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Merck

SAB4200597

Sigma-Aldrich

Monoclonal Anti-FMR1 antibody produced in mouse

clone FMR2.5, hybridoma cell culture supernatant

Sinónimos:

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

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

FMR2.5, monoclonal

form

buffered aqueous solution

mol wt

~71 kDa

species reactivity

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

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

General description

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.

Specificity

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

Immunogen

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

Biochem/physiol Actions

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.

Physical form

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

Storage and Stability

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.

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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Optional

Storage Class

10 - Combustible liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Visite la Librería de documentos

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)
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)
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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