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Rabbit anti-Human KMT2E Polyclonal Antibody

The antibody against KMT2E was raised in rabbit using the Recombinant Human Histone-lysine N-methyltransferase 2E protein (182-316AA) as the immunogen. This antibody exists as a non-conjugated isotype IgG, purified by protein G with a purity greater than 95%. This antibody has been validated on ELISA, WB.

ADC-02551A

The antibody against KMT2E was raised in rabbit using the Recombinant Human Histone-lysine N-methyltransferase 2E protein (182-316AA) as the immunogen. This antibody exists as a non-conjugated isotype IgG, purified by protein G with a purity greater than 95%. This antibody has been validated on ELISA, WB.

$299.00

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Specifications


Cat.No ADC-02551A ClonalityPolyclonal
Host SpeciesRabbitTarget NameKMT2E
FormLiquidSpecies ReactivityHuman, Mouse
IsotypeIgGStorage Buffer0.01M PBS, 0.03% Proclin 300; Constituents: 50% Glycerol, PH 7.4
Purification Method>95%, Protein G purifiedConjugateNon-conjugated
ApplicationELISA, WBStorageUpon receipt

Immunogen Information


Immunogen DescriptionRecombinant Human Histone-lysine N-methyltransferase 2E protein (182-316AA)Target SpeciesHuman
Immunogen SequenceComplete sequences for the immunogen, target protein, and peptides are available upon request.Uniprot IDQ8IZD2
Background Information
  • Uniprot Id

    Q8IZD2

  • Target Species

    Human

  • Target Name

    KMT2E

  • Target Full Name

    Inactive histone-lysine N-methyltransferase 2E

  • Target Function

    Associates with chromatin regions downstream of transcriptional start sites of active genes and thus regulates gene transcription. Chromatin interaction is mediated via the binding to tri-methylated histone H3 at 'Lys-4' (H3K4me3). Key regulator of hematopoiesis involved in terminal myeloid differentiation and in the regulation of hematopoietic stem cell (HSCs) self-renewal by a mechanism that involves DNA methylation. Also acts as an important cell cycle regulator, participating in cell cycle regulatory network machinery at multiple cell cycle stages including G1/S transition, S phase progression and mitotic entry. Recruited to E2F1 responsive promoters by HCFC1 where it stimulates tri-methylation of histone H3 at 'Lys-4' and transcriptional activation and thereby facilitates G1 to S phase transition. During myoblast differentiation, required to suppress inappropriate expression of S-phase-promoting genes and maintain expression of determination genes in quiescent cells.; Cellular ligand for NCR2/NKp44, may play a role as a danger signal in cytotoxicity and NK-cell-mediated innate immunity.

  • Target Subcellular Location

    Chromosome. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Nucleus speckle.; [Isoform 3]: Nucleus, nucleoplasm. Nucleus speckle.; [Isoform NKp44L]: Cytoplasm. Cell membrane; Peripheral membrane protein.

  • Target Protein Families

    Class V-like SAM-binding methyltransferase superfamily, Histone-lysine methyltransferase family, TRX/MLL subfamily

  • Target Tissue Specificity

    Widely expressed in both adult and fetal tissues. Highest levels of expression observed in fetal thymus and kidney and in adult hematopoietic tissues, jejunum and cerebellum. Isoform NKp44L: Not detected on circulating cells from healthy individuals, but

  • Target Research Area

    Cell cycle, Growth arrest, Transcription, Transcription regulation

  • Target Synonyms

    HDCMC04P; Histone lysine N methyltransferase MLL5; Histone-lysine N-methyltransferase MLL5; KMT2E; Lysine N methyltransferase 2E ; Lysine N-methyltransferase 2E; MGC70452; Mll5; MLL5_HUMAN; Myeloid/lymphoid or mixed lineage leukemia 5 (trithorax homolog; Drosophila); Myeloid/lymphoid or mixed lineage leukemia 5; Myeloid/lymphoid or mixed lineage leukemia protein 5; Myeloid/lymphoid or mixed-lineage leukemia protein 5

  • Target Background

    This gene is a member of the myeloid/lymphoid or mixed-lineage leukemia (MLL) family and encodes a protein with an N-terminal PHD zinc finger and a central SET domain. Overexpression of the protein inhibits cell cycle progression. Alternate transcriptional splice variants have been characterized.

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