Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OT0ZN08I)

DOT Name	Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7)
Synonyms	PPIase FKBP7; EC 5.2.1.8; 23 kDa FK506-binding protein; 23 kDa FKBP; FKBP-23; FK506-binding protein 7; FKBP-7; Rotamase
Gene Name	FKBP7
UniProt ID	FKBP7_HUMAN
3D Structure	Download 2D Sequence (FASTA) Download 3D Structure (PDB) Download
EC Number	5.2.1.8
Pfam ID	PF13202 ; PF00254
Sequence	MPKTMHFLFRFIVFFYLWGLFTAQRQKKEESTEEVKIEVLHRPENCSKTSKKGDLLNAHY DGYLAKDGSKFYCSRTQNEGHPKWFVLGVGQVIKGLDIAMTDMCPGEKRKVVIPPSFAYG KEGYAEGKIPPDATLIFEIELYAVTKGPRSIETFKQIDMDNDRQLSKAEINLYLQREFEK DEKPRDKSYQDAVLEDIFKKNDHDGDGFISPKEYNVYQHDEL
Function	PPIases accelerate the folding of proteins during protein synthesis.

Molecular Interaction Atlas (MIA) of This DOT

Molecular Interaction Atlas (MIA)

MIA Detail

Jump to Detail Molecular Interaction Atlas of This DOT

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 Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[1]
Ciclosporin	DMAZJFX	Approved	Ciclosporin decreases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[2]
Doxorubicin	DMVP5YE	Approved	Doxorubicin decreases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[3]
Cupric Sulfate	DMP0NFQ	Approved	Cupric Sulfate decreases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[4]
Vorinostat	DMWMPD4	Approved	Vorinostat increases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[5]
Acocantherin	DM7JT24	Approved	Acocantherin increases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[6]
Urethane	DM7NSI0	Phase 4	Urethane decreases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[7]
SNDX-275	DMH7W9X	Phase 3	SNDX-275 increases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[5]
Leflunomide	DMR8ONJ	Phase 1 Trial	Leflunomide decreases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[8]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 decreases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[9]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A increases the expression of Peptidyl-prolyl cis-trans isomerase FKBP7 (FKBP7).	[10]
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⏷ Show the Full List of 11 Drug(s)

References

1	Human embryonic stem cell-derived test systems for developmental neurotoxicity: a transcriptomics approach. Arch Toxicol. 2013 Jan;87(1):123-43.
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	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.
4	Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper. Physiol Genomics. 2009 Aug 7;38(3):386-401.
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	Ouabain at pathological concentrations might induce damage in human vascular endothelial cells. Acta Pharmacol Sin. 2006 Feb;27(2):165-72. doi: 10.1111/j.1745-7254.2006.00244.x.
7	Ethyl carbamate induces cell death through its effects on multiple metabolic pathways. Chem Biol Interact. 2017 Nov 1;277:21-32.
8	Endoplasmic reticulum stress and MAPK signaling pathway activation underlie leflunomide-induced toxicity in HepG2 Cells. Toxicology. 2017 Dec 1;392:11-21.
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	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.