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MLL2 C-terminal Antibody [L16L11]

Cat.No.: F6299

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:50
    1:1000
    Application
    WB, IP, IF
    Reactivity
    Human
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    80 kDa
    Positive Control A549 cells; NCCIT cells; MCF7 cells; A549 cells
    Negative Control HCT 116 cells

    Datasheet & SDS

    Biological Description

    Specificity
    MLL2 C-terminal Antibody [L16L11] detects endogenous levels of C-terminal of total MLL2 protein.
    Clone
    L16L11
    Synonym(s)
    Histone-lysine N-methyltransferase 2B; Trithorax homolog 2; WW domain-binding protein 7 (WBP-7); KMT2B; HRX2; KIAA0304; MLL2; MLL4; TRX2; WBP7
    Background
    MLL2 C-terminal is the enzymatically active fragment of MLL2, also known as KMT2B, a mammalian SET1-like histone H3 lysine 4 methyltransferase from the trithorax family that assembles into COMPASS-like complexes to catalyze H3K4 trimethylation at gene promoters. After being cleaved by Taspase 1 from the full 2715-amino-acid MLL2 protein, the C-terminal fragment, called MLL2-C, contains the signature SET domain, which forms a catalytic pocket that binds S-adenosylmethionine and the histone H3 N-terminal tail to drive methylation, and allows for non-covalent dimerization with the N-terminal fragment through adjacent FY-rich C-terminal and PHD domains. This core activity of MLL2-C activates transcription of developmental genes, bivalent promoters in embryonic stem cells, and genes involved in embryogenesis, hematopoiesis, stem and germinal cell differentiation, memory formation, glucose homeostasis, and cardiac lineage commitment. MLL2-C interacts with the WRAD complex, which includes WDR5, RBBP5, ASH2L, and DPY30, as well as HCF1, HCF2, and Menin subunits, to deposit H3K4 trimethylation at cis-regulatory sites, thereby ensuring precise epigenetic regulation of lineage specification and cell physiology. Dysregulation or mutations in MLL2-C are linked to diseases such as early-onset dystonia, gastrointestinal B-cell lymphoma, and modulation of MLL1-rearranged leukemias.
    References
    • https://pubmed.ncbi.nlm.nih.gov/20808952/
    • https://pubmed.ncbi.nlm.nih.gov/34440566/

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