Details of Drug Off-Target (DOT)

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

• DOT Name: Protein FAM89A (FAM89A)
• Gene Name: FAM89A
• Related Disease: Bacterial infection
• UniProt ID: FA89A_HUMAN
• Sequence:
  MSGARAAPGAAGNGAVRGLRVDGLPPLPKSLSGLLHSASGGGASGGWRHLERLYAQKSRI
  QDELSRGGPGGGGARAAALPAKPPNLDAALALLRKEMVGLRQLDMSLLCQLYSLYESIQE
  YKGACQAASSPDCTYALENGFFDEEEEYFQEQNSLHDRRDRGPPRDLSLPVSSLSSSDWI
  LESI

Molecular Interaction Atlas (MIA) of This DOT

1 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Bacterial infection	DIS5QJ9S	Limited	Altered Expression	[1]

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

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate increases the expression of Protein FAM89A (FAM89A).	[2]
Ciclosporin	DMAZJFX	Approved	Ciclosporin increases the expression of Protein FAM89A (FAM89A).	[3]
Acetaminophen	DMUIE76	Approved	Acetaminophen increases the expression of Protein FAM89A (FAM89A).	[4]
Cisplatin	DMRHGI9	Approved	Cisplatin increases the expression of Protein FAM89A (FAM89A).	[5]
Estradiol	DMUNTE3	Approved	Estradiol increases the expression of Protein FAM89A (FAM89A).	[3]
Temozolomide	DMKECZD	Approved	Temozolomide increases the expression of Protein FAM89A (FAM89A).	[6]
Vorinostat	DMWMPD4	Approved	Vorinostat increases the expression of Protein FAM89A (FAM89A).	[7]
Panobinostat	DM58WKG	Approved	Panobinostat increases the expression of Protein FAM89A (FAM89A).	[7]
Cidofovir	DMA13GD	Approved	Cidofovir increases the expression of Protein FAM89A (FAM89A).	[5]
Fenofibrate	DMFKXDY	Approved	Fenofibrate increases the expression of Protein FAM89A (FAM89A).	[5]
Ifosfamide	DMCT3I8	Approved	Ifosfamide increases the expression of Protein FAM89A (FAM89A).	[5]
Clodronate	DM9Y6X7	Approved	Clodronate increases the expression of Protein FAM89A (FAM89A).	[5]
Ibuprofen	DM8VCBE	Approved	Ibuprofen increases the expression of Protein FAM89A (FAM89A).	[5]
Amiodarone	DMUTEX3	Phase 2/3 Trial	Amiodarone increases the expression of Protein FAM89A (FAM89A).	[8]
(+)-JQ1	DM1CZSJ	Phase 1	(+)-JQ1 decreases the expression of Protein FAM89A (FAM89A).	[9]
Leflunomide	DMR8ONJ	Phase 1 Trial	Leflunomide increases the expression of Protein FAM89A (FAM89A).	[10]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A increases the expression of Protein FAM89A (FAM89A).	[11]
Milchsaure	DM462BT	Investigative	Milchsaure decreases the expression of Protein FAM89A (FAM89A).	[12]

References

• [1] A qPCR expression assay of IFI44L gene differentiates viral from bacterial infections in febrile children.Sci Rep. 2019 Aug 13;9(1):11780. doi: 10.1038/s41598-019-48162-9.
• [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] Multiple microRNAs function as self-protective modules in acetaminophen-induced hepatotoxicity in humans. Arch Toxicol. 2018 Feb;92(2):845-858.
• [5] Transcriptomics hit the target: monitoring of ligand-activated and stress response pathways for chemical testing. Toxicol In Vitro. 2015 Dec 25;30(1 Pt A):7-18.
• [6] 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.
• [7] 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.
• [8] Identification by automated screening of a small molecule that selectively eliminates neural stem cells derived from hESCs but not dopamine neurons. PLoS One. 2009 Sep 23;4(9):e7155.
• [9] CCAT1 is an enhancer-templated RNA that predicts BET sensitivity in colorectal cancer. J Clin Invest. 2016 Feb;126(2):639-52.
• [10] Endoplasmic reticulum stress and MAPK signaling pathway activation underlie leflunomide-induced toxicity in HepG2 Cells. Toxicology. 2017 Dec 1;392:11-21.
• [11] From transient transcriptome responses to disturbed neurodevelopment: role of histone acetylation and methylation as epigenetic switch between reversible and irreversible drug effects. Arch Toxicol. 2014 Jul;88(7):1451-68.
• [12] Transcriptional profiling of lactic acid treated reconstructed human epidermis reveals pathways underlying stinging and itch. Toxicol In Vitro. 2019 Jun;57:164-173.