Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OTZD8TQS)

• DOT Name: Solute carrier family 35 member E3 (SLC35E3)
• Synonyms: Bladder cancer-overexpressed gene 1 protein
• Gene Name: SLC35E3
• Related Disease: Cardiovascular disease
• UniProt ID: S35E3_HUMAN
• Pfam ID: PF03151
• Sequence:
  MALLVDRVRGHWRIAAGLLFNLLVSICIVFLNKWIYVYHGFPNMSLTLVHFVVTWLGLYI
  CQKLDIFAPKSLPPSRLLLLALSFCGFVVFTNLSLQNNTIGTYQLAKAMTTPVIIAIQTF
  CYQKTFSTRIQLTLIPITLGVILNSYYDVKFNFLGMVFAALGVLVTSLYQVWVGAKQHEL
  QVNSMQLLYYQAPMSSAMLLVAVPFFEPVFGEGGIFGPWSVSALLMVLLSGVIAFMVNLS
  IYWIIGNTSPVTYNMFGHFKFCITLFGGYVLFKDPLSINQALGILCTLFGILAYTHFKLS
  EQEGSRSKLAQRP
• Function: Putative transporter.

Molecular Interaction Atlas (MIA) of This DOT

1 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Cardiovascular disease	DIS2IQDX	Strong	Altered Expression	[1]

8 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 Solute carrier family 35 member E3 (SLC35E3).	[2]
Ciclosporin	DMAZJFX	Approved	Ciclosporin decreases the expression of Solute carrier family 35 member E3 (SLC35E3).	[3]
Tretinoin	DM49DUI	Approved	Tretinoin decreases the expression of Solute carrier family 35 member E3 (SLC35E3).	[4]
Acetaminophen	DMUIE76	Approved	Acetaminophen increases the expression of Solute carrier family 35 member E3 (SLC35E3).	[5]
Doxorubicin	DMVP5YE	Approved	Doxorubicin decreases the expression of Solute carrier family 35 member E3 (SLC35E3).	[6]
Cisplatin	DMRHGI9	Approved	Cisplatin increases the expression of Solute carrier family 35 member E3 (SLC35E3).	[7]
Benzo(a)pyrene	DMN7J43	Phase 1	Benzo(a)pyrene increases the expression of Solute carrier family 35 member E3 (SLC35E3).	[8]
Formaldehyde	DM7Q6M0	Investigative	Formaldehyde increases the expression of Solute carrier family 35 member E3 (SLC35E3).	[9]

References

• [1] SLC35E3 identified as a target of novelm1061?p via microRNA profiling of patients with cardiovascular disease.Mol Med Rep. 2018 Apr;17(4):5159-5167. doi: 10.3892/mmr.2018.8498. Epub 2018 Jan 25.
• [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] 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.
• [5] Predictive toxicology using systemic biology and liver microfluidic "on chip" approaches: application to acetaminophen injury. Toxicol Appl Pharmacol. 2012 Mar 15;259(3):270-80.
• [6] 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.
• [7] The thioxotriazole copper(II) complex A0 induces endoplasmic reticulum stress and paraptotic death in human cancer cells. J Biol Chem. 2009 Sep 4;284(36):24306-19.
• [8] 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.
• [9] Characterization of formaldehyde's genotoxic mode of action by gene expression analysis in TK6 cells. Arch Toxicol. 2013 Nov;87(11):1999-2012.