Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OT9GLJI6)

• DOT Name: Histone-lysine N-methyltransferase 2A (KMT2A)
• Synonyms: Lysine N-methyltransferase 2A; EC 2.1.1.364; ALL-1; CXXC-type zinc finger protein 7; Cysteine methyltransferase KMT2A; EC 2.1.1.-; Myeloid/lymphoid or mixed-lineage leukemia; Myeloid/lymphoid or mixed-lineage leukemia protein 1; Trithorax-like protein; Zinc finger protein HRX
• Gene Name: KMT2A
• Related Disease: Wiedemann-Steiner syndrome
• UniProt ID: KMT2A_HUMAN
• PDB ID: 2AGH ; 2J2S ; 2JYI ; 2KKF ; 2KU7 ; 2KYU ; 2LXS ; 2LXT ; 2MSR ; 2MTN ; 2W5Y ; 2W5Z ; 3EG6 ; 3EMH ; 3LQH ; 3LQI ; 3LQJ ; 3P4F ; 3U85 ; 3U88 ; 4ESG ; 4GQ6 ; 4NW3 ; 5F5E ; 5F6L ; 5SVH ; 6EMQ ; 6KIU ; 6KIV ; 6KIX ; 6KIZ ; 6PWV ; 6PWW ; 6U9K ; 6U9M ; 6U9N ; 6U9R ; 6W5I ; 6W5M ; 6W5N ; 7MBM ; 7MBN ; 7RZD ; 7RZJ ; 7S79 ; 7S7D ; 7S8A ; 7S8E ; 7S8F ; 7U5V ; 7W67 ; 7W6A ; 7W6I ; 7W6J ; 7ZEY ; 7ZEZ
• EC Number: 2.1.1.-; 2.1.1.364
• Pfam ID: PF05965 ; PF05964 ; PF00628 ; PF00856 ; PF02008 ; PF13771
• Sequence:
  MAHSCRWRFPARPGTTGGGGGGGRRGLGGAPRQRVPALLLPPGPPVGGGGPGAPPSPPAV
  AAAAAAAGSSGAGVPGGAAAASAASSSSASSSSSSSSSASSGPALLRVGPGFDAALQVSA
  AIGTNLRRFRAVFGESGGGGGSGEDEQFLGFGSDEEVRVRSPTRSPSVKTSPRKPRGRPR
  SGSDRNSAILSDPSVFSPLNKSETKSGDKIKKKDSKSIEKKRGRPPTFPGVKIKITHGKD
  ISELPKGNKEDSLKKIKRTPSATFQQATKIKKLRAGKLSPLKSKFKTGKLQIGRKGVQIV
  RRRGRPPSTERIKTPSGLLINSELEKPQKVRKDKEGTPPLTKEDKTVVRQSPRRIKPVRI
  IPSSKRTDATIAKQLLQRAKKGAQKKIEKEAAQLQGRKVKTQVKNIRQFIMPVVSAISSR
  IIKTPRRFIEDEDYDPPIKIARLESTPNSRFSAPSCGSSEKSSAASQHSSQMSSDSSRSS
  SPSVDTSTDSQASEEIQVLPEERSDTPEVHPPLPISQSPENESNDRRSRRYSVSERSFGS
  RTTKKLSTLQSAPQQQTSSSPPPPLLTPPPPLQPASSISDHTPWLMPPTIPLASPFLPAS
  TAPMQGKRKSILREPTFRWTSLKHSRSEPQYFSSAKYAKEGLIRKPIFDNFRPPPLTPED
  VGFASGFSASGTAASARLFSPLHSGTRFDMHKRSPLLRAPRFTPSEAHSRIFESVTLPSN
  RTSAGTSSSGVSNRKRKRKVFSPIRSEPRSPSHSMRTRSGRLSSSELSPLTPPSSVSSSL
  SISVSPLATSALNPTFTFPSHSLTQSGESAEKNQRPRKQTSAPAEPFSSSSPTPLFPWFT
  PGSQTERGRNKDKAPEELSKDRDADKSVEKDKSRERDREREKENKRESRKEKRKKGSEIQ
  SSSALYPVGRVSKEKVVGEDVATSSSAKKATGRKKSSSHDSGTDITSVTLGDTTAVKTKI
  LIKKGRGNLEKTNLDLGPTAPSLEKEKTLCLSTPSSSTVKHSTSSIGSMLAQADKLPMTD
  KRVASLLKKAKAQLCKIEKSKSLKQTDQPKAQGQESDSSETSVRGPRIKHVCRRAAVALG
  RKRAVFPDDMPTLSALPWEEREKILSSMGNDDKSSIAGSEDAEPLAPPIKPIKPVTRNKA
  PQEPPVKKGRRSRRCGQCPGCQVPEDCGVCTNCLDKPKFGGRNIKKQCCKMRKCQNLQWM
  PSKAYLQKQAKAVKKKEKKSKTSEKKDSKESSVVKNVVDSSQKPTPSAREDPAPKKSSSE
  PPPRKPVEEKSEEGNVSAPGPESKQATTPASRKSSKQVSQPALVIPPQPPTTGPPRKEVP
  KTTPSEPKKKQPPPPESGPEQSKQKKVAPRPSIPVKQKPKEKEKPPPVNKQENAGTLNIL
  STLSNGNSSKQKIPADGVHRIRVDFKEDCEAENVWEMGGLGILTSVPITPRVVCFLCASS
