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Primary Antibodies /
MBNL2 Antibody

MBNL2 Antibody #29733

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Supporting Data

REACTIVITY	H
SENSITIVITY	Endogenous
MW (kDa)	41
SOURCE	Rabbit

Application Key:

WB-Western Blotting

Species Cross-Reactivity Key:

H-Human

Product Information

Product Usage Information

Application	Dilution
Western Blotting	1:1000

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

Protocol

Specificity / Sensitivity

MBNL2 Antibody recognizes endogenous levels of total MBNL2 protein. This antibody does not cross-react with MBNL1 protein.

Species Reactivity:

Human

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly119 of human MBNL2 protein. Antibodies are purified by peptide affinity chromatography.

Background

Alternative splicing is a crucial biological process that promotes protein diversity and provides cells with an additional mechanism to regulate the expression of tissue-specific protein isoforms. Muscleblind-like proteins (MBNLs) are one such protein family responsible for tissue-specific alternative splicing regulation. MBNLs bind pre-mRNA through an evolutionarily conserved zinc finger domain, and act as either activators or repressors of splicing on specific pre-mRNA targets by promoting the inclusion or exclusion of exons (1). MBNLs are functionally antagonistic to CUG-BP and ETR-3-like factors (CELF proteins) that also control pre-mRNA splicing. The interplay between MBNL and CELF activity plays a key role in development, where predominant MBNL activity promotes adult differentiation, and predominant CELF activity promotes embryonic splicing patterns (1). Three MBNL homologs are expressed in humans (MBNL1, MBNL2, and MBNL3) that share similar structure and function, yet differ in their tissue- and developmental stage-specific expression patterns (2). MBNL1 is the predominant isoform in the majority of tissue, including muscle, and is therefore the most well characterized. MBNL2 is the predominant homolog in brain, and exhibits increased expression upon functional loss of MBNL1 in other tissue types, suggesting a compensatory role (3). MBNL3 appears to play a more specialized role, where it inhibits muscle differentiation in muscle precursor cells (4). Functional loss of MBNLs is observed in myotonic dystrophy (DM), where pathological repeats in the 3’-UTR of the myotonic dystrophy protein kinase (DMPK) gene or intron 1 of the cellular nucleic acid binding protein (CNBP) gene result in toxic RNA hairpins that sequester MBNLs in nuclear foci. This loss of available MBNLs causes an adult-to-fetal shift in alternative splicing patterns and ultimately results in respiratory and cardiac complications observed in DM patients (2,5).

Database Links

UniProt ID: Q5VZF2

Entrez-Gene Id: 10150

Limited Uses

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For Research Use Only. Not For Use In Diagnostic Procedures.

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