PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33898534-5	2021	Trio-WES revealed de novo pathogenic variations in KMT2D (p.Gly3465Aspfs*37) (NM_003482) and WDFY3 (p.Ser117Xfs*) (NM_014991), and CNV-seq identified a deletion of 150 kb encompassing NOTCH1.	gly3465aspfs	60-72	lysine methyltransferase 2D	Homo sapiens	51-56
33655698-8	2021	Histone-lysine N-methyltransferase 2 (KMT2) family members (KMT2A, KMT2C, and KMT2D) were frequently mutated in NSCLC tumors, and these mutations were associated with higher TMB and PD-L1 expression, as well as higher PD-L1+/TMB-H proportions.	tyrosyl-lysine	8-14	lysine methyltransferase 2D	Homo sapiens	78-83
33655698-8	2021	Histone-lysine N-methyltransferase 2 (KMT2) family members (KMT2A, KMT2C, and KMT2D) were frequently mutated in NSCLC tumors, and these mutations were associated with higher TMB and PD-L1 expression, as well as higher PD-L1+/TMB-H proportions.	Trimedoxime	174-177	lysine methyltransferase 2D	Homo sapiens	78-83
33655698-8	2021	Histone-lysine N-methyltransferase 2 (KMT2) family members (KMT2A, KMT2C, and KMT2D) were frequently mutated in NSCLC tumors, and these mutations were associated with higher TMB and PD-L1 expression, as well as higher PD-L1+/TMB-H proportions.	Trimedoxime	225-230	lysine methyltransferase 2D	Homo sapiens	78-83
33363385-10	2020	KMT2D mutations associated with sex (P = 0.035), tumor stage (P = 0.016), high TMB (P = 0.0072), and overall survival of patients (P = 0.0026).	1,2,4,5-tetramethoxybenzene	79-82	lysine methyltransferase 2D	Homo sapiens	0-5
33334222-5	2021	Results: Mutations in the KMT2D gene were identified in all of the 10 patients with KS.	Potassium	84-86	lysine methyltransferase 2D	Homo sapiens	26-31
33786580-0	2021	KDM5 inhibition offers a novel therapeutic strategy for the treatment of KMT2D mutant lymphomas.	kdm5	0-4	lysine methyltransferase 2D	Homo sapiens	73-78
33786580-3	2021	KDM5-inhibition increased H3K4me3 levels and caused an anti-proliferative response in vitro, which was markedly greater in both endogenous and CRISPR-edited KMT2D mutant DLBCL cell lines, while tumour growth was inhibited in KMT2D mutant xenografts in vivo.	kdm5	0-4	lysine methyltransferase 2D	Homo sapiens	157-162
33786580-3	2021	KDM5-inhibition increased H3K4me3 levels and caused an anti-proliferative response in vitro, which was markedly greater in both endogenous and CRISPR-edited KMT2D mutant DLBCL cell lines, while tumour growth was inhibited in KMT2D mutant xenografts in vivo.	kdm5	0-4	lysine methyltransferase 2D	Homo sapiens	225-230
33786580-4	2021	KDM5-inhibition reactivated both KMT2D-dependent and -independent genes, resulting in diminished B-cell signalling and altered expression of BCL2 family members, including BCL2 itself.	kdm5	0-4	lysine methyltransferase 2D	Homo sapiens	33-38
33786580-5	2021	KDM5-inhibition may offer an effective therapeutic strategy for ameliorating KMT2D loss-of-function mutations in GC-lymphomas.	kdm5	0-4	lysine methyltransferase 2D	Homo sapiens	77-82
32988590-1	2020	Histone lysine N-methyltransferase 2D (KMT2D), an important methyltransferase that is involved in the methylation of lysine 4 in histone H3 (H3K4) and related to the development of prostate cancer.	Lysine	8-14	lysine methyltransferase 2D	Homo sapiens	39-44
33291558-9	2020	CONCLUSIONS: The results suggest that certain histone lysine methyltransferase/demethylase, such as MLL4, UTX, and EZH2, regulate the expression of EMT-TFs such as Slug, ZEB1, and Twist epigenetically, which may thereby influence cancer metastasis from the lung to the brain.	Lysine	54-60	lysine methyltransferase 2D	Homo sapiens	100-104
32668765-1	2020	KMT2D encodes a methyltransferase responsible for histone 3 lysine 4 (H3K4) mono-/di-methylation, an epigenetic mark correlated with active transcription.	Lysine	60-66	lysine methyltransferase 2D	Homo sapiens	0-5
33004515-5	2020	Mutations in MNU were widely observed in chromatin remodeling genes such as KMT2D and KDM6A but rarely in TP53, PIK3CA, and FGFR3 KMT2D mutations were found to be common in urothelial cells, regardless of whether the cells experience exogenous mutagen exposure.	Methylnitrosourea	13-16	lysine methyltransferase 2D	Homo sapiens	76-81
