSA, IDH2, CARHSP1) were identified. We conclude that IVM of bovine oocytes at 37.5 °C induces significant proteomic changes without impacting nuclear maturation, cumulus cell expansion, or nitrite concentration in the IVM medium.

2024-05-01·Journal of Gastroenterology and Hepatology

Diagnostic algorithm for neonatal intrahepatic cholestasis integrating single‐gene testing and next‐generation sequencing in East Asia

Article

作者: Shin, MinSoo ; Seong, Moon Woo ; Lee, Heerah ; Ko, Jae Sung ; Hahn, Jong Woo ; Moon, Jin Soo

AbstractBackground and AimAdvances in molecular genetics have uncovered causative genes responsible for neonatal cholestasis. Panel‐based next‐generation sequencing has been used clinically in infants with neonatal cholestasis. We aimed to evaluate the clinical application of single‐gene testing and next‐generation sequencing and to develop a diagnostic algorithm for neonatal intrahepatic cholestasis.MethodsFrom January 2010 to July 2021, patients suspected of having neonatal intrahepatic cholestasis were tested at the Seoul National University Hospital. If there was a clinically suspected disease, single‐gene testing was performed. Alternatively, if it was clinically difficult to differentiate, a neonatal cholestasis gene panel test containing 34 genes was performed.ResultsOf the total 148 patients examined, 49 (33.1%) were received a confirmed genetic diagnosis, including 14 with Alagille syndrome, 14 with neonatal intrahepatic cholestasis caused by citrin deficiency, 7 with Dubin–Johnson syndrome, 5 with arthrogryposis‐renal dysfunction‐cholestasis syndrome, 5 with progressive familial intrahepatic cholestasis type II, 1 with Rotor syndrome, 1 with Niemann‐Pick disease type C, 1 with Kabuki syndrome, and 1 with Phenylalanyl‐tRNA synthetase subunit alpha mutation. Sixteen novel pathogenic or likely pathogenic variants of neonatal cholestasis were observed in this study. Based on the clinical characteristics and laboratory findings, we developed a diagnostic algorithm for neonatal intrahepatic cholestasis by integrating single‐gene testing and next‐generation sequencing.ConclusionsAlagille syndrome and neonatal intrahepatic cholestasis caused by citrin deficiency were the most common diseases associated with genetic neonatal cholestasis. Single‐gene testing and next‐generation sequencing are important and complementary tools for the diagnosis of genetic neonatal cholestasis.