Details of Drug Off-Target (DOT)

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

DOT Name TBC1 domain family member 8B (TBC1D8B)
Gene Name TBC1D8B
Related Disease
Nephrotic syndrome, type 2 ( )
Nephrotic syndrome, type 20 ( )
Steroid-resistant nephrotic syndrome ( )
Focal segmental glomerulosclerosis ( )
Nephrotic syndrome ( )
Familial idiopathic steroid-resistant nephrotic syndrome ( )
UniProt ID
TBC8B_HUMAN
3D Structure
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2D Sequence (FASTA)
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3D Structure (PDB)
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Pfam ID
PF02893 ; PF00566
Sequence
MWLKPEEVLLKNALKLWLMERSNDYFVLQRRRGYGEEGGGGLTGLLVGTLDSVLDSTAKV
APFRILHQTPDSQVYLSIACGANREEITKHWDWLEQNIMKTLSVFDSNEDITNFVQGKIR
GLIAEEGKHCFAKEDDPEKFREALLKFEKCFGLPEKEKLVTYYSCSYWKGRVPCQGWLYL
STNFLSFYSFLLGSEIKLIISWDEVSKLEKTSNVILTESIHVCSQGENHYFSMFLHINQT
YLLMEQLANYAIRRLFDKETFDNDPVLYNPLQITKRGLENRAHSEQFNAFFRLPKGESLK
EVHECFLWVPFSHFNTHGKMCISENYICFASQDGNQCSVIIPLREVLAIDKTNDSSKSVI
ISIKGKTAFRFHEVKDFEQLVAKLRLRCGAASTQYHDISTELAISSESTEPSDNFEVQSL
TSQRECSKTVNTEALMTVFHPQNLETLNSKMLKEKMKEQSWKILFAECGRGVSMFRTKKT
RDLVVRGIPETLRGELWMLFSGAVNDMATNPDYYTEVVEQSLGTCNLATEEIERDLRRSL
PEHPAFQSDTGISALRRVLTAYAYRNPKIGYCQAMNILTSVLLLYAKEEEAFWLLVAVCE
RMLPDYFNRRIIGALVDQAVFEELIRDHLPQLTEHMTDMTFFSSVSLSWFLTLFISVLPI
ESAVNVVDCFFYDGIKAILQLGLAILDYNLDKLLTCKDDAEAVTALNRFFDNVTNKDSPL
PSNVQQGSNVSDEKTSHTRVDITDLIRESNEKYGNIRYEDIHSMRCRNRLYVIQTLEETT
KQNVLRVVSQDVKLSLQELDELYVIFKKELFLSCYWCLGCPVLKHHDPSLPYLEQYQIDC
QQFRALYHLLSPWAHSANKDSLALWTFRLLDENSDCLINFKEFSSAIDIMYNGSFTEKLK
LLFKLHIPPAYTEVKSKDASKGDELSKEELLYFSQLHVSKPANEKEAESAKHSPEKGKGK
IDIQAYLSQWQDELFKKEENIKDLPRMNQSQFIQFSKTLYNLFHEDPEEESLYQAIAVVT
SLLLRMEEVGRKLHSPTSSAKGFSGTVCGSGGPSEEKTGSHLEKDPCSFREEPQWSFAFE
QILASLLNEPALVRFFEKPIDVKAKLENARISQLRSRTKM
Function Involved in vesicular recycling, probably as a RAB11B GTPase-activating protein.
Tissue Specificity Kidney (at protein level).
Reactome Pathway
Golgi Associated Vesicle Biogenesis (R-HSA-432722 )

