Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OTBE7V0P)

• DOT Name: Scrapie-responsive protein 1 (SCRG1)
• Synonyms: Scrapie-responsive gene 1 protein; ScRG-1
• Gene Name: SCRG1
• UniProt ID: SCRG1_HUMAN
• Pfam ID: PF15224
• Sequence:
  MKLMVLVFTIGLTLLLGVQAMPANRLSCYRKILKDHNCHNLPEGVADLTQIDVNVQDHFW
  DGKGCEMICYCNFSELLCCPKDVFFGPKISFVIPCNNQ
• Tissue Specificity: Expressed abundantly in the central nervous system of adult, but not at all in fetal brain. High levels of SCRG1 transcripts are also observed in testis and aorta.

Molecular Interaction Atlas (MIA) of This DOT

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

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate decreases the expression of Scrapie-responsive protein 1 (SCRG1).	[1]
Tretinoin	DM49DUI	Approved	Tretinoin decreases the expression of Scrapie-responsive protein 1 (SCRG1).	[2]
Temozolomide	DMKECZD	Approved	Temozolomide increases the expression of Scrapie-responsive protein 1 (SCRG1).	[3]
Vorinostat	DMWMPD4	Approved	Vorinostat increases the expression of Scrapie-responsive protein 1 (SCRG1).	[4]
Carbamazepine	DMZOLBI	Approved	Carbamazepine affects the expression of Scrapie-responsive protein 1 (SCRG1).	[5]
Selenium	DM25CGV	Approved	Selenium decreases the expression of Scrapie-responsive protein 1 (SCRG1).	[6]
Panobinostat	DM58WKG	Approved	Panobinostat increases the expression of Scrapie-responsive protein 1 (SCRG1).	[4]
Testosterone enanthate	DMB6871	Approved	Testosterone enanthate affects the expression of Scrapie-responsive protein 1 (SCRG1).	[7]
Indomethacin	DMSC4A7	Approved	Indomethacin increases the expression of Scrapie-responsive protein 1 (SCRG1).	[8]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 increases the expression of Scrapie-responsive protein 1 (SCRG1).	[9]
Bisphenol A	DM2ZLD7	Investigative	Bisphenol A decreases the expression of Scrapie-responsive protein 1 (SCRG1).	[10]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A increases the expression of Scrapie-responsive protein 1 (SCRG1).	[11]

References

• [1] Human embryonic stem cell-derived test systems for developmental neurotoxicity: a transcriptomics approach. Arch Toxicol. 2013 Jan;87(1):123-43.
• [2] 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.
• [3] 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.
• [4] 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.
• [5] 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.
• [6] Selenium and vitamin E: cell type- and intervention-specific tissue effects in prostate cancer. J Natl Cancer Inst. 2009 Mar 4;101(5):306-20.
• [7] Transcriptional profiling of testosterone-regulated genes in the skeletal muscle of human immunodeficiency virus-infected men experiencing weight loss. J Clin Endocrinol Metab. 2007 Jul;92(7):2793-802. doi: 10.1210/jc.2006-2722. Epub 2007 Apr 17.
• [8] Anti-inflammatory agent indomethacin reduces invasion and alters metabolism in a human breast cancer cell line. Neoplasia. 2007 Mar;9(3):222-35.
• [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] Bisphenol A and bisphenol S induce distinct transcriptional profiles in differentiating human primary preadipocytes. PLoS One. 2016 Sep 29;11(9):e0163318.
• [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.