33004515-5	2020	Mutations in MNU were widely observed in chromatin remodeling genes such as KMT2D and KDM6A but rarely in TP53, PIK3CA, and FGFR3 KMT2D mutations were found to be common in urothelial cells, regardless of whether the cells experience exogenous mutagen exposure.	Methylnitrosourea	13-16	lysine methyltransferase 2D	Homo sapiens	130-135
32817139-3	2020	KDM6A physically associates with histone H3 lysine 4 monomethyltransferases MLL3 (KMT2C) and MLL4 (KMT2D).	Lysine	44-50	lysine methyltransferase 2D	Homo sapiens	99-104
32599142-7	2020	Co-IP assay confirmed that H2O2 induced the phosphorylation of KMT2D to block the ubiquitination degradation, which was mainly mediated by phosphorylation of p38/MAPK.	Hydrogen Peroxide	27-31	lysine methyltransferase 2D	Homo sapiens	63-68
32599142-11	2020	In conclusion, we approved that oxidative stress induced ROS production promote the process of NP degeneration by enhancing KMT2D mediated transcriptional regulation of matrix degeneration related genes during NP degeneration.	ros	57-60	lysine methyltransferase 2D	Homo sapiens	124-129
32830475-9	2021	A heterozygous frameshift mutation (c.2579del, p.Leu860Argfs*70) was detected in the KMT2D gene.	leu860argfs	49-60	lysine methyltransferase 2D	Homo sapiens	85-90
32139118-5	2020	In this report, we examined MLL2 (KMT2D), a histone-lysine methyltransferase that catalyzes histone H3 lysine 4 methylation (H3K4me).	Lysine	52-58	lysine methyltransferase 2D	Homo sapiens	28-32
31949313-2	2020	METHODS: Multiple individuals, with MVs in exons 38 or 39 of KMT2D that encode a highly conserved region of 54 amino acids flanked by Val3527 and Lys3583, were identified and phenotyped.	valsartan	134-141	lysine methyltransferase 2D	Homo sapiens	61-66
31949313-2	2020	METHODS: Multiple individuals, with MVs in exons 38 or 39 of KMT2D that encode a highly conserved region of 54 amino acids flanked by Val3527 and Lys3583, were identified and phenotyped.	pentalysine	146-153	lysine methyltransferase 2D	Homo sapiens	61-66
32139118-5	2020	In this report, we examined MLL2 (KMT2D), a histone-lysine methyltransferase that catalyzes histone H3 lysine 4 methylation (H3K4me).	Lysine	52-58	lysine methyltransferase 2D	Homo sapiens	34-39
32139118-5	2020	In this report, we examined MLL2 (KMT2D), a histone-lysine methyltransferase that catalyzes histone H3 lysine 4 methylation (H3K4me).	Lysine	103-109	lysine methyltransferase 2D	Homo sapiens	28-32
32139118-5	2020	In this report, we examined MLL2 (KMT2D), a histone-lysine methyltransferase that catalyzes histone H3 lysine 4 methylation (H3K4me).	Lysine	103-109	lysine methyltransferase 2D	Homo sapiens	34-39
32139118-8	2020	Moreover, chromatin immunoprecipitation analyses demonstrated that MLL2 could co-occupy glucocorticoid response elements (GREs) of GR target genes along with GR following Dex stimulation.	Dextromethorphan	171-174	lysine methyltransferase 2D	Homo sapiens	67-71
32139118-9	2020	Finally, the FAIRE-qPCR results illustrated that MLL2 is pivotal in establishing chromatin structure accessibility at the GREs of ARPE-19 specific genes in the presence of Dex.	Dextromethorphan	172-175	lysine methyltransferase 2D	Homo sapiens	49-53
31876365-1	2020	Kabuki syndrome (KS, KS1: OMIM 147920 and KS2: OMIM 300867) is caused by pathogenic variations in KMT2D or KDM6A.	1-octyl-3-methylimidazolium hexafluorophosphate	26-37	lysine methyltransferase 2D	Homo sapiens	98-103
31935506-2	2020	Studies have determined that pathogenic variants of the lysine-specific methyltransferase 2D (KMT2D) and lysine-specific demethylase 6A (KDM6A) genes are the major causes of KS.	Lysine	56-62	lysine methyltransferase 2D	Homo sapiens	94-99
31876365-1	2020	Kabuki syndrome (KS, KS1: OMIM 147920 and KS2: OMIM 300867) is caused by pathogenic variations in KMT2D or KDM6A.	1-octyl-3-methylimidazolium hexafluorophosphate	47-58	lysine methyltransferase 2D	Homo sapiens	98-103
31654559-1	2020	Kabuki syndrome (KS) is a disorder of epigenetic dysregulation due to heterozygous mutations in KMT2D or KDM6A, genes encoding a lysine-specific methyltransferase or demethylase, respectively.	tyrosyl-lysine	129-135	lysine methyltransferase 2D	Homo sapiens	96-101
