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Rabbit anti-Human MLL5 Polyclonal Antibody

The antibody against MLL5 was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 200-500 of human MLL5 (NP_061152.3) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, IHC-P, IF/ICC, ELISA.

ADA-03160A

The antibody against MLL5 was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 200-500 of human MLL5 (NP_061152.3) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, IHC-P, IF/ICC, ELISA.

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Specifications


Cat.No ADA-03160A ClonalityPolyclonal
Host SpeciesRabbitTarget NameMLL5
Target SynonymsMLL5; NKp44L; ODLURO; SETD5B; HDCMC04PFormLiquid
Species ReactivityHuman, Mouse, RatIsotypeIgG
Storage Buffer50% Glycerol, PBS with 0.01% thimerosal, pH7.3.Purification MethodAffinity purification
Positive SamplesC2C12ApplicationELISA, WB, IF/ICC, IHC-P

Immunogen Information


Immunogen DescriptionRecombinant fusion protein containing a sequence corresponding to amino acids 200-500 of human MLL5 (NP_061152.3).Target SpeciesHuman
Uniprot IDQ8IZD2Immunogen Sequence
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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