Molecular Interaction Atlas (MIA) of This DOT

6 Disease(s) Related to This DOT
Disease Name Disease ID Evidence Level Mode of Inheritance REF
Nephrotic syndrome, type 2 DISIRFO1 Strong GermlineCausalMutation [1]
Nephrotic syndrome, type 20 DISSAJSU Strong X-linked [1]
Steroid-resistant nephrotic syndrome DISVEBC9 Strong Genetic Variation [1]
Focal segmental glomerulosclerosis DISJNHH0 moderate Biomarker [1]
Nephrotic syndrome DISSPSC2 moderate Biomarker [1]
Familial idiopathic steroid-resistant nephrotic syndrome DISQ53RS Supportive Autosomal dominant [1]
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⏷ Show the Full List of 6 Disease(s)
Molecular Interaction Atlas (MIA) Jump to Detail Molecular Interaction Atlas of This DOT
16 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 TBC1 domain family member 8B (TBC1D8B). [2]
Ciclosporin DMAZJFX Approved Ciclosporin decreases the expression of TBC1 domain family member 8B (TBC1D8B). [3]
Tretinoin DM49DUI Approved Tretinoin increases the expression of TBC1 domain family member 8B (TBC1D8B). [4]
Acetaminophen DMUIE76 Approved Acetaminophen decreases the expression of TBC1 domain family member 8B (TBC1D8B). [5]
Cupric Sulfate DMP0NFQ Approved Cupric Sulfate decreases the expression of TBC1 domain family member 8B (TBC1D8B). [6]
Quercetin DM3NC4M Approved Quercetin decreases the expression of TBC1 domain family member 8B (TBC1D8B). [7]
Selenium DM25CGV Approved Selenium decreases the expression of TBC1 domain family member 8B (TBC1D8B). [8]
Demecolcine DMCZQGK Approved Demecolcine decreases the expression of TBC1 domain family member 8B (TBC1D8B). [9]
Azathioprine DMMZSXQ Approved Azathioprine decreases the expression of TBC1 domain family member 8B (TBC1D8B). [10]
Clozapine DMFC71L Approved Clozapine increases the expression of TBC1 domain family member 8B (TBC1D8B). [11]
Clorgyline DMCEUJD Approved Clorgyline increases the expression of TBC1 domain family member 8B (TBC1D8B). [12]
Urethane DM7NSI0 Phase 4 Urethane decreases the expression of TBC1 domain family member 8B (TBC1D8B). [13]
SNDX-275 DMH7W9X Phase 3 SNDX-275 increases the expression of TBC1 domain family member 8B (TBC1D8B). [14]
PMID28460551-Compound-2 DM4DOUB Patented PMID28460551-Compound-2 increases the expression of TBC1 domain family member 8B (TBC1D8B). [16]
Trichostatin A DM9C8NX Investigative Trichostatin A increases the expression of TBC1 domain family member 8B (TBC1D8B). [19]
Formaldehyde DM7Q6M0 Investigative Formaldehyde decreases the expression of TBC1 domain family member 8B (TBC1D8B). [9]
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⏷ Show the Full List of 16 Drug(s)
3 Drug(s) Affected the Post-Translational Modifications of This DOT
Drug Name Drug ID Highest Status Interaction REF
Benzo(a)pyrene DMN7J43 Phase 1 Benzo(a)pyrene increases the methylation of TBC1 domain family member 8B (TBC1D8B). [15]
PMID28870136-Compound-52 DMFDERP Patented PMID28870136-Compound-52 decreases the phosphorylation of TBC1 domain family member 8B (TBC1D8B). [17]
Bisphenol A DM2ZLD7 Investigative Bisphenol A increases the methylation of TBC1 domain family member 8B (TBC1D8B). [18]
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References

1 TBC1D8B Loss-of-Function Mutations Lead to X-Linked Nephrotic Syndrome via Defective Trafficking Pathways. Am J Hum Genet. 2019 Feb 7;104(2):348-355. doi: 10.1016/j.ajhg.2018.12.016. Epub 2019 Jan 17.
2 Human embryonic stem cell-derived test systems for developmental neurotoxicity: a transcriptomics approach. Arch Toxicol. 2013 Jan;87(1):123-43.
3 Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro. Toxicol In Vitro. 2015 Apr;29(3):489-501.
4 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.
5 Gene expression analysis of precision-cut human liver slices indicates stable expression of ADME-Tox related genes. Toxicol Appl Pharmacol. 2011 May 15;253(1):57-69.
6 Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper. Physiol Genomics. 2009 Aug 7;38(3):386-401.
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 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.
9 Characterization of formaldehyde's genotoxic mode of action by gene expression analysis in TK6 cells. Arch Toxicol. 2013 Nov;87(11):1999-2012.
10 A transcriptomics-based in vitro assay for predicting chemical genotoxicity in vivo. Carcinogenesis. 2012 Jul;33(7):1421-9.
11 Cannabidiol Displays Proteomic Similarities to Antipsychotics in Cuprizone-Exposed Human Oligodendrocytic Cell Line MO3.13. Front Mol Neurosci. 2021 May 28;14:673144. doi: 10.3389/fnmol.2021.673144. eCollection 2021.
12 Anti-oncogenic and pro-differentiation effects of clorgyline, a monoamine oxidase A inhibitor, on high grade prostate cancer cells. BMC Med Genomics. 2009 Aug 20;2:55. doi: 10.1186/1755-8794-2-55.
13 Ethyl carbamate induces cell death through its effects on multiple metabolic pathways. Chem Biol Interact. 2017 Nov 1;277:21-32.
14 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.
15 Air pollution and DNA methylation alterations in lung cancer: A systematic and comparative study. Oncotarget. 2017 Jan 3;8(1):1369-1391. doi: 10.18632/oncotarget.13622.
16 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.
17 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.
18 Expression and DNA methylation changes in human breast epithelial cells after bisphenol A exposure. Int J Oncol. 2012 Jul;41(1):369-77.
19 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.