  GHVEFVYCQVCCEPFHKFCLEENERPLEDQLENWCCRRCKFCHVCGRQHQATKQLLECNK
  CRNSYHPECLGPNYPTKPTKKKKVWICTKCVRCKSCGSTTPGKGWDAQWSHDFSLCHDCA
  KLFAKGNFCPLCDKCYDDDDYESKMMQCGKCDRWVHSKCENLSDEMYEILSNLPESVAYT
  CVNCTERHPAEWRLALEKELQISLKQVLTALLNSRTTSHLLRYRQAAKPPDLNPETEESI
  PSRSSPEGPDPPVLTEVSKQDDQQPLDLEGVKRKMDQGNYTSVLEFSDDIVKIIQAAINS
  DGGQPEIKKANSMVKSFFIRQMERVFPWFSVKKSRFWEPNKVSSNSGMLPNAVLPPSLDH
  NYAQWQEREENSHTEQPPLMKKIIPAPKPKGPGEPDSPTPLHPPTPPILSTDRSREDSPE
  LNPPPGIEDNRQCALCLTYGDDSANDAGRLLYIGQNEWTHVNCALWSAEVFEDDDGSLKN
  VHMAVIRGKQLRCEFCQKPGATVGCCLTSCTSNYHFMCSRAKNCVFLDDKKVYCQRHRDL
  IKGEVVPENGFEVFRRVFVDFEGISLRRKFLNGLEPENIHMMIGSMTIDCLGILNDLSDC
  EDKLFPIGYQCSRVYWSTTDARKRCVYTCKIVECRPPVVEPDINSTVEHDENRTIAHSPT
  SFTESSSKESQNTAEIISPPSPDRPPHSQTSGSCYYHVISKVPRIRTPSYSPTQRSPGCR
  PLPSAGSPTPTTHEIVTVGDPLLSSGLRSIGSRRHSTSSLSPQRSKLRIMSPMRTGNTYS
  RNNVSSVSTTGTATDLESSAKVVDHVLGPLNSSTSLGQNTSTSSNLQRTVVTVGNKNSHL
  DGSSSSEMKQSSASDLVSKSSSLKGEKTKVLSSKSSEGSAHNVAYPGIPKLAPQVHNTTS
  RELNVSKIGSFAEPSSVSFSSKEALSFPHLHLRGQRNDRDQHTDSTQSANSSPDEDTEVK
  TLKLSGMSNRSSIINEHMGSSSRDRRQKGKKSCKETFKEKHSSKSFLEPGQVTTGEEGNL
  KPEFMDEVLTPEYMGQRPCNNVSSDKIGDKGLSMPGVPKAPPMQVEGSAKELQAPRKRTV
  KVTLTPLKMENESQSKNALKESSPASPLQIESTSPTEPISASENPGDGPVAQPSPNNTSC
  QDSQSNNYQNLPVQDRNLMLPDGPKPQEDGSFKRRYPRRSARARSNMFFGLTPLYGVRSY
  GEEDIPFYSSSTGKKRGKRSAEGQVDGADDLSTSDEDDLYYYNFTRTVISSGGEERLASH
  NLFREEEQCDLPKISQLDGVDDGTESDTSVTATTRKSSQIPKRNGKENGTENLKIDRPED
  AGEKEHVTKSSVGHKNEPKMDNCHSVSRVKTQGQDSLEAQLSSLESSRRVHTSTPSDKNL
  LDTYNTELLKSDSDNNNSDDCGNILPSDIMDFVLKNTPSMQALGESPESSSSELLNLGEG
  LGLDSNREKDMGLFEVFSQQLPTTEPVDSSVSSSISAEEQFELPLELPSDLSVLTTRSPT
  VPSQNPSRLAVISDSGEKRVTITEKSVASSESDPALLSPGVDPTPEGHMTPDHFIQGHMD
  ADHISSPPCGSVEQGHGNNQDLTRNSSTPGLQVPVSPTVPIQNQKYVPNSTDSPGPSQIS
  NAAVQTTPPHLKPATEKLIVVNQNMQPLYVLQTLPNGVTQKIQLTSSVSSTPSVMETNTS
  VLGPMGGGLTLTTGLNPSLPTSQSLFPSASKGLLPMSHHQHLHSFPAATQSSFPPNISNP
  PSGLLIGVQPPPDPQLLVSESSQRTDLSTTVATPSSGLKKRPISRLQTRKNKKLAPSSTP
  SNIAPSDVVSNMTLINFTPSQLPNHPSLLDLGSLNTSSHRTVPNIIKRSKSSIMYFEPAP
  LLPQSVGGTAATAAGTSTISQDTSHLTSGSVSGLASSSSVLNVVSMQTTTTPTSSASVPG
  HVTLTNPRLLGTPDIGSISNLLIKASQQSLGIQDQPVALPPSSGMFPQLGTSQTPSTAAI
  TAASSICVLPSTQTTGITAASPSGEADEHYQLQHVNQLLASKTGIHSSQRDLDSASGPQV
  SNFTQTVDAPNSMGLEQNKALSSAVQASPTSPGGSPSSPSSGQRSASPSVPGPTKPKPKT
  KRFQLPLDKGNGKKHKVSHLRTSSSEAHIPDQETTSLTSGTGTPGAEAEQQDTASVEQSS
  QKECGQPAGQVAVLPEVQVTQNPANEQESAEPKTVEEEESNFSSPLMLWLQQEQKRKESI
  TEKKPKKGLVFEISSDDGFQICAESIEDAWKSLTDKVQEARSNARLKQLSFAGVNGLRML
  GILHDAVVFLIEQLSGAKHCRNYKFRFHKPEEANEPPLNPHGSARAEVHLRKSAFDMFNF
  LASKHRQPPEYNPNDEEEEEVQLKSARRATSMDLPMPMRFRHLKKTSKEAVGVYRSPIHG
