Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OTJN8P3K)

DOT Name	Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2)
Synonyms	Acyl-CoA thioesterase MBLAC2; EC 3.1.2.2; Beta-lactamase MBLAC2; EC 3.5.2.6; Metallo-beta-lactamase domain-containing protein 2; Palmitoyl-coenzyme A thioesterase MBLAC2
Gene Name	MBLAC2
UniProt ID	MBLC2_HUMAN
3D Structure	Download 2D Sequence (FASTA) Download 3D Structure (PDB) Download
EC Number	3.1.2.2; 3.5.2.6
Pfam ID	PF00753
Sequence	MSALEWYAHKSLGDGIFWIQERFYESGNRANIWLVRGSEQDVVIDTGLGLRSLPEYLYSS GLLQDREAKEDAARRPLLAVATHVHFDHSGGLYQFDRVAVHHAEAEALARGDNFETVTWL SDSEVVRTPSPGWRARQFRVQAVQPTLILQDGDVINLGDRQLTVMHMPGHSRGSICLHDK DRKILFSGDVVYDGSLIDWLPYSRISDYVGTCERLIELVDRGLVEKVLPGHFNTFGAERL FRLASNYISKAGICHKVSTFAMRSLASLALRVTNSRTSP
Function	Acyl-CoA thioesterases are a group of enzymes that catalyze the hydrolysis of acyl-CoAs to the free fatty acid and coenzyme A (CoASH), providing the potential to regulate intracellular levels of acyl-CoAs, free fatty acids and CoASH. Has an acyl-CoA thioesterase activity towards the long chain fatty acyl-CoA thioester palmitoyl-CoA (hexadecanoyl-CoA; C16:0-CoA). Displays a substrate preference for fatty acyl-CoAs with chain-lengths C12-C18. Possesses beta-lactamase activity, catalyzing the hydrolysis of penicillin G and nitrocefin. Exhibits no activity towards other beta-lactam antibiotic classes including cephalosporins (cefotaxime) and carbapenems (imipenem).

Molecular Interaction Atlas (MIA) of This DOT

Molecular Interaction Atlas (MIA)

MIA Detail

Jump to Detail Molecular Interaction Atlas of This DOT

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

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate decreases the methylation of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[1]
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10 Drug(s) Affected the Gene/Protein Processing of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Ciclosporin	DMAZJFX	Approved	Ciclosporin decreases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[2]
Doxorubicin	DMVP5YE	Approved	Doxorubicin decreases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[3]
Cisplatin	DMRHGI9	Approved	Cisplatin decreases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[4]
Estradiol	DMUNTE3	Approved	Estradiol increases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[5]
Ivermectin	DMDBX5F	Approved	Ivermectin decreases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[6]
Quercetin	DM3NC4M	Approved	Quercetin decreases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[7]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 increases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[8]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A increases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[9]
Formaldehyde	DM7Q6M0	Investigative	Formaldehyde decreases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[10]
Acetaldehyde	DMJFKG4	Investigative	Acetaldehyde decreases the expression of Acyl-coenzyme A thioesterase MBLAC2 (MBLAC2).	[11]
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⏷ Show the Full List of 10 Drug(s)

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	Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro. Toxicol In Vitro. 2015 Apr;29(3):489-501.
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	Activation of AIFM2 enhances apoptosis of human lung cancer cells undergoing toxicological stress. Toxicol Lett. 2016 Sep 6;258:227-236.
5	17-Estradiol Activates HSF1 via MAPK Signaling in ER-Positive Breast Cancer Cells. Cancers (Basel). 2019 Oct 11;11(10):1533. doi: 10.3390/cancers11101533.
6	Quantitative proteomics reveals a broad-spectrum antiviral property of ivermectin, benefiting for COVID-19 treatment. J Cell Physiol. 2021 Apr;236(4):2959-2975. doi: 10.1002/jcp.30055. Epub 2020 Sep 22.
7	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.
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.
9	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.
10	Gene expression changes in primary human nasal epithelial cells exposed to formaldehyde in vitro. Toxicol Lett. 2010 Oct 5;198(2):289-95.
11	In vitro effects of aldehydes present in tobacco smoke on gene expression in human lung alveolar epithelial cells. Toxicol In Vitro. 2013 Apr;27(3):1072-81.