07-702
Anti-FOXO3a/FKHRL1 Antibody
Upstate®, from rabbit
Synonym(s):
AF6q21 protein, Forkhead in rhabdomyosarcoma-like 1, forkhead box O3, forkhead box O3A, forkhead homolog (rhabdomyosarcoma) like 1, forkhead, Drosophila, homolog of, in rhabdomyosarcoma-like 1
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
species reactivity
human, mouse
manufacturer/tradename
Upstate®
technique(s)
western blot: suitable
isotype
IgG
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... FOXO3(2309)
Related Categories
General description
The forkhead family of transcription factors is a large group of proteins that share a common conserved 100 amino acid DNA binding domain, which is termed a winged-helix or forkhead domain after the founding member of this group, the forkhead gene in Drosophila. In addition to their roles during normal development, recent studies have demonstrated that members of the forkhead family may participate in several kinds of neoplasia. In particular, 3 genes of the human forkhead family, FKHR, FKHRL1, and AFX, which are orthologues of DAF-16 in Caenorhabditis elegans, were identified at the chromosomal breakpoints in human neoplasms. These three genes have been assigned to the FOXO (named for “Forkhead Box, group O”) subfamily of forkhead transcription factors. The forkhead factors, including FKHRL1, regulate their activation through phosphorylation by proto-oncogene Akt (protein kinase B) and/or SGK (serum- and glucocorticoid- induced kinases) in mammalian cells and the phosphorylated form localized at the cytoplasm is recognized to be an inactivated form, whereas nuclear-imported dephosphorylated FKHRL1 is functional as an active transcriptional factor.
Specificity
Not tested on other species.
Recognizes FKHRL1/FOXO3A, Mr 90-95 kDa.
Immunogen
Epitope: a.a. 330-673
GST fusion protein corresponding to residues 330-673 of human FKHRL1/FOXO3A.
Application
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Transcription Factors
Transcription Factors
Use Anti-FOXO3a/FKHRL1 Antibody (Rabbit Polyclonal Antibody) validated in WB to detect FOXO3a/FKHRL1 also known as AF6q21 protein, Forkhead in rhabdomyosarcoma-like 1, forkhead box O3A.
Quality
Routinely evaluated by Western Blot on 3T3/A31 cell lysates.
Western Blot Analysis:
A 0.5 g/mL dilution of this antibody was used to detect FOXO3a/FKHRL1 in 3T3/A31 cell lysate.
Western Blot Analysis:
A 0.5 g/mL dilution of this antibody was used to detect FOXO3a/FKHRL1 in 3T3/A31 cell lysate.
Target description
Approx. 90-95 kDa
Linkage
Replaces: 04-1007
Physical form
Affinity purified
Antigen affinity purified rabbit polyclonal, followed by anti-GST depletion, in 0.1M Tris-Glycine (pH7.4), 150mM NaCl with 0.05% sodium azide.
Format: Purified
Storage and Stability
Stable for 1 year at 2-8ºC from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.
Analysis Note
Control
Positive Antigen Control: Catalog #12-305, 3T3/A31 lysate. Add 2.5 μL of 2-mercapto-ethanol/100 μL of lysate and boil for 5 minutes to reduce the preparation. Load 20 μg of reduced lysate per lane for minigels.
Positive Antigen Control: Catalog #12-305, 3T3/A31 lysate. Add 2.5 μL of 2-mercapto-ethanol/100 μL of lysate and boil for 5 minutes to reduce the preparation. Load 20 μg of reduced lysate per lane for minigels.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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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Product No.
Description
Pricing
Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Find documentation for the products that you have recently purchased in the Document Library.
Stephane Tarrade et al.
International journal of molecular sciences, 16(12), 29996-30014 (2015-12-24)
Histone H2AX plays a crucial role in molecular and cellular responses to DNA damage and in the maintenance of genome stability. It is downstream of ataxia telangiectasia mutated (ATM) damage signaling pathway and there is an emerging role of the
Bortezomib treatment causes remission in a Ph+ALL patient and reveals FoxO as a theranostic marker.
Dewar, R; Chen, ST; Yeckes-Rodin, H; Miller, K; Khosravi-Far, R
Cancer Biology & Therapy null
Céline Charvet et al.
Molecular cell, 42(5), 584-596 (2011-06-11)
Activation of p53 by DNA damage results in either cell-cycle arrest, allowing DNA repair and cell survival, or induction of apoptosis. As these opposite outcomes are both mediated by p53 stabilization, additional mechanisms to determine this decision must exist. Here
Igor Shats et al.
Cancer research, 73(19), 6056-6067 (2013-08-24)
The transcription factor E2F1 is a key regulator of proliferation and apoptosis but the molecular mechanisms that mediate these cell fate decisions remain unclear. Here, we identify FOXO transcription factors as E2F1 target genes that act in a feed-forward regulatory
FOXO3a mediates the cytotoxic effects of cisplatin in colon cancer cells.
Fernandez de Mattos, S; Villalonga, P; Clardy, J; Lam, EW
Molecular Cancer Therapeutics null
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