Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OTC2S7J3)

• DOT Name: Protein FAM53C (FAM53C)
• Gene Name: FAM53C
• Related Disease: Schizophrenia
• UniProt ID: FA53C_HUMAN
• Pfam ID: PF15242
• Sequence:
  MITLITEQLQKQTLDELKCTRFSISLPLPDHADISNCGNSFQLVSEGASWRGLPHCSCAE
  FQDSLNFSYHPSGLSLHLRPPSRGNSPKEQPFSQVLRPEPPDPEKLPVPPAPPSKRHCRS
  LSVPVDLSRWQPVWRPAPSKLWTPIKHRGSGGGGGPQVPHQSPPKRVSSLRFLQAPSASS
  QCAPAHRPYSPPFFSLALAQDSSRPCAASPQSGSWESDAESLSPCPPQRRFSLSPSLGPQ
  ASRFLPSARSSPASSPELPWRPRGLRNLPRSRSQPCDLDARKTGVKRRHEEDPRRLRPSL
  DFDKMNQKPYSGGLCLQETAREGSSISPPWFMACSPPPLSASCSPTGGSSQVLSESEEEE
  EGAVRWGRQALSKRTLCQRDFGDLDLNLIEEN

Molecular Interaction Atlas (MIA) of This DOT

1 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Schizophrenia	DISSRV2N	Strong	Genetic Variation	[1]

4 Drug(s) Affected the Post-Translational Modifications of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate increases the methylation of Protein FAM53C (FAM53C).	[2]
Arsenic	DMTL2Y1	Approved	Arsenic affects the methylation of Protein FAM53C (FAM53C).	[6]
PMID28870136-Compound-52	DMFDERP	Patented	PMID28870136-Compound-52 increases the phosphorylation of Protein FAM53C (FAM53C).	[12]
Coumarin	DM0N8ZM	Investigative	Coumarin decreases the phosphorylation of Protein FAM53C (FAM53C).	[12]

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

Drug Name	Drug ID	Highest Status	Interaction	REF
Acetaminophen	DMUIE76	Approved	Acetaminophen increases the expression of Protein FAM53C (FAM53C).	[3]
Cupric Sulfate	DMP0NFQ	Approved	Cupric Sulfate increases the expression of Protein FAM53C (FAM53C).	[4]
Cisplatin	DMRHGI9	Approved	Cisplatin increases the expression of Protein FAM53C (FAM53C).	[5]
Quercetin	DM3NC4M	Approved	Quercetin increases the expression of Protein FAM53C (FAM53C).	[7]
Temozolomide	DMKECZD	Approved	Temozolomide increases the expression of Protein FAM53C (FAM53C).	[8]
Urethane	DM7NSI0	Phase 4	Urethane increases the expression of Protein FAM53C (FAM53C).	[9]
Benzo(a)pyrene	DMN7J43	Phase 1	Benzo(a)pyrene increases the expression of Protein FAM53C (FAM53C).	[10]
(+)-JQ1	DM1CZSJ	Phase 1	(+)-JQ1 increases the expression of Protein FAM53C (FAM53C).	[11]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A affects the expression of Protein FAM53C (FAM53C).	[13]

References

• [1] Genome-Wide Association Study Detected Novel Susceptibility Genes for Schizophrenia and Shared Trans-Populations/Diseases Genetic Effect.Schizophr Bull. 2019 Jun 18;45(4):824-834. doi: 10.1093/schbul/sby140.
• [2] Integrative omics data analyses of repeated dose toxicity of valproic acid in vitro reveal new mechanisms of steatosis induction. Toxicology. 2018 Jan 15;393:160-170.
• [3] Gene expression analysis of precision-cut human liver slices indicates stable expression of ADME-Tox related genes. Toxicol Appl Pharmacol. 2011 May 15;253(1):57-69.
• [4] Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper. Physiol Genomics. 2009 Aug 7;38(3):386-401.
• [5] The thioxotriazole copper(II) complex A0 induces endoplasmic reticulum stress and paraptotic death in human cancer cells. J Biol Chem. 2009 Sep 4;284(36):24306-19.
• [6] Prenatal arsenic exposure and the epigenome: identifying sites of 5-methylcytosine alterations that predict functional changes in gene expression in newborn cord blood and subsequent birth outcomes. Toxicol Sci. 2015 Jan;143(1):97-106. doi: 10.1093/toxsci/kfu210. Epub 2014 Oct 10.
• [7] 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.
• [8] 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.
• [9] Ethyl carbamate induces cell death through its effects on multiple metabolic pathways. Chem Biol Interact. 2017 Nov 1;277:21-32.
• [10] 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.
• [11] Inhibition of BRD4 attenuates tumor cell self-renewal and suppresses stem cell signaling in MYC driven medulloblastoma. Oncotarget. 2014 May 15;5(9):2355-71.
• [12] Quantitative phosphoproteomics reveal cellular responses from caffeine, coumarin and quercetin in treated HepG2 cells. Toxicol Appl Pharmacol. 2022 Aug 15;449:116110. doi: 10.1016/j.taap.2022.116110. Epub 2022 Jun 7.
• [13] A trichostatin A expression signature identified by TempO-Seq targeted whole transcriptome profiling. PLoS One. 2017 May 25;12(5):e0178302. doi: 10.1371/journal.pone.0178302. eCollection 2017.