Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OTO2EE3K)

• DOT Name: Protein FMC1 homolog (FMC1)
• Synonyms: ATP synthase assembly factor FMC1, mitochondrial; Formation of mitochondrial complex V assembly factor 1 homolog
• Gene Name: FMC1
• Related Disease: Idiopathic parkinson disease
• UniProt ID: FMC1_HUMAN
• Pfam ID: PF13233
• Sequence:
  MAALGSPSHTFRGLLRELRYLSAATGRPYRDTAAYRYLVKAFRAHRVTSEKLCRAQHELH
  FQAATYLCLLRSIRKHVALHQEFHGKGERSVEESAGLVGLKLPHQPGGKGWEP
• Function: Plays a role in the assembly/stability of the mitochondrial membrane ATP synthase (F(1)F(0) ATP synthase or Complex V).

Molecular Interaction Atlas (MIA) of This DOT

1 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Idiopathic parkinson disease	DIS18PD0	moderate	Biomarker	[1]

9 Drug(s) Affected the Gene/Protein Processing of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate decreases the expression of Protein FMC1 homolog (FMC1).	[2]
Ciclosporin	DMAZJFX	Approved	Ciclosporin decreases the expression of Protein FMC1 homolog (FMC1).	[3]
Cisplatin	DMRHGI9	Approved	Cisplatin decreases the expression of Protein FMC1 homolog (FMC1).	[4]
Estradiol	DMUNTE3	Approved	Estradiol decreases the expression of Protein FMC1 homolog (FMC1).	[5]
Quercetin	DM3NC4M	Approved	Quercetin decreases the expression of Protein FMC1 homolog (FMC1).	[6]
Temozolomide	DMKECZD	Approved	Temozolomide decreases the expression of Protein FMC1 homolog (FMC1).	[7]
Hydrogen peroxide	DM1NG5W	Approved	Hydrogen peroxide affects the expression of Protein FMC1 homolog (FMC1).	[8]
SNDX-275	DMH7W9X	Phase 3	SNDX-275 decreases the expression of Protein FMC1 homolog (FMC1).	[9]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A decreases the expression of Protein FMC1 homolog (FMC1).	[10]

References

• [1] Knockdown of the mitochondria-localized protein p13 protects against experimental parkinsonism.EMBO Rep. 2018 Mar;19(3):e44860. doi: 10.15252/embr.201744860. Epub 2018 Jan 25.
• [2] Human embryonic stem cell-derived test systems for developmental neurotoxicity: a transcriptomics approach. Arch Toxicol. 2013 Jan;87(1):123-43.
• [3] Comparison of HepG2 and HepaRG by whole-genome gene expression analysis for the purpose of chemical hazard identification. Toxicol Sci. 2010 May;115(1):66-79.
• [4] Activation of AIFM2 enhances apoptosis of human lung cancer cells undergoing toxicological stress. Toxicol Lett. 2016 Sep 6;258:227-236.
• [5] Genistein and bisphenol A exposure cause estrogen receptor 1 to bind thousands of sites in a cell type-specific manner. Genome Res. 2012 Nov;22(11):2153-62.
• [6] Comparison of phenotypic and transcriptomic effects of false-positive genotoxins, true genotoxins and non-genotoxins using HepG2 cells. Mutagenesis. 2011 Sep;26(5):593-604.
• [7] Temozolomide induces activation of Wnt/-catenin signaling in glioma cells via PI3K/Akt pathway: implications in glioma therapy. Cell Biol Toxicol. 2020 Jun;36(3):273-278. doi: 10.1007/s10565-019-09502-7. Epub 2019 Nov 22.
• [8] Global gene expression analysis reveals differences in cellular responses to hydroxyl- and superoxide anion radical-induced oxidative stress in caco-2 cells. Toxicol Sci. 2010 Apr;114(2):193-203. doi: 10.1093/toxsci/kfp309. Epub 2009 Dec 31.
• [9] Definition of transcriptome-based indices for quantitative characterization of chemically disturbed stem cell development: introduction of the STOP-Toxukn and STOP-Toxukk tests. Arch Toxicol. 2017 Feb;91(2):839-864.
• [10] A transcriptome-based classifier to identify developmental toxicants by stem cell testing: design, validation and optimization for histone deacetylase inhibitors. Arch Toxicol. 2015 Sep;89(9):1599-618.