Histone methyltransferase that catalyzes methyl group transfer from S-adenosyl-L-methionine to the epsilon-amino group of 'Lys-4' of histone H3 (H3K4) (PubMed:25561738). Part of chromatin remodeling machinery predominantly forms H3K4me1 methylation marks at active chromatin sites where transcription and DNA repair take place (PubMed:25561738, PubMed:24081332, PubMed:22266653). Likely plays a redundant role with KMT2D in enriching H3K4me1 mark on primed and active enhancer elements (PubMed:24081332). L-lysyl(4)-[histone H3] + S-adenosyl-L-methionine = H(+) + N(6)-methyl-L-lysyl(4)-[histone H3] + S-adenosyl-L-homocysteine Component of the MLL3 complex (also named ASCOM complex), at least composed of catalytic subunit KMT2C/MLL3, ASH2L, RBBP5, WDR5, NCOA6, DPY30, KDM6A, PAXIP1/PTIP, PAGR1 and alpha- and beta-tubulin (PubMed:17021013, PubMed:17500065, PubMed:23508102). Forms a core complex with the evolutionary conserved subcomplex WRAD composed of WDR5, RBBP5, ASH2L/ASH2 and DPY30 subunits; WRAD differentially stimulates the methyltransferase activity (PubMed:25561738). Interacts (via WIN motif) with WDR5 (PubMed:22665483, PubMed:22266653). Highly expressed in testis and ovary, followed by brain and liver. Also expressed in placenta, peripherical blood, fetal thymus, heart, lung and kidney. Within brain, expression was highest in hippocampus, caudate nucleus, and substantia nigra. Not detected in skeletal muscle and fetal liver. The SET domain interacts with histone H3 but not H2A, H2B and H4, and may have a H3 lysine specific methylation activity. The disease is caused by variants affecting the gene represented in this entry. Found in a critical region of chromosome 7, which is commonly deleted in malignant myeloid disorders. Partial duplication of the KMT2C gene are found in the juxtacentromeric region of chromosomes 1, 2, 13 and 21. Juxtacentromeric reshuffling of the KMT2C gene has generated the BAGE genes. Belongs to the class V-like SAM-binding methyltransferase superfamily. Histone-lysine methyltransferase family. TRX/MLL subfamily. Intron retention.