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Last update 08 May 2025

TSFM

Last update 08 May 2025

Basic Info

Synonyms

EF-TS, EF-Tsmt, Elongation factor Ts, mitochondrial

+ [2]

Introduction

Associates with the EF-Tu.GDP complex and induces the exchange of GDP to GTP. It remains bound to the aminoacyl-tRNA.EF-Tu.GTP complex up to the GTP hydrolysis stage on the ribosome.

Drugs associated with TSFM

CN116462743

Patent Mining

Target

TSFM

Mechanism-

Active Org.

West China Hospital

Originator Org.

West China Hospital

Active Indication

Infectious Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TSFM

100 Translational Medicine associated with TSFM

0 Patents (Medical) associated with TSFM

286

Literatures (Medical) associated with TSFM

01 Dec 2024·Molecular Biology Reports

Short-term regulation of TSFM level does not alter amyloidogenesis and mitochondrial function in type-specific cells

Article

Author: Li, Chen-Lu ; Xie, Xiong-Yong ; Wang, Lu ; Li, Xiao-Yun ; Chen, Guo-Jun ; Yang, Jie ; -Chen, Xue ; Pu, Ya-Lan ; Zhou, Gui-Feng

BACKGROUNDMitochondrial Ts translation elongation factor (TSFM) is an enzyme that catalyzes exchange of guanine nucleotides. By forming a complex with mitochondrial Tu translation elongation factor (TUFM), TSFM participates in mitochondrial protein translation. We have previously reported that TUFM regulates translation of beta-site APP cleaving enzyme 1 (BACE1) via ROS (reactive oxygen species)-dependent mechanism, suggesting a potential role in amyloid precursor protein (APP) processing associated with Alzheimer's disease (AD), which led to the speculation that TSFM may regulate APP processing in a similar way to TUFM.METHODS AND RESULTSHere, we report that in cultured cells, knockdown or overexpression TSFM did not change protein levels in BACE1 and APP. Besides, the levels of cytoplasmic ROS and mitochondrial superoxide, in addition to ATP level, cell viability and mitochondrial membrane potential were not significantly altered by TSFM knockdown in the short term. Further transcriptome analysis revealed that expression of majority of mitochondrial genes were not remarkably changed by TSFM silencing. The possibility of TSFM involved in cardiomyopathy and cancer development was uncovered using bioinformatics analysis.CONCLUSIONSCollectively, short-term regulation of TSFM level in cultured cells does not cause a significant change in proteins involved in APP processing, levels in ROS and ATP associated with mitochondrial function. Whereas our study could contribute to comprehend certain clinical features of TSFM mutations, the roles of TSFM in cardiomyopathy and cancer development might deserve further investigation.

01 Jul 2024·Translational Cancer Research

Novel mitochondrial-related gene signature predicts prognosis and immunological status in glioma

Article

Author: Chen, Guangliang ; Cai, Lize ; Liu, Yongsheng ; Yao, Lin ; Zhang, Kai ; Zhou, Youxin ; Wang, Hao

BackgroundMitochondria are the center of cellular metabolism. The relationship between mitochondria and diseases has also been studied for a long time. However, the prognostic role of mitochondrial-related genes (MRGs) in patients with glioma and their biological effects are still unclear. The aim of the study was to construct a mitochondria-related model to assess prognosis and potential biological effects like immune infiltration, gene pathway and mutation, and give some predictive chemotherapeutic agents.MethodsThe data of 675 patients from The Cancer Genome Atlas (TCGA) database were used to identify MRG signature and construct a prognostic model. After validating its robustness in Chinese Glioma Genome Atlas (CGGA), two risk groups derived from the prognostic model were then conducted with Gene Set Enrichment Analysis (GSEA), immune status, mutation status and chemotherapeutic agents prediction.ResultsThe prognostic model built from six gene signatures can successfully predict the prognosis and reflect clinicopathological characteristics. Patients in high-risk group displayed significantly worse overall survival (OS), immunosuppression effects, and mutation markers with worse prognosis. Twelve chemotherapeutic agents with strongly correlated sensitivity and risk scores were selected as potential agents.ConclusionsThe novel MRG signatures (TYMP, TSFM, MGME1, BOLA3, TRMT5, NDUFA9) can predict prognosis and immunological status in glioma.

01 May 2023·Biological Psychiatry

Prioritization of Drug Targets for Neurodegenerative Diseases by Integrating Genetic and Proteomic Data From Brain and Blood