  RGLFCKRNIDAGEMVIEYAGNVIRSIQTDKREKYYDSKGIGCYMFRIDDSEVVDATMHGN
  AARFINHSCEPNCYSRVINIDGQKHIVIFAMRKIYRGEELTYDYKFPIEDASNKLPCNCG
  AKKCRKFLN
• Function: Histone methyltransferase that plays an essential role in early development and hematopoiesis. Catalytic subunit of the MLL1/MLL complex, a multiprotein complex that mediates both methylation of 'Lys-4' of histone H3 (H3K4me) complex and acetylation of 'Lys-16' of histone H4 (H4K16ac). Catalyzes methyl group transfer from S-adenosyl-L-methionine to the epsilon-amino group of 'Lys-4' of histone H3 (H3K4) via a non-processive mechanism. Part of chromatin remodeling machinery predominantly forms H3K4me1 and H3K4me2 methylation marks at active chromatin sites where transcription and DNA repair take place. Has weak methyltransferase activity by itself, and requires other component of the MLL1/MLL complex to obtain full methyltransferase activity. Has no activity toward histone H3 phosphorylated on 'Thr-3', less activity toward H3 dimethylated on 'Arg-8' or 'Lys-9', while it has higher activity toward H3 acetylated on 'Lys-9'. Binds to unmethylated CpG elements in the promoter of target genes and helps maintain them in the nonmethylated state. Required for transcriptional activation of HOXA9. Promotes PPP1R15A-induced apoptosis. Plays a critical role in the control of circadian gene expression and is essential for the transcriptional activation mediated by the CLOCK-BMAL1 heterodimer. Establishes a permissive chromatin state for circadian transcription by mediating a rhythmic methylation of 'Lys-4' of histone H3 (H3K4me) and this histone modification directs the circadian acetylation at H3K9 and H3K14 allowing the recruitment of CLOCK-BMAL1 to chromatin. Also has auto-methylation activity on Cys-3882 in absence of histone H3 substrate.
• Tissue Specificity: Heart, lung, brain and T- and B-lymphocytes.
• KEGG Pathway:
  Lysine degradation (hsa00310)
  Metabolic pathways (hsa01100)
  Cushing syndrome (hsa04934)
  Transcriptio.l misregulation in cancer (hsa05202)
• Reactome Pathway:
  RUNX1 regulates genes involved in megakaryocyte differentiation and platelet function (R-HSA-8936459)
  RUNX1 regulates transcription of genes involved in differentiation of HSCs (R-HSA-8939236)
  Transcriptional regulation of granulopoiesis (R-HSA-9616222)
  Formation of WDR5-containing histone-modifying complexes (R-HSA-9772755)
  PKMTs methylate histone lysines (R-HSA-3214841)
• BioCyc Pathway: MetaCyc:HS04188-MONOMER

