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Merck
CN

05-621

Anti-CUGBP1 Antibody, clone 3B1

clone 3B1, Upstate®, from mouse

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
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产品名称

Anti-CUGBP1 Antibody, clone 3B1, clone 3B1, Upstate®, from mouse

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

3B1, monoclonal

species reactivity

bovine, mouse, human, rabbit, rat, pig

manufacturer/tradename

Upstate®

technique(s)

electrophoretic mobility shift assay: suitable
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... CELF1(10658)

Analysis Note

Control
Positive Antigen Control: Catalog #12-309, Hela cell nuclear extract. Add an equal volume of Laemmli reducing sample buffer to 10 μL of extract and boil for 5 minutes to reduce the preparation. Load 20 μg of reduced extract per lane for minigels.
routinely evaluated by immunoblot on HeLa nuclear extract

Application

Anti-CUGBP1 Antibody, clone 3B1 is a high quality Mouse Monoclonal Antibody for the detection of CUGBP1 & has been validated in EMSA, IP, WB, ICC.
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Cell Cycle, DNA Replication & Repair

RNA Binding Protein (RBP)

Biochem/physiol Actions

CUG-BP1

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.

General description

50kDa
Myotonic dystrophy (MD) is an autosomal dominant neuromuscular disease that is associated with a (CTG)n repeat expansion in the 3′-untranslated region of the myotonin protein kinase (Mt-PK) gene. A (CUG)n oligonucleotides triplet repeat pre-mRNA/mRNA binding protein may play an important role in DM pathogenesis. HeLa cell protein, CUG-BP1, has been purified based upon its ability to bind specifically to (CUG)8 oligonucleotides in vitro. CUG-BP1 is the major (CUG)8 binding activity in normal cells. CUG-BP1 has been identified as isoforms of a novel heterogeneous nuclear ribonucleoprotein (hnRNP), hNab50. The CUG-BP/hNab50 protein is localized predominantly in the nucleus and is associated with polyadenylated RNAs in vivo. In vitro RNA-binding/photocrosslinking studies demonstrate that CUG-BP/hNab50 binds to RNAs containing the Mt-PK 3′-UTR.

Immunogen

Full-length GST fusion protein corresponding to human CUG-BP1, also known as heterogeneous nuclear ribonucleoprotein (hnRNP) hNab50

Physical form

0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.05% sodium azide before the addition of glycerol to 30%
Format: Purified
Protein G Chromatography

Preparation Note

2 years at -20°C

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

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存储类别

10 - Combustible liquids

wgk

WGK 1


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N Muge Kuyumcu-Martinez et al.
Molecular cell, 28(1), 68-78 (2007-10-16)
The genetic basis of myotonic dystrophy type 1 (DM1) is a CTG expansion in the 3' untranslated region (UTR) of DMPK. The pathogenic mechanism involves an RNA gain of function in which the repeat-containing transcripts accumulate in nuclei and alter
James P Orengo et al.
Annals of neurology, 69(4), 681-690 (2011-03-15)
Dysregulation of alternative splicing has become a molecular hallmark of myotonic dystrophy type 1 (DM1), in which neonatal splice variants are expressed in adult skeletal muscle. Splicing dysregulation is induced by RNA containing expanded CUG repeats expressed from the expanded
Ashish N Rao et al.
JCI insight, 6(5) (2021-01-27)
Myotonic dystrophy type 1 (DM1) is caused by a CTG repeat expansion in the DMPK gene. Expression of pathogenic expanded CUG repeat (CUGexp) RNA causes multisystemic disease by perturbing the functions of RNA-binding proteins, resulting in expression of fetal protein
Reversible model of RNA toxicity and cardiac conduction defects in myotonic dystrophy.
Mahadevan, MS; Yadava, RS; Yu, Q; Balijepalli, S; Frenzel-McCardell, CD; Bourne, TD; Phillips, LH
Nature Genetics null
Rafal Goraczniak et al.
The Journal of biological chemistry, 283(4), 2286-2296 (2007-11-29)
The 3'-untranslated regions (UTRs) of human papillomavirus 16 (HPV16) and bovine papillomavirus 1 (BPV1) contain a negative regulatory element (NRE) that inhibits viral late gene expression. The BPV1 NRE consists of a single 9-nucleotide (nt) U1 small nuclear ribonucleoprotein (snRNP)

相关内容

All eukaryotic organisms require tight regulation of gene expression for complex processes such as development, differentiation, cell specification, and responses to environmental stimuli. Many genes are regulated post-transcriptionally, in addition to transcriptional mechanisms of gene regulation. RNA-binding proteins (RBPs) are essential for post-transcriptional gene regulation, linking transcription and translation in many processes including transcription, splicing, export, rate of translation and turnover. In all of these events, RBPs coordinate regulation of the amount of protein produced from mRNA transcripts.

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