Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OTJWBPL3)

• DOT Name: Uncharacterized protein C9orf85 (C9ORF85)
• Gene Name: C9ORF85
• UniProt ID: CI085_HUMAN
• Pfam ID: PF10217
• Sequence:
  MSSQKGNVARSRPQKHQNTFSFKNDKFDKSVQTKKINAKLHDGVCQRCKEVLEWRVKYSK
  YKPLSKPKKCVKCLQKTVKDSYHIMCRPCACELEVCAKCGKKEDIVIPWSLPLLPRLECS
  GRILAHHNLRLPCSSDSPASASRVAGTTGAHHHAQLIFVFLVEMGFHYVGQAGLELLTS

Molecular Interaction Atlas (MIA) of This DOT

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

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate decreases the methylation of Uncharacterized protein C9orf85 (C9ORF85).	[1]

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

Drug Name	Drug ID	Highest Status	Interaction	REF
Ciclosporin	DMAZJFX	Approved	Ciclosporin increases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[2]
Acetaminophen	DMUIE76	Approved	Acetaminophen decreases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[3]
Doxorubicin	DMVP5YE	Approved	Doxorubicin decreases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[4]
Quercetin	DM3NC4M	Approved	Quercetin increases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[5]
Calcitriol	DM8ZVJ7	Approved	Calcitriol increases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[6]
Folic acid	DMEMBJC	Approved	Folic acid decreases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[7]
Bortezomib	DMNO38U	Approved	Bortezomib increases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[8]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 decreases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[9]
Formaldehyde	DM7Q6M0	Investigative	Formaldehyde decreases the expression of Uncharacterized protein C9orf85 (C9ORF85).	[10]

References

• [1] 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.
• [2] 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.
• [3] Predictive toxicology using systemic biology and liver microfluidic "on chip" approaches: application to acetaminophen injury. Toxicol Appl Pharmacol. 2012 Mar 15;259(3):270-80.
• [4] Bringing in vitro analysis closer to in vivo: studying doxorubicin toxicity and associated mechanisms in 3D human microtissues with PBPK-based dose modelling. Toxicol Lett. 2018 Sep 15;294:184-192.
• [5] 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.
• [6] Large-scale in silico and microarray-based identification of direct 1,25-dihydroxyvitamin D3 target genes. Mol Endocrinol. 2005 Nov;19(11):2685-95.
• [7] Folic acid supplementation dysregulates gene expression in lymphoblastoid cells--implications in nutrition. Biochem Biophys Res Commun. 2011 Sep 9;412(4):688-92. doi: 10.1016/j.bbrc.2011.08.027. Epub 2011 Aug 16.
• [8] The proapoptotic effect of zoledronic acid is independent of either the bone microenvironment or the intrinsic resistance to bortezomib of myeloma cells and is enhanced by the combination with arsenic trioxide. Exp Hematol. 2011 Jan;39(1):55-65.
• [9] Cell-based two-dimensional morphological assessment system to predict cancer drug-induced cardiotoxicity using human induced pluripotent stem cell-derived cardiomyocytes. Toxicol Appl Pharmacol. 2019 Nov 15;383:114761. doi: 10.1016/j.taap.2019.114761. Epub 2019 Sep 15.
• [10] Cellular reactions to long-term volatile organic compound (VOC) exposures. Sci Rep. 2016 Dec 1;6:37842. doi: 10.1038/srep37842.