31813957-3	2020	The major cause of Kabuki syndrome are mutations in KMT2D, a gene encoding a histone H3 lysine 4 (H3K4) methyltransferase belonging to the group of chromatin modifiers.	tyrosyl-lysine	88-96	lysine methyltransferase 2D	Homo sapiens	52-57
31813957-3	2020	The major cause of Kabuki syndrome are mutations in KMT2D, a gene encoding a histone H3 lysine 4 (H3K4) methyltransferase belonging to the group of chromatin modifiers.	H-2K(K) antigen	98-102	lysine methyltransferase 2D	Homo sapiens	52-57
31813957-9	2020	Importantly, Kmt2d knockdown correlates with a decrease in H3K4 monomethylation and H3K27 acetylation supporting a role of Kmt2d in the transcriptional activation of target genes.	H-2K(K) antigen	59-63	lysine methyltransferase 2D	Homo sapiens	13-18
31924266-1	2020	The type 2 lysine methyltransferases KMT2C and KMT2D are large, enzymatically active scaffold proteins that form the core of nuclear regulatory structures known as KMT2C/D COMPASS complexes (complex of proteins associating with Set1).	tyrosyl-lysine	11-17	lysine methyltransferase 2D	Homo sapiens	47-52
32024448-8	2020	Seven patients also had somatic mutations in APC, and seven patients harbored somatic mutations in KMT2D, which encodes a lysine methyl transferase.	tyrosyl-lysine	122-135	lysine methyltransferase 2D	Homo sapiens	99-104
29305415-8	2018	In vitro, chidamide significantly inhibited the growth of EP300-mutated T-lymphoma cells and KMT2D-mutated T-lymphoma cells when combined with the hypomethylating agent decitabine.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	10-19	lysine methyltransferase 2D	Homo sapiens	93-98
30337373-14	2019	CONCLUSION: Together our findings define a new tumour suppressor function of KMT2D through the regulation of glucose/fatty acid metabolism in pancreatic cancer.	Glucose	109-116	lysine methyltransferase 2D	Homo sapiens	77-82
30337373-14	2019	CONCLUSION: Together our findings define a new tumour suppressor function of KMT2D through the regulation of glucose/fatty acid metabolism in pancreatic cancer.	Fatty Acids	117-127	lysine methyltransferase 2D	Homo sapiens	77-82
30990809-6	2019	RESULTS: We identified KMT2D, SETD1A and SETD2, included in the lysine methyltransferase activity function, as linked with poor prognosis in invasive breast cancer.	Lysine	64-70	lysine methyltransferase 2D	Homo sapiens	23-28
31232159-0	2019	Loss of KMT2D induces prostate cancer ROS-mediated DNA damage by suppressing the enhancer activity and DNA binding of antioxidant transcription factor FOXO3.	Reactive Oxygen Species	38-41	lysine methyltransferase 2D	Homo sapiens	8-13
31232159-4	2019	Knockdown of KMT2D sensitized cells to DNA damage through the disturbance of antioxidative gene expression and increased levels of intracellular reactive oxygen species, which led to cell apoptosis and senescence.	Reactive Oxygen Species	145-168	lysine methyltransferase 2D	Homo sapiens	13-18
31587141-1	2019	BACKGROUND: Kabuki syndrome (KS), is a infrequent inherited malformation syndrome caused by mutations in a H3 lysine 4 methylase (KMT2D) or an X-linked histone H3 lysine 27 demethylase (UTX/KDM6A).	Lysine	110-116	lysine methyltransferase 2D	Homo sapiens	130-135
31446696-13	2019	KMT2D and KDM6A are two pathogenic genes that have been identified for KS.	Potassium	71-73	lysine methyltransferase 2D	Homo sapiens	0-5
30943409-5	2019	Elevated SGK1, in turn, phosphorylates KMT2D, suppressing its function, leading to a loss of methylation of lysine 4 on histone H3 (H3K4) and a repressive chromatin state at ER loci to attenuate ER activity.	lysine 4	108-116	lysine methyltransferase 2D	Homo sapiens	39-44
30107592-4	2018	Here, we expanded the mutation spectrum of KMT2D and KDM6A in KS by identifying 37 new KMT2D sequence variants.	Potassium	62-64	lysine methyltransferase 2D	Homo sapiens	43-48
30107592-4	2018	Here, we expanded the mutation spectrum of KMT2D and KDM6A in KS by identifying 37 new KMT2D sequence variants.	Potassium	62-64	lysine methyltransferase 2D	Homo sapiens	87-92
