Details of Drug Off-Target (DOT)

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

• DOT Name: Protein FAM83G (FAM83G)
• Synonyms: Protein associated with SMAD1
• Gene Name: FAM83G
• UniProt ID: FA83G_HUMAN
• Pfam ID: PF07894
• Sequence:
  MAFSQVQCLDDNHVNWRSSESKPEFFYSEEQRLALEALVARGRDAFYEVLKRENIRDFLS
  ELELKRILETIEVYDPGSEDPRGTGPSQGPEDNGVGDGEEASGADGVPIEAEPLPSLEYW
  PQKSDRSIPQLDLGWPDTIAYRGVTRASVYMQPPIDGQAHIKEVVRKMISQAQKVIAVVM
  DMFTDVDIFKDLLDAGFKRKVAVYIIVDESNVKYFLHMCERACMHLGHLKNLRVRSSGGT
  EFFTRSATKFKGALAQKFMFVDGDRAVCGSYSFTWSAARTDRNVISVLSGQVVEMFDRQF
  QELYLMSHSVSLKGIPMEKEPEPEPIVLPSVVPLVPAGTVAKKLVNPKYALVKAKSVDEI
  AKISSEKQEAKKPLGLKGPALAEHPGELPELLPPIHPGLLHLERANMFEYLPTWVEPDPE
  PGSDILGYINIIDPNIWNPQPSQMNRIKIRDTSQASAQHQLWKQSQDSRPRPEPCPPPEP
  SAPQDGVPAENGLPQGDPEPLPPVPKPRTVPVADVLARDSSDIGWVLELPKEEAPQNGTD
  HRLPRMAGPGHAPLQRQLSVTQDDPESLGVGLPNGLDGVEEEDDDDYVTLSDQDSHSGSS
  GRGPGPRRPSVASSVSEEYFEVREHSVPLRRRHSEQVANGPTPPPRRQLSAPHITRGTFV
  GPQGGSPWAQSRGREEADALKRMQAQRSTDKEAQGQQFHHHRVPASGTRDKDGFPGPPRY
  RSAADSVQSSTRNAGPAMAGPHHWQAKGGQVPRLLPDPGSPRLAQNARPMTDGRATEEHP
  SPFGIPYSKLSQSKHLKARTGGSQWASSDSKRRAQAPRDRKDP
• Function: Substrate for type I BMP receptor kinase involved in regulation of some target genes of the BMP signaling pathway. Also regulates the expression of several non-BMP target genes, suggesting a role in other signaling pathways.

Molecular Interaction Atlas (MIA) of This DOT

2 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 FAM83G (FAM83G).	[1]
PMID28870136-Compound-52	DMFDERP	Patented	PMID28870136-Compound-52 increases the phosphorylation of Protein FAM83G (FAM83G).	[7]

6 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 FAM83G (FAM83G).	[2]
Cisplatin	DMRHGI9	Approved	Cisplatin decreases the expression of Protein FAM83G (FAM83G).	[3]
Estradiol	DMUNTE3	Approved	Estradiol increases the expression of Protein FAM83G (FAM83G).	[4]
Epigallocatechin gallate	DMCGWBJ	Phase 3	Epigallocatechin gallate increases the expression of Protein FAM83G (FAM83G).	[5]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 increases the expression of Protein FAM83G (FAM83G).	[6]
Bisphenol A	DM2ZLD7	Investigative	Bisphenol A affects the expression of Protein FAM83G (FAM83G).	[8]

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] 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.
• [3] Activation of AIFM2 enhances apoptosis of human lung cancer cells undergoing toxicological stress. Toxicol Lett. 2016 Sep 6;258:227-236.
• [4] 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.
• [5] Comparative proteomics reveals concordant and discordant biochemical effects of caffeine versus epigallocatechin-3-gallate in human endothelial cells. Toxicol Appl Pharmacol. 2019 Sep 1;378:114621. doi: 10.1016/j.taap.2019.114621. Epub 2019 Jun 10.
• [6] 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.
• [7] 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.
• [8] Comprehensive analysis of transcriptomic changes induced by low and high doses of bisphenol A in HepG2 spheroids in vitro and rat liver in vivo. Environ Res. 2019 Jun;173:124-134. doi: 10.1016/j.envres.2019.03.035. Epub 2019 Mar 18.