Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OTZ31RP5)

• DOT Name: Protein FAM162B (FAM162B)
• Gene Name: FAM162B
• Related Disease: Neoplasm
• UniProt ID: F162B_HUMAN
• Pfam ID: PF06388
• Sequence:
  MLRAVGSLLRLGRGLTVRCGPGAPLEATRRPAPALPPRGLPCYSSGGAPSNSGPQGHGEI
  HRVPTQRRPSQFDKKILLWTGRFKSMEEIPPRIPPEMIDTARNKARVKACYIMIGLTIIA
  CFAVIVSAKRAVERHESLTSWNLAKKAKWREEAALAAQAKAK

Molecular Interaction Atlas (MIA) of This DOT

1 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Neoplasm	DISZKGEW	Strong	Biomarker	[1]

11 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 FAM162B (FAM162B).	[2]
Tretinoin	DM49DUI	Approved	Tretinoin increases the expression of Protein FAM162B (FAM162B).	[3]
Cisplatin	DMRHGI9	Approved	Cisplatin affects the expression of Protein FAM162B (FAM162B).	[4]
Estradiol	DMUNTE3	Approved	Estradiol affects the expression of Protein FAM162B (FAM162B).	[5]
Vorinostat	DMWMPD4	Approved	Vorinostat increases the expression of Protein FAM162B (FAM162B).	[7]
Carbamazepine	DMZOLBI	Approved	Carbamazepine affects the expression of Protein FAM162B (FAM162B).	[8]
Decitabine	DMQL8XJ	Approved	Decitabine affects the expression of Protein FAM162B (FAM162B).	[4]
Panobinostat	DM58WKG	Approved	Panobinostat increases the expression of Protein FAM162B (FAM162B).	[7]
SNDX-275	DMH7W9X	Phase 3	SNDX-275 increases the expression of Protein FAM162B (FAM162B).	[7]
Belinostat	DM6OC53	Phase 2	Belinostat increases the expression of Protein FAM162B (FAM162B).	[7]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A increases the expression of Protein FAM162B (FAM162B).	[10]

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

Drug Name	Drug ID	Highest Status	Interaction	REF
Arsenic	DMTL2Y1	Approved	Arsenic affects the methylation of Protein FAM162B (FAM162B).	[6]
Benzo(a)pyrene	DMN7J43	Phase 1	Benzo(a)pyrene increases the methylation of Protein FAM162B (FAM162B).	[9]

References

• [1] Read-through transcripts in normal human lung parenchyma are down-regulated in lung adenocarcinoma.Oncotarget. 2016 May 10;7(19):27889-98. doi: 10.18632/oncotarget.8556.
• [2] Human embryonic stem cell-derived test systems for developmental neurotoxicity: a transcriptomics approach. Arch Toxicol. 2013 Jan;87(1):123-43.
• [3] Development of a neural teratogenicity test based on human embryonic stem cells: response to retinoic acid exposure. Toxicol Sci. 2011 Dec;124(2):370-7.
• [4] Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine is associated with global DNA Damage-associated p53 activation, anti-pluripotency and DNA demethylation. PLoS One. 2012;7(12):e53003. doi: 10.1371/journal.pone.0053003. Epub 2012 Dec 27.
• [5] Identification of novel low-dose bisphenol a targets in human foreskin fibroblast cells derived from hypospadias patients. PLoS One. 2012;7(5):e36711. doi: 10.1371/journal.pone.0036711. Epub 2012 May 4.
• [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] 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] Gene Expression Regulation and Pathway Analysis After Valproic Acid and Carbamazepine Exposure in a Human Embryonic Stem Cell-Based Neurodevelopmental Toxicity Assay. Toxicol Sci. 2015 Aug;146(2):311-20. doi: 10.1093/toxsci/kfv094. Epub 2015 May 15.
• [9] Air pollution and DNA methylation alterations in lung cancer: A systematic and comparative study. Oncotarget. 2017 Jan 3;8(1):1369-1391. doi: 10.18632/oncotarget.13622.
• [10] 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.