Molecular Interaction Atlas (MIA) of This DOT

1 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Wiedemann-Steiner syndrome	DIS67KX5	Definitive	Autosomal dominant	[1]

This DOT Affected the Drug Response of 4 Drug(s)

Drug Name	Drug ID	Highest Status	Interaction	REF
Doxorubicin	DMVP5YE	Approved	Histone-lysine N-methyltransferase 2A (KMT2A) decreases the response to substance of Doxorubicin.	[29]
Cytarabine	DMZD5QR	Approved	Histone-lysine N-methyltransferase 2A (KMT2A) increases the response to substance of Cytarabine.	[29]
Prednisolone	DMQ8FR2	Approved	Histone-lysine N-methyltransferase 2A (KMT2A) decreases the response to substance of Prednisolone.	[29]
Cladribine	DM3JDRP	Approved	Histone-lysine N-methyltransferase 2A (KMT2A) increases the response to substance of Cladribine.	[29]

26 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 Histone-lysine N-methyltransferase 2A (KMT2A).	[2]
Tretinoin	DM49DUI	Approved	Tretinoin decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[3]
Acetaminophen	DMUIE76	Approved	Acetaminophen increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[4]
Cupric Sulfate	DMP0NFQ	Approved	Cupric Sulfate decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[5]
Cisplatin	DMRHGI9	Approved	Cisplatin decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[6]
Estradiol	DMUNTE3	Approved	Estradiol decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[7]
Quercetin	DM3NC4M	Approved	Quercetin increases the mutagenesis of Histone-lysine N-methyltransferase 2A (KMT2A).	[8]
Vorinostat	DMWMPD4	Approved	Vorinostat decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[9]
Marinol	DM70IK5	Approved	Marinol increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[10]
Ethanol	DMDRQZU	Approved	Ethanol decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[11]
Testosterone enanthate	DMB6871	Approved	Testosterone enanthate affects the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[13]
Clozapine	DMFC71L	Approved	Clozapine increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[14]
Malathion	DMXZ84M	Approved	Malathion increases the mutagenesis of Histone-lysine N-methyltransferase 2A (KMT2A).	[15]
Permethrin	DMZ0Q1G	Approved	Permethrin increases the mutagenesis of Histone-lysine N-methyltransferase 2A (KMT2A).	[16]
Rigosertib	DMOSTXF	Phase 3	Rigosertib increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[17]
Genistein	DM0JETC	Phase 2/3	Genistein increases the mutagenesis of Histone-lysine N-methyltransferase 2A (KMT2A).	[8]
Benzo(a)pyrene	DMN7J43	Phase 1	Benzo(a)pyrene decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[18]
Geldanamycin	DMS7TC5	Discontinued in Phase 2	Geldanamycin increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[20]
Torcetrapib	DMDHYM7	Discontinued in Phase 2	Torcetrapib increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[21]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[23]
Formaldehyde	DM7Q6M0	Investigative	Formaldehyde increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[24]
Milchsaure	DM462BT	Investigative	Milchsaure increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[25]
Nickel chloride	DMI12Y8	Investigative	Nickel chloride increases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[26]
crotylaldehyde	DMTWRQI	Investigative	crotylaldehyde decreases the expression of Histone-lysine N-methyltransferase 2A (KMT2A).	[27]
Chlorpyrifos	DMKPUI6	Investigative	Chlorpyrifos increases the mutagenesis of Histone-lysine N-methyltransferase 2A (KMT2A).	[28]
Kaempferol	DMHEMUB	Investigative	Kaempferol increases the mutagenesis of Histone-lysine N-methyltransferase 2A (KMT2A).	[8]