Article

Author: Seeley, William W. ; Tan, Lan ; Waldö, Maria Landqvist ; Cappa, Stefano F. ; Ferrucci, Luigi ; Halliday, Glenda M. ; Benussi, Luisa ; Boeve, Bradley F. ; Puca, Annibale A. ; Rubino, Elisa ; Anfossi, Maria ; Grossman, Murray ; Huey, Edward D. ; Pasquier, Florence ; Momeni, Parastoo ; Nalls, Michael A. ; Deng, Yue-Ting ; Gerhard, Alexander ; Chiang, Huei-Hsin ; Rossi, Giacomina ; Hsiung, Ging-Yuek R. ; Mayhaus, Manuel ; Rainero, Innocenzo ; Nilsson, Christer ; Lebert, Florence ; Yang, Liu ; Fox, Nick C. ; Danek, Adrian ; Pichler, Sabrina ; Wassermann, Eric M. ; Attems, Johannes ; Miller, Bruce L. ; Brooks, William S. ; Heutink, Peter ; Lleó, Alberto ; Karydas, Anna M. ; van der Zee, Julie ; Dong, Qiang ; Nilsson, Karin ; Wu, Bang-Sheng ; Trojanowski, John Q. ; Rohrer, Jonathan D. ; Smirne, Nicoletta ; Chen, Shi-Dong ; Hannequin, Didier ; Mead, Simon ; Pickering-Brown, Stuart ; Kwok, John B.J. ; Mackenzie, Ian R.A. ; Yu, Jin-Tai ; Ghidoni, Roberta ; Seelaar, Harro ; Thomas, Alan J. ; Van Broeckhoven, Christine ; Hernandez, Dena G. ; Ge, Yi-Jun ; Piaceri, Irene ; Uphill, James ; Dickson, Dennis W. ; Schlachetzki, Johannes C.M. ; Capozzo, Rosa ; Warren, Jason D. ; Thompson, Elizabeth ; Ou, Ya-Nan ; Cairns, Nigel J. ; Rizzu, Patrizia ; Rademakers, Rosa ; Pinessi, Lorenzo ; Perneczky, Robert ; Cupidi, Chiara ; Ferrari, Raffaele ; Clarimón, Jordi ; Cruts, Marc ; Kapogiannis, Dimitrios ; Novelli, Valeria ; Deramecourt, Vincent ; Kristiansen, Mark ; Parisi, Joseph E. ; Jaros, Evelyn ; Ramasamy, Adaikalavan ; Borroni, Barbara ; St. George-Hyslop, Peter ; Le Ber, Isabelle ; Alexopoulos, Panagiotis ; Razquin, Cristina ; Forloni, Gianluigi ; Frangipane, Francesca ; van Swieten, John C. ; Rossor, Martin N. ; Tagliavini, Fabrizio ; Hjermind, Lena E. ; Morris, Huw R. ; Riemenschneider, Matthias ; Gallo, Maura ; Bernardi, Livia ; Dobson-Stone, Carol ; Gasparoni, Gilles ; Sorbi, Sandro ; Petersen, Ronald C. ; Hernández, Isabel ; Rollinson, Sara ; Serpente, Maria ; Padovani, Alessandro ; Morris, Christopher M. ; Pietrini, P. ; Diehl-Schmid, Janine ; Cruchaga, Carlos ; Fenoglio, Chiara ; Singleton, Andrew B. ; Dopper, Elise G.P. ; Milan, Graziella ; Graff-Radford, Neill R. ; Schofield, Peter R. ; Graff, Caroline ; Conidi, Maria Elena ; Richardson, Anna ; Hardy, John ; Baborie, Atik ; Griffiths, Timothy D. ; Huang, Yu-Yuan ; Postiglione, Alfredo ; Ruiz, Agustín ; Scarpini, Elio ; Snowden, Julie S. ; Zhang, Ya-Ru ; Pastor, Pau ; Knopman, David ; Collinge, John ; Nielsen, Jørgen E. ; Baker, Matt ; Sorrentino, Paolo ; Bartley, Lauren ; Scheltens, Philip ; Spillantini, Maria Grazia ; Pijnenburg, Yolande A.L. ; Piguet, Olivier ; Rogaeva, Ekaterina ; Rosen, Howard ; Binetti, Giuliano ; Vercelletto, Martine ; Josephs, Keith A. ; Giaccone, Giorgio ; Haan, Eric ; Mann, David M.A. ; Nacmias, Benedetta ; Van Langenhove, Tim ; Rowe, James B. ; Logroscino, Giancarlo ; Boada, Mercè ; Franceschi, Massimo ; Golfier, Véronique ; Kurz, Alexander ; Bagnoli, Silvia ; Gu, Wei ; Maletta, Raffaele ; Hodges, John R. ; Ortega-Cubero, Sara ; Van Deerlin, Vivianna M. ; Tierney, Michael C. ; Rollin, Adeline ; Galimberti, Daniela ; Alonso, Elena ; Blesa, Rafael ; Brice, Alexis ; Grafman, Jordan ; Bruni, Amalia C. ; McKeith, Ian G. ; Ibach, Bernd ; Deschamps, William

BACKGROUNDNeurodegenerative diseases are among the most prevalent and devastating neurological disorders, with few effective prevention and treatment strategies. We aimed to integrate genetic and proteomic data to prioritize drug targets for neurodegenerative diseases.METHODSWe screened human proteomes through Mendelian randomization to identify causal mediators of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, frontotemporal dementia, and Lewy body dementia. For instruments, we used brain and blood protein quantitative trait loci identified from one genome-wide association study with 376 participants and another with 3301 participants, respectively. Causal associations were subsequently validated by sensitivity analyses and colocalization. The safety and druggability of identified targets were also evaluated.RESULTSOur analyses showed targeting BIN1, GRN, and RET levels in blood as well as ACE, ICA1L, MAP1S, SLC20A2, and TOM1L2 levels in brain might reduce Alzheimer's disease risk, while ICA1L, SLC20A2, and TOM1L2 were not recommended as prioritized drugs due to the identified potential side effects. Brain CD38, DGKQ, GPNMB, and SEC23IP were candidate targets for Parkinson's disease. Among them, GPNMB was the most promising target for Parkinson's disease with their causal relationship evidenced by studies on both brain and blood tissues. Interventions targeting FCRL3, LMAN2, and MAPK3 in blood and DHRS11, FAM120B, SHMT1, and TSFM in brain might affect multiple sclerosis risk. The risk of amyotrophic lateral sclerosis might be reduced by medications targeting DHRS11, PSMB3, SARM1, and SCFD1 in brain.CONCLUSIONSOur study prioritized 22 proteins as targets for neurodegenerative diseases and provided preliminary evidence for drug development. Further studies are warranted to validate these targets.

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