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96-Well Plate
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48-602MAG
Buffer Detection Kit for Magnetic Beads
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AB4130
Sigma-AldrichAnti-FOXO1 Antibody
Anti-FOXO1 Antibody is a Rabbit Polyclonal Antibody for detection of FOXO1 also known as Forkhead Box Protein O1, FKHR & has been validated in ICC.
More>>Anti-FOXO1 Antibody is a Rabbit Polyclonal Antibody for detection of FOXO1 also known as Forkhead Box Protein O1, FKHR & has been validated in ICC. Less<<
Anti-FOXO1 Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
This gene belongs to the forkhead family of transcription factors which are characterized by a distinct forkhead domain. The specific function of this gene has not yet been determined; however, it may play a role in myogenic growth and differentiation. Translocation of this gene with PAX3 has been associated with alveolar rhabdomyosarcoma.
FUNCTION: SwissProt: Q12778 # Transcription factor. SIZE: 655 amino acids; 69662 Da SUBUNIT: Interacts with LRPPRC (By similarity). SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note=Shuttles between cytoplasm and nucleus. TISSUE SPECIFICITY: Ubiquitous. PTM: Phosphorylated by AKT1; insulin-induced (By similarity). IGF1 rapidly induces phosphorylation of Thr-24, Ser-256 and Ser-319. Phosphorylation of Ser-256 decreases DNA-binding activity and promotes the phosphorylation of Thr-24, and Ser-319, which leads to nuclear exclusion and loss of function. Phosphorylation of Ser- 329 is independent of IGF1 and leads to reduced function. Phosphorylated upon DNA damage, probably by ATM or ATR. DISEASE: SwissProt: Q12778 # Chromosomal aberrations involving FOXO1 are a cause of rhabdomyosarcoma 2 (RMS2) [MIM:268220]; also known as alveolar rhabdomyosarcoma. Translocation (2;13)(q35;q14) with PAX3; translocation t(1;13)(p36;q14) with PAX7. The resulting protein is a transcriptional activator. SIMILARITY: SwissProt: Q12778 ## Contains 1 fork-head DNA-binding domain.
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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 Conditions
Maintain unopened vial at -20°C for up to 6 months. Avoid repeated freeze/thaw cycles.
The rehydrated antibody solutions can be stored undiluted at 2-8°C for 2 months without any significant loss of activity. Note, the solution is not sterile, thus care should be taken if product is stored at 2-8°C.
For storage at -20°C, the addition of an equal volume of glycerol can be used, however, it is recommended that ACS grade or higher glycerol be used, as significant loss of activity can occur if the glycerol used is not of high quality.
For freezing, it is recommended that the rehydrated antibody solution be further diluted 1:1 with a 2% BSA (fraction V, highest-grade available) solution made with the rehydration buffer. The resulting 1% BSA/antibody solution can be aliquoted and stored frozen at -70°C for up to 6 months. Avoid repeated freeze/thaw cycles.
PREPARATION AND USE:
To reconstitute the antibody, centrifuge the antibody vial at moderate speed (5,000 rpm) for 5 minutes to pellet the precipitated antibody product. Carefully remove the ammonium sulfate/PBS buffer solution and discard. It is not necessary to remove all of the ammonium sulfate/PBS solution: 10 μL of residual ammonium sulfate solution will not effect the resuspension of the antibody. Do not let the protein pellet dry, as severe loss of antibody reactivity can occur.
Resuspend the antibody pellet in any suitable biological buffer, standard PBS or TBS (pH 7.3-7.5) are typical. Volumes required are not critical but it is suggested that the final antibody concentration be between 0.1 mg/mL and 1.0 mg/mL. For example, to achieve a1 mg/mL concentration with 50 μg of precipitated antibody, the amount of buffer needed would be 50 μL.
Carefully add the liquid buffer to the pellet. DO NOT VORTEX. Mix by gentle stirring with a wide pipet tip or gentle finger-tapping. Let the precipitated antibody rehydrate for 1 hour at 4-25°C prior to use. Small particles of precipitated antibody that fail to resuspend are normal. Vials are overfilled to compensate for any losses.
Peroxisome proliferator-activated receptor γ (PPARγ) and its target genes are downstream effectors of FoxO1 protein in islet β-cells: mechanism of β-cell compensation and failure. Gupta, D; Leahy, AA; Monga, N; Peshavaria, M; Jetton, TL; Leahy, JL The Journal of biological chemistry
288
25440-9
2013
The molecular mechanisms and signaling pathways that drive islet β-cell compensation and failure are not fully resolved. We have used in vitro and in vivo systems to show that FoxO1, an integrator of metabolic stimuli, inhibits PPARγ expression in β-cells, thus transcription of its target genes (Pdx1, glucose-dependent insulinotropic polypeptide (GIP) receptor, and pyruvate carboxylase) that are important regulators of β-cell function, survival, and compensation. FoxO1 inhibition of target gene transcription is normally relieved when upstream activation induces its translocation from the nucleus to the cytoplasm. Attesting to the central importance of this pathway, islet expression of PPARγ and its target genes was enhanced in nondiabetic insulin-resistant rats and markedly reduced with diabetes induction. Insight into the impaired PPARγ signaling with hyperglycemia was obtained with confocal microscopy of pancreas sections that showed an intense nuclear FoxO1 immunostaining pattern in the β-cells of diabetic rats in contrast to the nuclear and cytoplasmic FoxO1 in nondiabetic rats. These findings suggest a FoxO1/PPARγ-mediated network acting as a core component of β-cell adaptation to metabolic stress, with failure of this response from impaired FoxO1 activation causing or exacerbating diabetes.
Transcriptional regulatory mechanisms of cardiac oxidative stress resistance are not well defined. FoxO transcription factors are critical mediators of oxidative stress resistance in multiple cell types, but cardioprotective functions have not been reported previously. FoxO function in oxidative stress resistance was investigated in cultured cardiomyocytes and in mice with cardiomyocyte-specific combined deficiency of FoxO1 and FoxO3 subjected to myocardial infarction (MI) or acute ischemia/reperfusion (I/R) injury. Induction of oxidative stress in cardiomyocytes promotes FoxO1 and FoxO3 nuclear localization and target gene activation. Infection of cardiomyocytes with a dominant-negative FoxO1(Δ256) adenovirus results in a significant increase in reactive oxygen species and cell death, whereas increased FoxO1 or FoxO3 expression reduces reactive oxygen species and cell death. Mice generated with combined conditional deletion of FoxO1 and FoxO3 specifically in cardiomyocytes were subjected to I/R or MI. Loss of FoxO1 and FoxO3 in cardiomyocytes results in a significant increase in infarct area with decreased expression of the antiapoptotic molecules, PTEN-induced kinase1 (PINK1) and CBP/P300-interacting transactivator (CITED2). Expressions of the antioxidants catalase and manganese superoxide dismutase-2 (SOD2) and the autophagy-related proteins LC3II and Gabarapl1 also are decreased following I/R compared with controls. Mice with cardiomyocyte-specific FoxO deficiency subjected to MI have reduced cardiac function, increased scar formation, induction of stress-responsive signaling, and increased apoptotic cell death relative to controls. These data support a critical role for FoxOs in promoting cardiomyocyte survival during conditions of oxidative stress through induction of antioxidants and cell survival pathways.
