Table 1: Protein Methyltransferases, their Methylation Marks, and Links to Disease

Methyltransferase	Major Target Site(s)	Function or Links to Disease
SUV39H1	H3K9	Increased expression in colorectal tumors [20]
SUV39H2	H3K9	Mice lacking both SUV39H genes showed cytogenetic abnormalities and increased incidence of lymphoma [21]
SUV420H1	H4K20	Function or link to disease not yet elucidated
SUV420H2	H4K20	Decreased expression found in human breast cancer cells [22]
EZH1	H3K27	Function or link to disease not yet elucidated
EZH2	H3K27	Overexpressed in various human cancers, including prostate, breast, colon, skin, and lung cancers; [23] dominant, gain-of-function mutation (Tyr641) increases H3K27me3 levels leading to tumorigenesis; [24]malignant phenotype of follicular and diffuse-large B-cell lymphomas of the germinal-center origin is the result of the overall gain of function [25]
G9a	H3K9, p53K373	Overexpressed in various human cancers including leukemia, prostate carcinoma, hepatocellular carcinoma and lung cancer [26-29]
GLP	H3K9, p53K373	Overexpressed in gland tumors [30]
SETDB1	H3K9	Cooperation with DNA methyltransferase silencing of promoter regions in tumor cells [31]
SET7/9	H3K4, p53K372, p65 subunit NF-κB	Modulates p53 activity in human cancer cells; [32] regulates NF-κB-dependent inflammatory genes [33]
SETD8	H4K20, p53K372, p53K382	Implicated in cell cycle dependent gene silencing and mitotic regulation; [34,35] suppresses p53 dependent transcription [36]
MLL1	H3K4	Mutations/rearrangements observed in patients with acute leukemia including MLL partial tandem duplications and MLL fusions [37-39]
MLL2	H3K4	Mutations of MLL2 found in renal cell carcinoma [40]and Kabuki syndrome [41]
MLL3	H3K4	Function or link to disease not yet elucidated [42]
MLL4	H3K4	Serves as a cellular target for hepatitis B virus in liver oncogenesis [43]
SMYD2	H3K36, p53K370	Suppresses p53 transcriptional activity [44]
SMYD3	H3K4	Overexpression correlated with the development of colorectal and hepatocellular carcinoma; [45] enhanced breast cancer cell growth due to overexpression [46]
NSD1	H3K36, H4K20	NSD1 deletions and intragenic mutations are identified in patients with Sotos and Weaver syndromes [47]
NSD2	H3K4, H3K27, H3K36, H4K20	Translocated in some cases of myeloma [48]
NSD3	H3K4, H3K27, H3K36	Fused with NUP98 in acute myeloid leukemia; [49] amplified in breast cancers [50]
DOT1L	H3K79	Recruited by MLL fusion partners to Hox genes; directly involved in acute myeloid leukemia [51,52]
PRMT1	H4R3, NAB2p, NPL3p, ERαR260 and other GAR motifs	Coactivator of hormone receptor function; aberrant expression observed in several tumor states including breast and colon cancers; [53-56]deregulation of H4R3 suggestive marker of prostate cancer; [57]essential component of MLL oncogenic transcriptional complex and activity required for malignant transformation [58]
PRMT2	H4(site of methylation unknown)[59]	Coactivator of both the androgen receptor and ERα [59]
PRMT4 (CARM1)	H3R2, H3R17, H3R26, and other PGM motifs	Steroid receptor coactivator; overexpressed in both human breast tumors and castration-resistant prostate cancer; [60-62]knockdown impedes androgen receptor signaling
PRMT5	H3R8, H4R3, H2AR3	Acts as a strong repressor of numerous genes; recruited to the promoters of tumor suppressor genes such as ST7 and NM23; [63]overexpression observed in a variety of lymphoma and leukemia cells, [64,65]gastric carcinoma,[66]and immortalized fibroblast cells [63]
PRMT6	H3R2, H4R3, H2AR3	Transcriptional repressor [59]
PRMT7	H4R3, H2AR3	Downregulation sensitizes cancer cells to camptothecin treatment [67]