The acute lymphoblastic leukaemia (ALL)-1 (also known as MLL, HRX, HTRX, and TRX1) gene on human chromosome 11q23 is the site of many locally clustered chromosomal alterations associated with several types of acute leukaemias, including deletions, partial duplications and translocations. Structurally variant proteins derived from the altered gene presumably cause the malignant transformation of early haemopoietic progenitor cells.
Specificity
Recognizes N-terminal proteolytic fragment of MLL (MLLN).
Immunogen
MBP fusion protein corresponding to residues 161-356 of human mixed lineage leukemia, MLL
Application
Detect MLL/HRX with Anti-MLL/HRX Antibody, N-term., clone N4.4 (Mouse Monoclonal Antibody), that has been shown to work in IP & WB.
Quality
routinely evaluated by immunoblot on nuclear extract from K562 cells
Target description
300 kDa
Physical form
Format: Purified
Immunoaffinity Purified immunoglobulin in 0.014M phosphate buffer, pH 7.6, 0.175M NaCl, 0.07% sodium azide, and 30% glycerol.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Different fusion oncogenes in acute myeloid leukemia (AML) have distinct clinical and laboratory features suggesting different modes of malignant transformation. Here we compare the in vitro effects of representatives of 4 major groups of AML fusion oncogenes on primary human
The MLL-AF4 fusion gene is a hallmark genomic aberration in high-risk acute lymphoblastic leukemia in infants. Although it is well established that MLL-AF4 arises prenatally during human development, its effects on hematopoietic development in utero remain unexplored. We have created
Inducible MLL-AF9 Expression Drives an AML Program during Human Pluripotent Stem Cell-Derived Hematopoietic Differentiation.
Permanent middle cerebral artery occlusion (MCAO) causes neuronal cell death in the striatum and cortex. In rodents, estradiol treatment protects the cortex from cell death in an estrogen receptor alpha (ERalpha) dependent manner. ERalpha is only transiently expressed in the
Elucidation of activation mechanisms governing protein fusions is essential for therapeutic development. MLL undergoes rearrangement with numerous partners, including a recurrent translocation fusing the epigenetic regulator to a cytoplasmic RAS effector, AF6/afadin. We show here that AF6 employs a non-canonical
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