30126979-8	2018	However, KMT2D was less commonly mutated in DTFL (52%) and LSTFL (24%) as compared with ASTFL (79%).	dtfl	44-48	lysine methyltransferase 2D	Homo sapiens	9-14
30126979-8	2018	However, KMT2D was less commonly mutated in DTFL (52%) and LSTFL (24%) as compared with ASTFL (79%).	lstfl	59-64	lysine methyltransferase 2D	Homo sapiens	9-14
30126979-9	2018	In ASTFL, 41% of KMT2D-mutated cases harbored multiple mutations in KMT2D, as compared with only 12% in LSTFL (P = .019) and 0% in DTFL (P < .0001).	astfl	3-8	lysine methyltransferase 2D	Homo sapiens	17-22
30126979-9	2018	In ASTFL, 41% of KMT2D-mutated cases harbored multiple mutations in KMT2D, as compared with only 12% in LSTFL (P = .019) and 0% in DTFL (P < .0001).	astfl	3-8	lysine methyltransferase 2D	Homo sapiens	68-73
29663555-9	2018	Furthermore, dehydroleucodine downregulated expression of histone demethylase JMJD2B as well as repressed the expression of histone methyltransferase MLL4, which in turn diminished the expression of C/EBPbeta and PPARgamma, respectively.	dehydroleucodine	13-29	lysine methyltransferase 2D	Homo sapiens	150-154
29305415-9	2018	Mechanistically, decitabine acted synergistically with chidamide to enhance the interaction of KMT2D with transcription factor PU.1, regulated H3K4me-associated signaling pathways, and sensitized T-lymphoma cells to chidamide.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	216-225	lysine methyltransferase 2D	Homo sapiens	95-100
29305415-10	2018	In a xenograft KMT2D-mutated T-lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D/H3K4me axis.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	67-76	lysine methyltransferase 2D	Homo sapiens	15-20
29305415-10	2018	In a xenograft KMT2D-mutated T-lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D/H3K4me axis.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	67-76	lysine methyltransferase 2D	Homo sapiens	181-186
29305415-10	2018	In a xenograft KMT2D-mutated T-lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D/H3K4me axis.	Decitabine	81-91	lysine methyltransferase 2D	Homo sapiens	15-20
29305415-9	2018	Mechanistically, decitabine acted synergistically with chidamide to enhance the interaction of KMT2D with transcription factor PU.1, regulated H3K4me-associated signaling pathways, and sensitized T-lymphoma cells to chidamide.	Decitabine	17-27	lysine methyltransferase 2D	Homo sapiens	95-100
29305415-10	2018	In a xenograft KMT2D-mutated T-lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D/H3K4me axis.	Decitabine	81-91	lysine methyltransferase 2D	Homo sapiens	181-186
29305415-9	2018	Mechanistically, decitabine acted synergistically with chidamide to enhance the interaction of KMT2D with transcription factor PU.1, regulated H3K4me-associated signaling pathways, and sensitized T-lymphoma cells to chidamide.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	55-64	lysine methyltransferase 2D	Homo sapiens	95-100
29367767-4	2018	BBN tumors showed overexpression of markers of basal cancer subtype, and had a high mutation burden with frequent Trp53 (80%), Kmt2d (70%), and Kmt2c (90%) mutations by exome sequencing, similar to human MIBC.	Butylhydroxybutylnitrosamine	0-3	lysine methyltransferase 2D	Homo sapiens	127-132
29483845-0	2018	MLL2/KMT2D and MLL3/KMT2C expression correlates with disease progression and response to imatinib mesylate in chronic myeloid leukemia.	Imatinib Mesylate	89-97	lysine methyltransferase 2D	Homo sapiens	0-4
27875625-7	2017	SMAD4 and lysine methyltransferase 2D (KMT2D) mutations were associated with reduced OS.	Osmium	85-87	lysine methyltransferase 2D	Homo sapiens	10-37
29404406-2	2018	Mll4 (Kmt2d), a member of the COMPASS (COMplex of Proteins ASsociated with Set1) protein family that implements histone H3 lysine 4 monomethylation (H3K4me1) at enhancers, is essential for embryonic development and functions as a pancancer tumor suppressor.	Lysine	123-129	lysine methyltransferase 2D	Homo sapiens	0-4
29404406-2	2018	Mll4 (Kmt2d), a member of the COMPASS (COMplex of Proteins ASsociated with Set1) protein family that implements histone H3 lysine 4 monomethylation (H3K4me1) at enhancers, is essential for embryonic development and functions as a pancancer tumor suppressor.	Lysine	123-129	lysine methyltransferase 2D	Homo sapiens	6-11
