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

DOT Name Partitioning defective 6 homolog beta (PARD6B)
Synonyms PAR-6 beta; PAR-6B
Gene Name PARD6B
UniProt ID
PAR6B_HUMAN
3D Structure
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2D Sequence (FASTA)
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3D Structure (PDB)
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Pfam ID
PF00564 ; PF00595
Sequence
MNRSHRHGAGSGCLGTMEVKSKFGAEFRRFSLERSKPGKFEEFYGLLQHVHKIPNVDVLV
GYADIHGDLLPINNDDNYHKAVSTANPLLRIFIQKKEEADYSAFGTDTLIKKKNVLTNVL
RPDNHRKKPHIVISMPQDFRPVSSIIDVDILPETHRRVRLYKYGTEKPLGFYIRDGSSVR
VTPHGLEKVPGIFISRLVPGGLAQSTGLLAVNDEVLEVNGIEVSGKSLDQVTDMMIANSR
NLIITVRPANQRNNVVRNSRTSGSSGQSTDNSLLGYPQQIEPSFEPEDEDSEEDDIIIED
NGVPQQIPKAVPNTESLESLTQIELSFESGQNGFIPSNEVSLAAIASSSNTEFETHAPDQ
KLLEEDGTIITL
Function
Adapter protein involved in asymmetrical cell division and cell polarization processes. Probably involved in formation of epithelial tight junctions. Association with PARD3 may prevent the interaction of PARD3 with F11R/JAM1, thereby preventing tight junction assembly. The PARD6-PARD3 complex links GTP-bound Rho small GTPases to atypical protein kinase C proteins.
Tissue Specificity Expressed in pancreas and in both adult and fetal kidney. Weakly expressed in placenta and lung. Not expressed in other tissues.
KEGG Pathway
Rap1 sig.ling pathway (hsa04015 )
Endocytosis (hsa04144 )
Axon guidance (hsa04360 )
Hippo sig.ling pathway (hsa04390 )
Tight junction (hsa04530 )
Human papillomavirus infection (hsa05165 )
Reactome Pathway
RHOV GTPase cycle (R-HSA-9013424 )
Tight junction interactions (R-HSA-420029 )

Molecular Interaction Atlas (MIA) of This DOT

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 decreases the expression of Partitioning defective 6 homolog beta (PARD6B). [1]
Tretinoin DM49DUI Approved Tretinoin increases the expression of Partitioning defective 6 homolog beta (PARD6B). [2]
Cupric Sulfate DMP0NFQ Approved Cupric Sulfate increases the expression of Partitioning defective 6 homolog beta (PARD6B). [3]
Ivermectin DMDBX5F Approved Ivermectin decreases the expression of Partitioning defective 6 homolog beta (PARD6B). [4]
Triclosan DMZUR4N Approved Triclosan increases the expression of Partitioning defective 6 homolog beta (PARD6B). [5]
Amphotericin B DMTAJQE Approved Amphotericin B increases the expression of Partitioning defective 6 homolog beta (PARD6B). [6]
Benzo(a)pyrene DMN7J43 Phase 1 Benzo(a)pyrene increases the expression of Partitioning defective 6 homolog beta (PARD6B). [8]
Leflunomide DMR8ONJ Phase 1 Trial Leflunomide increases the expression of Partitioning defective 6 homolog beta (PARD6B). [9]
PMID28460551-Compound-2 DM4DOUB Patented PMID28460551-Compound-2 decreases the expression of Partitioning defective 6 homolog beta (PARD6B). [10]
Bisphenol A DM2ZLD7 Investigative Bisphenol A increases the expression of Partitioning defective 6 homolog beta (PARD6B). [12]
Trichostatin A DM9C8NX Investigative Trichostatin A decreases the expression of Partitioning defective 6 homolog beta (PARD6B). [13]
Formaldehyde DM7Q6M0 Investigative Formaldehyde increases the expression of Partitioning defective 6 homolog beta (PARD6B). [14]
Milchsaure DM462BT Investigative Milchsaure decreases the expression of Partitioning defective 6 homolog beta (PARD6B). [15]
3R14S-OCHRATOXIN A DM2KEW6 Investigative 3R14S-OCHRATOXIN A increases the expression of Partitioning defective 6 homolog beta (PARD6B). [8]
Tributylstannanyl DMHN7CB Investigative Tributylstannanyl increases the expression of Partitioning defective 6 homolog beta (PARD6B). [8]
Methyl Mercury Ion DM6YEW4 Investigative Methyl Mercury Ion increases the expression of Partitioning defective 6 homolog beta (PARD6B). [8]
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⏷ Show the Full List of 16 Drug(s)
2 Drug(s) Affected the Post-Translational Modifications of This DOT
Drug Name Drug ID Highest Status Interaction REF
G1 DMTV42K Phase 1/2 G1 increases the phosphorylation of Partitioning defective 6 homolog beta (PARD6B). [7]
PMID28870136-Compound-52 DMFDERP Patented PMID28870136-Compound-52 increases the phosphorylation of Partitioning defective 6 homolog beta (PARD6B). [11]
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References

1 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.
2 Transcriptional and Metabolic Dissection of ATRA-Induced Granulocytic Differentiation in NB4 Acute Promyelocytic Leukemia Cells. Cells. 2020 Nov 5;9(11):2423. doi: 10.3390/cells9112423.
3 Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper. Physiol Genomics. 2009 Aug 7;38(3):386-401.
4 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.
5 Transcriptome and DNA methylome dynamics during triclosan-induced cardiomyocyte differentiation toxicity. Stem Cells Int. 2018 Oct 29;2018:8608327.
6 Differential expression of microRNAs and their predicted targets in renal cells exposed to amphotericin B and its complex with copper (II) ions. Toxicol Mech Methods. 2017 Sep;27(7):537-543. doi: 10.1080/15376516.2017.1333554. Epub 2017 Jun 8.
7 The G Protein-Coupled Estrogen Receptor Agonist G-1 Inhibits Nuclear Estrogen Receptor Activity and Stimulates Novel Phosphoproteomic Signatures. Toxicol Sci. 2016 Jun;151(2):434-46. doi: 10.1093/toxsci/kfw057. Epub 2016 Mar 29.
8 Inhibition of CXCL12-mediated chemotaxis of Jurkat cells by direct immunotoxicants. Arch Toxicol. 2016 Jul;90(7):1685-94. doi: 10.1007/s00204-015-1585-7. Epub 2015 Aug 28.
9 Endoplasmic reticulum stress and MAPK signaling pathway activation underlie leflunomide-induced toxicity in HepG2 Cells. Toxicology. 2017 Dec 1;392:11-21.
10 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.
11 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.
12 Characterization of the Molecular Alterations Induced by the Prolonged Exposure of Normal Colon Mucosa and Colon Cancer Cells to Low-Dose Bisphenol A. Int J Mol Sci. 2022 Oct 1;23(19):11620. doi: 10.3390/ijms231911620.
13 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.
14 Characterization of formaldehyde's genotoxic mode of action by gene expression analysis in TK6 cells. Arch Toxicol. 2013 Nov;87(11):1999-2012.
15 Transcriptional profiling of lactic acid treated reconstructed human epidermis reveals pathways underlying stinging and itch. Toxicol In Vitro. 2019 Jun;57:164-173.