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SAB4200597

Sigma-Aldrich

Monoclonal Anti-FMR1 antibody produced in mouse

clone FMR2.5, hybridoma cell culture supernatant

Synonyme(s) :

FMRP, FRAXA, POF, POF1, fragile X mental retardation 1

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

FMR2.5, monoclonal

Forme

buffered aqueous solution

Poids mol.

~71 kDa

Espèces réactives

rat, human, mouse, hamster

Concentration

~1 mg/mL

Technique(s)

flow cytometry: 2.0-5.0 μg/test using HeLa cells
immunoblotting: 1.0-2.0  μg/mL using HepG2 total cell extracts.
immunocytochemistry: suitable
immunofluorescence: 5-10 μg/mL using HepG2 cells.

Isotype

IgG1

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... FMR1(2332)
mouse ... Fmr1(14265)
rat ... Fmr1(24948)

Description générale

Monoclonal Anti-FMR1 (mouse IgG1 isotype) is derived from the hybridoma FMR2.5 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a synthetic peptide. Fragile X mental retardation 1 (FMR1) is encoded by the gene mapped to human chromosome Xq27.3q28. FMR1 localizes to both the nucleus and the cytoplasm.

Spécificité

Monoclonal Anti- FMR1 recognizes human, hamster, rat and mouse FMR1.

Immunogène

synthetic peptide corresponding to a sequence at the C-terminal region of human FMR1

Application

Monoclonal Anti-FMR1 antibody produced in mouse may be used in:
  • immunoblotting
  • immunocytochemistry
  • immunofluorescence
  • flow cytometry

Actions biochimiques/physiologiques

Fragile X mental retardation 1 (FMR1) protein functions as an RNA-binding protein that associates with polyribosomes and is a likely component of a messenger ribonuclear protein (mRNP) particle. Since, FMR1 contains both a nuclear localization signal and a nuclear export signal it is also implicated in nucleocytoplasmic transport. Mutation in the gene leads to the development of fragile X mental retardation (FXMR) syndrome.

Forme physique

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

Stockage et stabilité

For extended storage, freeze at 20 °C in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilution samples should be discarded if not used within 12 hours.

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Familial interstitial Xq27.3q28 duplication encompassing the FMR1 gene but not the MECP2 gene causes a new syndromic mental retardation condition
Rio M,et al.
European Journal of Human Genetics, 18, 285-285 (2010)
FMRP Associates with Polyribosomes as an mRNP, and the I304N Mutation of Severe Fragile X Syndrome Abolishes This Association
Feng Y, et al.
Molecular Cell, 1, 109-118 (1997)
Fragile X Mental Retardation Protein FMRP Binds mRNAs in the Nucleus
Kim M, et al.
Molecular and Cellular Biology, 29, 214-228 (2009)
Kan Yang et al.
Cell reports, 37(5), 109939-109939 (2021-11-04)
Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental disorder, causing defects of social interaction and repetitive behaviors. Here, we identify a de novo heterozygous gene-truncating mutation of the Sentrin-specific peptidase1 (SENP1) gene in people with ASD without neurodevelopmental delay.

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