29440247-5	2018	Depletion of KMT2D results in a broad loss of enhancer histone modifications H3 Lys 4 (H3K4) monomethylation (H3K4me1) and H3K27 acetylation (H3K27ac) as well as reduced expression of p63 target genes, including key genes involved in epithelial development and adhesion.	Lysine	80-83	lysine methyltransferase 2D	Homo sapiens	13-18
27875625-7	2017	SMAD4 and lysine methyltransferase 2D (KMT2D) mutations were associated with reduced OS.	Osmium	85-87	lysine methyltransferase 2D	Homo sapiens	39-44
27280393-7	2016	Kmt2d depletion in KC/KPC cell lines also led to an increased response to the nucleoside analogue 5-fluorouracil, suggesting that lower levels of this methyltransferase may mediate the sensitivity of PDAC to particular treatments.	Nucleosides	78-88	lysine methyltransferase 2D	Homo sapiens	0-5
28007623-8	2017	We found that KMT2D mutation in human SCLC cell lines was associated with reduced lysine methyltransferase 2D protein levels and reduced monomethylation of histone H3 lysine 4, a mark associated with transcriptional enhancers.	HS 3	164-166	lysine methyltransferase 2D	Homo sapiens	14-19
28007623-8	2017	We found that KMT2D mutation in human SCLC cell lines was associated with reduced lysine methyltransferase 2D protein levels and reduced monomethylation of histone H3 lysine 4, a mark associated with transcriptional enhancers.	lysine 4	167-175	lysine methyltransferase 2D	Homo sapiens	14-19
27280393-7	2016	Kmt2d depletion in KC/KPC cell lines also led to an increased response to the nucleoside analogue 5-fluorouracil, suggesting that lower levels of this methyltransferase may mediate the sensitivity of PDAC to particular treatments.	Fluorouracil	98-112	lysine methyltransferase 2D	Homo sapiens	0-5
27280393-7	2016	Kmt2d depletion in KC/KPC cell lines also led to an increased response to the nucleoside analogue 5-fluorouracil, suggesting that lower levels of this methyltransferase may mediate the sensitivity of PDAC to particular treatments.	pdac	200-204	lysine methyltransferase 2D	Homo sapiens	0-5
26640146-5	2016	ASXL2 forms a complex with histone methylation modifiers including LSD1, UTX and MLL2, which all are recruited to the E2-responsive genes via ASXL2 and regulate methylations at histone H3 lysine 4, 9 and 27.	Lysine	188-194	lysine methyltransferase 2D	Homo sapiens	81-85
27055146-6	2016	For example, EZH2 somatic mutations drive silencing of bivalent gene promoters through histone 3 lysine 27 trimethylation, whereas KMT2D (MLL2) mutations disrupt specific sets of enhancers through depletion of histone 3 lysine 4 mono and dimethylation (H3K4me1/me2).	Lysine	220-226	lysine methyltransferase 2D	Homo sapiens	131-136
27055146-6	2016	For example, EZH2 somatic mutations drive silencing of bivalent gene promoters through histone 3 lysine 27 trimethylation, whereas KMT2D (MLL2) mutations disrupt specific sets of enhancers through depletion of histone 3 lysine 4 mono and dimethylation (H3K4me1/me2).	Lysine	220-226	lysine methyltransferase 2D	Homo sapiens	138-142
26841698-5	2016	This revealed several notable genomic alterations, including mutations of DICER1 (6 tumors) and KMT2D (also known as MLL2; 5 tumors)-which are frequently recurrent and mutually exclusive molecular events for IO-MEPL.	io-mepl	208-215	lysine methyltransferase 2D	Homo sapiens	96-101
26841698-5	2016	This revealed several notable genomic alterations, including mutations of DICER1 (6 tumors) and KMT2D (also known as MLL2; 5 tumors)-which are frequently recurrent and mutually exclusive molecular events for IO-MEPL.	io-mepl	208-215	lysine methyltransferase 2D	Homo sapiens	117-121
26841698-8	2016	The high proportion of recurrent somatic DICER1 and KMT2D mutations in this series of sporadic IO-MEPL points to their likely important roles in the molecular pathogenesis of these rare embryonal tumors, and perhaps suggests the existence of distinct molecular variants of IO-MEPL.	io-mepl	95-102	lysine methyltransferase 2D	Homo sapiens	52-57
