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HPA023084

Sigma-Aldrich

Anti-MLXIP antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

Synonym(s):

Anti-MLX-interacting protein, Anti-Transcriptional activator MondoA

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About This Item

UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

Pricing and availability is not currently available.

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human

technique(s)

immunohistochemistry: 1:50- 1:200

immunogen sequence

LKREGMLASTVSQSNVVIAPAAIARAPGVPEFHSSILVTDLGHGTSSPPAPVSRLFPSTAQDPLGKGEQVPLHGGSPQVTVTGPSRDCPNSGQASPCASEQSPSPQSPQNNCSGKSDPKNVAALKNRQMK

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This Item
HPA064640HPA029252AV39966
conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

IgG fraction of antiserum

product line

Prestige Antibodies® Powered by Atlas Antibodies

product line

Prestige Antibodies® Powered by Atlas Antibodies

product line

Prestige Antibodies® Powered by Atlas Antibodies

product line

-

clone

polyclonal

clone

polyclonal

clone

polyclonal

clone

polyclonal

UniProt accession no.

Q9HAP2

UniProt accession no.

Q9NP71

UniProt accession no.

Q5VWP3

UniProt accession no.

Q9UH92

General description

MLXIP (MLX interacting protein) belongs to the basic helix-loop-helix leucine zipper (bHLHZip) family of transcription factors. The gene is mapped to human chromosome 12q24.

Immunogen

MLX-interacting protein recombinant protein epitope signature tag (PrEST)

Application

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

Biochem/physiol Actions

MLXIP (MLX interacting protein) associates with MLX (max-like protein X) and together they are needed for the regulation of glucose-mediated gene expression. MLXIP is important for glucose homeostasis in cells. The MLXIP-MLX complex moves between the nucleus and cytoplasm. MLXIP is upregulated in acute lymphoblastic leukemia cells and is associated with leukemia aggressiveness.

Features and Benefits

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Linkage

Corresponding Antigen APREST73752

Physical form

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Legal Information

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Orazio Palumbo et al.
American journal of medical genetics. Part A, 167A(2), 438-444 (2014-11-28)
We provide a detailed clinical and molecular characterization of an 11-year-old female patient presenting with neurodevelopmental delay (NDD), intellectual disability (ID), seizures, stereotypies and dysmorphic features. Chromosomal microarrays analysis (CMA) detected a small, rare de novo deletion on chromosome 12q24.31
Caroline M Wernicke et al.
Leukemia research, 36(9), 1185-1192 (2012-07-04)
Acute lymphoblastic leukemia (ALL) is the most common childhood cancer. To identify novel candidates for targeted therapy, we performed a comprehensive transcriptome analysis identifying MondoA (MLXIP) - a transcription factor regulating glycolysis - to be overexpressed in ALL compared to
Mohan R Kaadige et al.
Molecular and cellular biology, 35(1), 101-110 (2014-10-22)
Mammalian target of rapamycin (mTOR) integrates multiple signals, including nutrient status, growth factor availability, and stress, to regulate cellular and organismal growth. How mTOR regulates transcriptional programs in response to these diverse stimuli is poorly understood. MondoA and its obligate
Jie Luo et al.
Journal of immunology (Baltimore, Md. : 1950), 193(10), 5044-5055 (2014-10-08)
Myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG) are caused by Ab-mediated autoimmune responses to muscle nicotinic acetylcholine receptors (AChRs) that impair neuromuscular transmission, thereby causing muscle weakness. Previously, we discovered that i.p. injection of a therapeutic vaccine consisting

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