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Anti-MLL.N Antibody

Mouse Monoclonal Antibody specific to MLL (N-terminus)

Product Specifications

CAS Number

9007-83-4

Product Name Alternative

Anti-MLL (N-terminus) Mouse Monoclonal Antibody

Gene Name

MLL

NCBI Gene ID

<a href="https://www.ncbi.nlm.nih.gov/gene/?term=MLL">MLL</a>

UniProt

Q9Y6P1

Host

Mouse

Reactivity

Human, Mouse

Immunogen

Maltose-binding fusion protein containing MLL amino acids 161-356 (Uniprot #Q03164).

Target Antigen

MLL

Target

MLL.N

Clonality

Monoclonal

Isotype

IgG1

Type

Antibody

Applications

WB, IP

Field of Research

Cancer research

Purification Method

Purified by Protein G affinity chromatography

Concentration

Lot Specific

Dilution

Dilute in PBS or medium that is identical to that used in the assay system.

Format

Purified

Form

Liquid

Buffer

Phosphate Buffered Saline

Additionnal Information

Immunoblotting: use at 2ug/mL. A band of ~300kDa is detected. <br><br>Immunoprecipitation: use 2-10ug per 500ul (1-3mg/ml) of cell lysate. <br><br>Positive control: K562 cell lysate. <br><br>These are recommended concentrations. <br><br>Endusers should determine optimal concentrations for their applications.

Storage Conditions

This antibody is stable for at least one (1) year at -20°C. Avoid multiple freeze-thaw cycles.

Specificity

This antibody recognizes human and mouse MLLN.

Formulation

PBS, pH 7.4.

Buffer pH

pH 7.4

Target Background

MLL (Mixed Lineage Leukemia) is a proto- oncogene that is mutated in a variety of acute leukemias. MLL is proteolytically processed into 2 fragments, MLLN and MLLC, that display opposite transcriptional properties. Processed MLLN and MLLC associate with each other via N-terminal and C-terminal intramolecular interaction domains. MLL processing occurs rapidly after translation and is followed by phosphorylation of MLLC. MLLN displays transcriptional repression activity, whereas MLLC has strong transcriptional activation properties. Leukemia-associated MLL fusion proteins lack the MLL processing sites, do not undergo cleavage, and are unable to interact with MLLC. These observations suggest that posttranslational modifications of MLL may be involved in regulating MLL activity as a transcription factor, and this aspect of its function is perturbed by leukemogenic fusions.
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