26461093-3	2015	We found that an epigenetic pathway involving MLL2 is crucial for growth of HER2(+) cells and MLL2 reduces sensitivity of the cancer cells to a HER2 inhibitor, lapatinib.	Lapatinib	160-169	lysine methyltransferase 2D	Homo sapiens	46-50
26932671-0	2016	KMT2D regulates specific programs in heart development via histone H3 lysine 4 di-methylation.	HS 3	67-69	lysine methyltransferase 2D	Homo sapiens	0-5
26932671-0	2016	KMT2D regulates specific programs in heart development via histone H3 lysine 4 di-methylation.	Lysine	70-76	lysine methyltransferase 2D	Homo sapiens	0-5
26437033-5	2015	Second, phyllodes tumors exhibited mutations in FLNA, SETD2 and KMT2D, suggesting a role in driving phyllodes tumor development.	phyllodes	8-17	lysine methyltransferase 2D	Homo sapiens	64-69
26437033-5	2015	Second, phyllodes tumors exhibited mutations in FLNA, SETD2 and KMT2D, suggesting a role in driving phyllodes tumor development.	phyllodes	100-109	lysine methyltransferase 2D	Homo sapiens	64-69
26461093-3	2015	We found that an epigenetic pathway involving MLL2 is crucial for growth of HER2(+) cells and MLL2 reduces sensitivity of the cancer cells to a HER2 inhibitor, lapatinib.	Lapatinib	160-169	lysine methyltransferase 2D	Homo sapiens	94-98
26461093-4	2015	Lapatinib-induced FOXO transcription factors, normally tumor-suppressing, paradoxically upregulate c-Myc epigenetically in concert with a cascade of MLL2-associating epigenetic regulators to dampen sensitivity of the cancer cells to lapatinib.	Lapatinib	0-9	lysine methyltransferase 2D	Homo sapiens	149-153
26461093-4	2015	Lapatinib-induced FOXO transcription factors, normally tumor-suppressing, paradoxically upregulate c-Myc epigenetically in concert with a cascade of MLL2-associating epigenetic regulators to dampen sensitivity of the cancer cells to lapatinib.	Lapatinib	233-242	lysine methyltransferase 2D	Homo sapiens	149-153
26032282-6	2015	Two somatic mutations and one constitutional variant in the well-established cancer gene lysine (K)-specific methyltransferase 2D (KMT2D, MLL2) were discovered in one sample each, prompting KMT2D screening using focused exome-sequencing in the verification cohort.	Lysine	89-95	lysine methyltransferase 2D	Homo sapiens	131-136
26032282-6	2015	Two somatic mutations and one constitutional variant in the well-established cancer gene lysine (K)-specific methyltransferase 2D (KMT2D, MLL2) were discovered in one sample each, prompting KMT2D screening using focused exome-sequencing in the verification cohort.	Lysine	89-95	lysine methyltransferase 2D	Homo sapiens	138-142
26032282-6	2015	Two somatic mutations and one constitutional variant in the well-established cancer gene lysine (K)-specific methyltransferase 2D (KMT2D, MLL2) were discovered in one sample each, prompting KMT2D screening using focused exome-sequencing in the verification cohort.	Lysine	89-95	lysine methyltransferase 2D	Homo sapiens	190-195
26280580-2	2015	Dominant mutations in the chromatin regulators lysine (K)-specific methyltransferase 2D (KMT2D) (also known as MLL2) and lysine (K)-specific demethylase 6A (KDM6A) underlie the majority of cases.	Lysine	47-53	lysine methyltransferase 2D	Homo sapiens	89-94
26280580-2	2015	Dominant mutations in the chromatin regulators lysine (K)-specific methyltransferase 2D (KMT2D) (also known as MLL2) and lysine (K)-specific demethylase 6A (KDM6A) underlie the majority of cases.	Lysine	47-53	lysine methyltransferase 2D	Homo sapiens	111-115
25135975-1	2014	The growing list of mutations implicated in monogenic disorders of the developing brain includes at least seven genes (ARX, CUL4B, KDM5A, KDM5C, KMT2A, KMT2C, KMT2D) with loss-of-function mutations affecting proper regulation of histone H3 lysine 4 methylation, a chromatin mark which on a genome-wide scale is broadly associated with active gene expression, with its mono-, di- and trimethylated forms differentially enriched at promoter and enhancer and other regulatory sequences.	Lysine	240-246	lysine methyltransferase 2D	Homo sapiens	159-164
24346842-0	2014	A novel mutation in SOX3 polyalanine tract: a case of Kabuki syndrome with combined pituitary hormone deficiency harboring double mutations in MLL2 and SOX3.	polyalanine	25-36	lysine methyltransferase 2D	Homo sapiens	143-147