1 Drug(s) Affected the Protein Interaction/Cellular Processes of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Etoposide	DMNH3PG	Approved	Etoposide increases the cleavage of Histone-lysine N-methyltransferase 2A (KMT2A).	[12]

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

Drug Name	Drug ID	Highest Status	Interaction	REF
PMID28870136-Compound-52	DMFDERP	Patented	PMID28870136-Compound-52 affects the phosphorylation of Histone-lysine N-methyltransferase 2A (KMT2A).	[19]
Bisphenol A	DM2ZLD7	Investigative	Bisphenol A increases the methylation of Histone-lysine N-methyltransferase 2A (KMT2A).	[22]
Coumarin	DM0N8ZM	Investigative	Coumarin affects the phosphorylation of Histone-lysine N-methyltransferase 2A (KMT2A).	[19]

References

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• [12] The broken MLL gene is frequently located outside the inherent chromosome territory in human lymphoid cells treated with DNA topoisomerase II poison etoposide. PLoS One. 2013 Sep 25;8(9):e75871. doi: 10.1371/journal.pone.0075871. eCollection 2013.
• [13] Transcriptional profiling of testosterone-regulated genes in the skeletal muscle of human immunodeficiency virus-infected men experiencing weight loss. J Clin Endocrinol Metab. 2007 Jul;92(7):2793-802. doi: 10.1210/jc.2006-2722. Epub 2007 Apr 17.
• [14] Prefrontal dysfunction in schizophrenia involves mixed-lineage leukemia 1-regulated histone methylation at GABAergic gene promoters. J Neurosci. 2007 Oct 17;27(42):11254-62. doi: 10.1523/JNEUROSCI.3272-07.2007.
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• [19] 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.
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• [21] Clarifying off-target effects for torcetrapib using network pharmacology and reverse docking approach. BMC Syst Biol. 2012 Dec 10;6:152.
• [22] Expression and DNA methylation changes in human breast epithelial cells after bisphenol A exposure. Int J Oncol. 2012 Jul;41(1):369-77.
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• [26] Zerovalent Fe, Co and Ni nanoparticle toxicity evaluated on SKOV-3 and U87 cell lines. J Appl Toxicol. 2016 Mar;36(3):385-93.
• [27] Gene expression profile and cytotoxicity of human bronchial epithelial cells exposed to crotonaldehyde. Toxicol Lett. 2010 Aug 16;197(2):113-22.
• [28] Chlorpyrifos Induces MLL Translocations Through Caspase 3-Dependent Genomic Instability and Topoisomerase II Inhibition in Human Fetal Liver Hematopoietic Stem Cells. Toxicol Sci. 2015 Oct;147(2):588-606. doi: 10.1093/toxsci/kfv153. Epub 2015 Jul 20.
• [29] In vitro drug-resistance profile in infant acute lymphoblastic leukemia in relation to age, MLL rearrangements and immunophenotype. Leukemia. 2004 Mar;18(3):521-9. doi: 10.1038/sj.leu.2403253.