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Key Documents

SAB4300410

Sigma-Aldrich

Anti-FOXO1 (Ab-256) antibody produced in rabbit

affinity isolated antibody

Sinónimos:

Anti-FKH1 antibody produced in rabbit, Anti-FKHR antibody produced in rabbit, Anti-FOXO1A antibody produced in rabbit, Anti-forkhead box O1 antibody produced in rabbit

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

78-82 kDa

species reactivity

mouse, human, rat

concentration

1 mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:50-1:100
indirect immunofluorescence: 1:100-1:200
western blot: 1:500-1:1000

isotype

IgG

immunogen sequence

(A-A-S-M-D)

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... FOXO1(2308)

General description

FOXO1 (forkhead box O1) is a transcription factor , that belongs to the Foxo subfamily. It is located on human chromosome 13q14.

Immunogen

Peptide sequence around aa. 254-258 (A-A-S-M-D), according to the protein FOXO1.

Application

Anti-FOXO1 (Ab-256) antibody has been used in immunohistochemistry, immunofluorescence and western blotting .

Biochem/physiol Actions

FOXO1 (forkhead box O1) blocks the differentiation of cell in fetal pancreatic progenitor cells. It controls the differentiation of adipocyte.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Target description

FKHR belongs to the forkhead family of transcription factors, which are characterized by a distinct forkhead domain. It may play a role in myogenic growth and differentiation. The mammalian DAF-16-like transcription factors, FKHR, FKHRL1, and AFX, function as key regulators of insulin signaling, cell cycle progression, and apoptosis downstream of phosphoinositide 3-kinase. Gene activation through binding to insulin response sequences has been essential for mediating these functions. D-type Cyclins (in Class III) is required for FKHR mediated inhibition of cell cycle progression and transformation. FKHR gene is mapped to chromosome 13q14

Physical form

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

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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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

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

Forkhead Protein FoxO1 Acts as a Repressor to Inhibit Cell Differentiation in Human Fetal Pancreatic Progenitor Cells
Jiang Z, et al.
Journal of Diabetes Research (2017)
Differential effects of angiotensin receptor blockers on pancreatic islet remodelling and glucose homeostasis in diet-induced obese mice
Graus-Nunes F, et al.
Molecular and Cellular Endocrinology, 439, 54-64 (2017)
The insulin-signaling pathway of the pancreatic islet is impaired in adult mice offspring of mothers fed a high-fat diet
Bringhenti I, et al.
Nutrition, 32(10), 1138-1143 (2016)
The forkhead transcription factor Foxo1 regulates adipocyte differentiation
Nakae J, et al.
Developmental Cell, 4(1), 119-129 (2003)
The forkhead transcription factor Foxo1 links insulin signaling to Pdx1 regulation of pancreatic beta cell growth
Kitamura T, et al.
The Journal of Clinical Investigation, 110(12), 1839-1847 (2002)

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