24311525-8	2014	Our observations suggest that patients with KS may have hypoglycemia due to different mechanisms and that MLL2 gene may have a role in glucose physiology.	Glucose	135-142	lysine methyltransferase 2D	Homo sapiens	106-110
24633898-7	2014	Our experimental data showed that both KMT2D and KDM6A nonsense mutations displayed high levels of readthrough in response to gentamicin treatment, paving the way to further studies aimed at eventually treating some Kabuki patients with readthrough inducers.	Gentamicins	126-136	lysine methyltransferase 2D	Homo sapiens	39-44
24240169-0	2013	KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation.	HS 3	65-67	lysine methyltransferase 2D	Homo sapiens	0-5
24240169-0	2013	KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation.	Lysine	68-74	lysine methyltransferase 2D	Homo sapiens	0-5
23045699-6	2012	A combinatorial analysis of the MLL2 binding profile and gene expression in MLL2 wild-type versus MLL2-null isogenic cell lines identified direct transcriptional target genes and revealed the connection of MLL2 to multiple cellular signaling pathways, including the p53 pathway, cAMP-mediated signaling, and cholestasis signaling.	Cyclic AMP	279-283	lysine methyltransferase 2D	Homo sapiens	32-36
23045699-6	2012	A combinatorial analysis of the MLL2 binding profile and gene expression in MLL2 wild-type versus MLL2-null isogenic cell lines identified direct transcriptional target genes and revealed the connection of MLL2 to multiple cellular signaling pathways, including the p53 pathway, cAMP-mediated signaling, and cholestasis signaling.	Cyclic AMP	279-283	lysine methyltransferase 2D	Homo sapiens	76-80
23045699-6	2012	A combinatorial analysis of the MLL2 binding profile and gene expression in MLL2 wild-type versus MLL2-null isogenic cell lines identified direct transcriptional target genes and revealed the connection of MLL2 to multiple cellular signaling pathways, including the p53 pathway, cAMP-mediated signaling, and cholestasis signaling.	Cyclic AMP	279-283	lysine methyltransferase 2D	Homo sapiens	76-80
23045699-6	2012	A combinatorial analysis of the MLL2 binding profile and gene expression in MLL2 wild-type versus MLL2-null isogenic cell lines identified direct transcriptional target genes and revealed the connection of MLL2 to multiple cellular signaling pathways, including the p53 pathway, cAMP-mediated signaling, and cholestasis signaling.	Cyclic AMP	279-283	lysine methyltransferase 2D	Homo sapiens	76-80
34758724-9	2021	Finally, using 1,6-hexanediol (HD), an inhibitor of LLPS, we determined cell activities associated with KMT2D function in wild-type PANC-1 cells.	hexamethylene glycol	15-29	lysine methyltransferase 2D	Homo sapiens	104-109
20433758-1	2010	BACKGROUND: MLL2, an epigenetic regulator in mammalian cells, mediates histone 3 lysine 4 tri-methylation (H3K4me3) through the formation of a multiprotein complex.	Lysine	81-87	lysine methyltransferase 2D	Homo sapiens	12-16
21067415-3	2010	The results of acridine orange staining indicated that MLL-2 caused apoptosis in MCF-7 cells.	Acridine Orange	15-30	lysine methyltransferase 2D	Homo sapiens	55-60
21067415-6	2010	The MLL-2 induced a sustained increase in concentration of intracellular free calcium.	Calcium	78-85	lysine methyltransferase 2D	Homo sapiens	4-9
18372346-1	2008	Activating signal cointegrator-2 (ASC-2), a coactivator of multiple nuclear receptors and transcription factors, including the liver X receptors (LXRs), is associated with histone H3 lysine 4 (H3K4) methyltransferase (H3K4MT) MLL3 or its paralogue MLL4 in a steady-state complex named ASCOM (ASC-2 complex).	histone h3 lysine 4	172-191	lysine methyltransferase 2D	Homo sapiens	248-252
33782741-5	2021	KMT2D and SETD2 mutations were present in both the conventional phyllodes tumour and endometriosis-like areas and are also described in endometriosis raising interesting questions about these lesions.	phyllodes	64-73	lysine methyltransferase 2D	Homo sapiens	0-5
20808952-0	2010	MLL2 is required in oocytes for bulk histone 3 lysine 4 trimethylation and transcriptional silencing.	Lysine	47-53	lysine methyltransferase 2D	Homo sapiens	0-4
