Anti-MLL monoclonal antibody, clone 20G9E8

Name: Anti-MLL monoclonal antibody, clone 20G9E8
SKU: DCABH-12367
Rating: 5 (1 reviews)

Mouse anti-Human MLL monoclonal antibody for WB, IHC-P, ELISA

COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG1

Clone

20G9E8

Species Reactivity

Human

Immunogen

Recombinant protein corresponding to amino acids 3751-3968 of human MLL.

Conjugate

Unconjugated

Applications

Application Notes

ELISA (1:10000); WB (1:500-1:2000); Immunohistochemistry (1:200-1:1000) & The optimal working dilution should be determined by the end user.

Target

Alternative Names

MLL; myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); myeloid/lymphoid or mixed lineage leukemia (trithorax (Drosophila) homolog); histone-lysine N-methyltransferase MLL; ALL 1; CXXC7; HRX; HTRX1; KMT2A; MLL1A; TRX1; trithorax-l

Entrez Gene ID

4297

UniProt ID

Q03164

Product Background

Antigen Description

The MLL gene encodes a DNA-binding protein that methylates histone H3 (see MIM 601128) lys4 (H3K4) and positively regulates expression of target genes, including multiple HOX genes (see MIM 142980). MLL is a frequent target for recurrent translocations in acute leukemias that may be characterized as acute myeloid leukemia (AML; MIM 601626), acute lymphoblastic leukemia (ALL), or mixed lineage (biphenotypic) leukemia (MLL). Leukemias with translocations involving MLL possess unique clinical and biologic characteristics and are often associated with poor prognosis. MLL rearrangements are found in more than 70% of infant leukemias, whether the immunophenotype is more consistent with ALL or AML6, but are less frequent in leukemias from older children. MLL translocations are also found in approximately 10% of AMLs in adults, as well as in therapy-related leukemias, most often characterized as AML, that develop in patients previously treated with topoisomerase II inhibitors for other malignancies. More than 50 different MLL fusion partners have been identified. Leukemogenic MLL translocations encode MLL fusion proteins that have lost H3K4 methyltransferase activity. A key feature of MLL fusion proteins is their ability to efficiently transform hematopoietic cells into leukemia stem cells (Krivtsov and Armstrong, 2007 [PubMed 17957188]).

Pathway

Lysine degradation, organism-specific biosystem; Lysine degradation, conserved biosystem; Senescence and Autophagy, organism-specific biosystem; Transcriptional misregulation in cancer, organism-specific biosystem; Transcriptional misregulation in cancer, conserved biosystem;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Antitumor effect of baicalin from the Scutellaria baicalensis radix extract in B-acute lymphoblastic leukemia with different chromosomal rearrangements

INTERNATIONAL IMMUNOPHARMACOLOGY

Authors: Orzechowska, Beata U.; Wrobel, Grazyna; Turlej, Eliza; Jatczak, Bogna; Sochocka, Marta; Chaber, Radoslaw

Abstract

Acute B-lymphoblastic leukemia (B-ALL) is the most common hematologic malignancy in children. Many cases of B-ALL harbor chromosomal translocations which are often critical determinants of prognosis. Most of them represent altered transcription factors that impact gene transcription or enhance signaling. B-ALLs harboring the mixed-lineage leukemia 1 (MLL1) gene rearrangements represent aggressive, high-risk type of early childhood leukemias that are usually associated with a very poor prognosis. Therefore, there is an urgent need for novel therapeutic agents as well as new treatment strategies. The objective was to examine the vitro inhibitory effects of Scutellaria baicalensis root extract (SBE) in B-ALL cell lines with different chromosomal rearrangements and in leukemic blasts derived from patients' bone marrow (BMCs). In this study we showed that baicalin which is the main component of the SBE possess antitumor activity against all leukemic cell lines especially those with MLL and PBX1 gene rearrangements. Baicalin inhibited cell proliferation, arrested the cell cycle at the G0/G1 phase, and induced cell death through caspase 3/7 activation. Moreover, baicalin treatment inhibited the glycogen synthase kinase-3 beta (GSK-3 beta) by suppressing its phosphorylation at Y216, and upregulated the downstream mediator of the cell cycle arrest - cyclin dependent kinase inhibitor p27(Kip1). Bone marrow derived blasts from B-ALL patients also exhibited varied sensitivity towards baicalin with 72% patients sensitive to the SBE and baicalin treatment. Taken together, our findings provide new insights into the anti-cancer properties of baicalin by showing its diverse mode of action which might be related to the different genetic background.

A complex karyotype with t(11;12)(q23;p13) translocation with coexistent clones of deletion 5q and cryptic deletion 7q in acute myeloid leukemia

INDIAN JOURNAL OF CANCER

Authors: Pais, Anurita; Pande, Shailesh; Pradhan, Gauri; Patil, Smita

Abstract

We report a rare case of acute myeloid leukemia (AML) with a cytogenetically complex karyotype with coexistence of KMT2A/MLL Mixed Lineage Leukemia (11q23) rearrangement with 5q deletion and 7q deletion as unrelated clones along with evolution of a subclone with translocation between chromosomes 6 and 17. A novel MLL fusion partner region 12p13 was identified in a 52 year old woman who presented with pyrexia of unknown origin. Unraveling the complexity of genomic alterations occurring in AML patients will lead to better understanding of leukemic transformation and identification of subsets of patients that may respond differently to therapy.