Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OT5PTQSH)

DOT Name	Spindlin-3 (SPIN3)
Synonyms	Spindlin-like protein 3; SPIN-3
Gene Name	SPIN3
Related Disease	Advanced cancer ( ) Colorectal carcinoma ( ) Neoplasm ( ) Seminoma ( )
UniProt ID	SPIN3_HUMAN
3D Structure	Download 2D Sequence (FASTA) Download 3D Structure (PDB) Download
PDB ID	5A1H
Pfam ID	PF02513
Sequence	MKTPFGKAAAGQRSRTGAGHGSVSVTMIKRKAAHKKHRSRPTSQPRGNIVGCRIQHGWKD GDEPLTQWKGTVLDQVPVNPSLYLIKYDGFDCVYGLELHRDERVSSLEVLPNRVASSRIS DTHLAEIMVGKAVEHIFETEEGSKNEWRGMVLAQAPVMNTWFYITYEKDPVLYMYQLLDD YKDGDLRILQDSNDSPLAEREPGEVIDSLVGKQVEYAKDDGSKRTGMVIHQVEAKPSVYF IKFDDDFHIYVYDLVKTS
Function	Exhibits H3K4me3-binding activity.

Molecular Interaction Atlas (MIA) of This DOT

4 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance
Advanced cancer	DISAT1Z9	Strong	Biomarker	[1]
Colorectal carcinoma	DIS5PYL0	Strong	Genetic Variation	[2]
Neoplasm	DISZKGEW	Strong	Biomarker	[1]
Seminoma	DIS3J8LJ	Strong	Altered Expression	[1]
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Molecular Interaction Atlas (MIA)

MIA Detail

Jump to Detail Molecular Interaction Atlas of This DOT

6 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 Spindlin-3 (SPIN3).	[3]
Quercetin	DM3NC4M	Approved	Quercetin decreases the expression of Spindlin-3 (SPIN3).	[4]
SNDX-275	DMH7W9X	Phase 3	SNDX-275 decreases the expression of Spindlin-3 (SPIN3).	[5]
APR-246	DMNFADH	Phase 2	APR-246 affects the expression of Spindlin-3 (SPIN3).	[6]
Benzo(a)pyrene	DMN7J43	Phase 1	Benzo(a)pyrene decreases the expression of Spindlin-3 (SPIN3).	[7]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 increases the expression of Spindlin-3 (SPIN3).	[8]
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⏷ Show the Full List of 6 Drug(s)

References

1	SPIN1 is a proto-oncogene and SPIN3 is a tumor suppressor in human seminoma.Oncotarget. 2018 Aug 21;9(65):32466-32477. doi: 10.18632/oncotarget.25977. eCollection 2018 Aug 21.
2	Pooled sample-based GWAS: a cost-effective alternative for identifying colorectal and prostate cancer risk variants in the Polish population.PLoS One. 2012;7(4):e35307. doi: 10.1371/journal.pone.0035307. Epub 2012 Apr 19.
3	Human embryonic stem cell-derived test systems for developmental neurotoxicity: a transcriptomics approach. Arch Toxicol. 2013 Jan;87(1):123-43.
4	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.
5	Definition of transcriptome-based indices for quantitative characterization of chemically disturbed stem cell development: introduction of the STOP-Toxukn and STOP-Toxukk tests. Arch Toxicol. 2017 Feb;91(2):839-864.
6	Mutant p53 reactivation by PRIMA-1MET induces multiple signaling pathways converging on apoptosis. Oncogene. 2010 Mar 4;29(9):1329-38. doi: 10.1038/onc.2009.425. Epub 2009 Nov 30.
7	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.
8	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.