10732797-5	1998	The validity of this approach is supported by the detection of nervous system-specific genes (e.g., glial fibrillary acid protein) and genes known to show trinucleotide expansions in disease (e.g., AAD10 associated with spino cerebellar ataxia type 2).	trinucleotide	155-168	lysine methyltransferase 2D	Homo sapiens	198-203
34724040-1	2021	KMT2D, as one of the key histone methyltransferases responsible for histone 3 lysine 4 methylation (H3K4me), has been proved to be the main pathogenic gene of Kabuki syndrome disease.	Lysine	78-84	lysine methyltransferase 2D	Homo sapiens	0-5
34724040-9	2021	Moreover, LiCl partially reversed the decrease of cell proliferation activity and G1 arrest, and the downregulation of Wnt-related genes in Kmt2d knockdown cells.	Lithium Chloride	10-14	lysine methyltransferase 2D	Homo sapiens	140-145
34705580-1	2021	To investigate the function of histone-lysine N-methyltransferase 2D (KMT2D) on the methylation of H3 lysine 4 (H3K4) in the progression of Ovarian cancer (OV).	Lysine	102-108	lysine methyltransferase 2D	Homo sapiens	31-68
34859145-1	2021	We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen.	Lysine	28-34	lysine methyltransferase 2D	Homo sapiens	60-65
34168983-6	2021	We found a significant association between TMB-H (>=10.3muts/Mb) and ATM (P=0.023), CREBBP (P=0.010), KMT2D(P=0.050) and LRP1B (P=0.005) gene mutations in Chinese SCLC patients.	1,2,4,5-tetramethoxybenzene	43-46	lysine methyltransferase 2D	Homo sapiens	102-107
34745101-7	2021	The comprehensive results showed that high IPI-IPM risk scores were correlated with immune-related signaling pathways, high KMT2D and CD79B mutation rates, and upregulation of inhibitory immune checkpoints, including PD-L1, BTLA, and SIGLEC7, indicating a greater potential response to ICB therapy.	diprotin A	43-46	lysine methyltransferase 2D	Homo sapiens	124-129
34156443-3	2021	MLL3/KMT2C and MLL4/KMT2D are two paralogous histone modifiers that belong to the SET1/MLL (also named COMPASS) family of lysine methyltransferases and play critical roles in enhancer-regulated gene activation.	Lysine	122-128	lysine methyltransferase 2D	Homo sapiens	15-19
34156443-3	2021	MLL3/KMT2C and MLL4/KMT2D are two paralogous histone modifiers that belong to the SET1/MLL (also named COMPASS) family of lysine methyltransferases and play critical roles in enhancer-regulated gene activation.	Lysine	122-128	lysine methyltransferase 2D	Homo sapiens	20-25
34156443-5	2021	MLL3 and MLL4 form identical multi-protein complexes for modifying mono-methylation of histone H3 lysine 4 (H3K4) at enhancers, which together with the p300/CBP-mediated H3K27 acetylation can generate an active enhancer landscape for long-range target gene activation.	Lysine	98-104	lysine methyltransferase 2D	Homo sapiens	9-13
34705580-1	2021	To investigate the function of histone-lysine N-methyltransferase 2D (KMT2D) on the methylation of H3 lysine 4 (H3K4) in the progression of Ovarian cancer (OV).	Lysine	102-108	lysine methyltransferase 2D	Homo sapiens	70-75
35411237-3	2022	Lysine-specific histone methyltransferase 2D (KMT2D) has a two-fold higher mutation frequency in metastatic cSCCs relative to primary non-metastatic associated cSCCs.	Lysine	0-6	lysine methyltransferase 2D	Homo sapiens	46-51
35229282-5	2022	PROSER1 stabilizes TET2, a member of the TET family of DNA demethylases which is involved in recruiting the enhancer-associated KMT2C/KMT2D complexes and mediating DNA demethylation, activating gene expression.	tetramethylenedisulfotetramine	41-44	lysine methyltransferase 2D	Homo sapiens	134-139
35196069-5	2022	Transcriptome-wide analysis revealed a coordinated regulation of metabolic enzymes related to one-carbon metabolism, including three methyltransferase enzymes (KMT2D, SETD1B, and ASH1L), key enzymes for both carnitine synthesis and histone modification.	Carbon	98-104	lysine methyltransferase 2D	Homo sapiens	160-165
34980601-7	2022	Conversely, KMT2D mutations significantly stratified DhE but not non-DhE DLBCL.	Dihydroergotamine	53-56	lysine methyltransferase 2D	Homo sapiens	12-17