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Merck

M3320

Sigma-Aldrich

Monoclonal Anti-MBNL1 antibody produced in mouse

~1 mg/mL, clone HL 1822 (3A4-1E9), purified immunoglobulin, buffered aqueous solution

Synonym(e):

Anti-CUG Triplet Repeat Expansion Double-stranded RNA-binding protein, Anti-EXP, Anti-KIAA0428, Anti-Muscleblind-like protein, Anti-Triplet-expansion RNA-binding protein

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About This Item

MDL-Nummer:
UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

mouse

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

HL 1822 (3A4-1E9), monoclonal

Form

buffered aqueous solution

Mol-Gew.

antigen ~42 kDa

Speziesreaktivität

monkey, mouse, human

Konzentration

~1 mg/mL

Methode(n)

immunocytochemistry: suitable
immunohistochemistry: suitable
microarray: suitable
western blot: 0.2-0.5 μg/mL using HeLa nuclear cell extract

Isotyp

IgG1

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... MBNL1(4154)
mouse ... Mbnl1(56758)

Allgemeine Beschreibung

Muscle blind-like 1 (MBNL1) is a homolog of human muscle blind like proteins. Proteins of the MBNL (muscleblind-like) family are mainly expressed in skeletal muscle neuronal tissues, thymus, liver and kidney.

Immunogen

recombinant muscleblind-like1 (MBNL1) fusion protein.

Anwendung

Monoclonal Anti-MBNL1 antibody produced in mouse has been used in: immunoblotting, immunohistochemistry and immunocytochemistry

Biochem./physiol. Wirkung

Proteins of the MBNL (muscleblind-like) family enhance inclusion or exclusion of specific exons on different pre-mRNAs by inhibiting the activity of CUG-BP and ETR-3-like factors (CELF proteins) bound to distinct intronic sites. MBNL1 may be implicated in the stimulation of muscle differentiation. Mice knockouts for the MBNL1 gene develop muscle, eye, and RNA splicing abnormalities that are characteristic of the neuromuscular disease myotonic dystrophy (DM) disease.

Physikalische Form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

The Muscleblind family of proteins: an emerging class of regulators of developmentally programmed alternative splicing
Pascual M, et al.
Differentiation, 74, 65-80 (2006)
Muscleblind-like 1 (Mbnl1) regulates pre-mRNA alternative splicing during terminal erythropoiesis
Cheng AW, et al.
Blood, 124, 598-610 (2014)
A Muscleblind Knockout Model for Myotonic Dystrophy
Kanadia RN, et al.
Science, 302, 1978-1980 (2003)
Curtis A Nutter et al.
Muscle & nerve, 56(4), 744-749 (2017-02-07)
Type 1 diabetic patients can develop skeletal muscle weakness and atrophy by molecular mechanisms that are not well understood. Alternative splicing (AS) is critical for gene expression in the skeletal muscle, and its dysregulation is implicated in muscle weakness and
Debra A O'Leary et al.
Current chemical genomics, 4, 9-18 (2010-05-27)
Myotonic dystrophy type 1 (DM1) is a genetic disorder characterized by muscle wasting, myotonia, cataracts, cardiac arrhythmia, hyperinsulinism and intellectual deficits, and is caused by expansion of a CTG repeat in the 3'UTR of the Dystrophia Myotonica-Protein Kinase (DMPK) gene.

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