Anti-PKB beta (aa 455-469) polyclonal antibody (CABT-BL6346)

Sheep Anti-Mouse PKB beta (aa 455-469) polyclonal antibody for WB, IP


Host Species
Antibody Isotype
Species Reactivity
PKB beta (residues 455-469) [RYDSLDPLELDQRTH]


Application Notes
WB: 1 µg/ml
IP: Use 10 µg/mg of cell extract
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
AKT2; v-akt murine thymoma viral oncogene homolog 2; RAC-beta serine/threonine-protein kinase; PKB beta; RAC-PK-beta; protein kinase Akt-2
Entrez Gene ID
UniProt ID


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Identification of single nucleotide polymorphisms of the PI3K-AKT-mTOR pathway as a risk factor of central nervous system metastasis in metastatic breast cancer


Authors: Le Rhun, Emilie; Bertrand, Nicolas; Dumont, Aurelie; Tresch, Emmanuelle; Le Deley, Marie-Cecile; Mailliez, Audrey; Preusser, Matthias; Weller, Michael; Revillion, Francoise; Bonneterre, Jacques

Introduction: The PI3K-AKT-mTOR pathway may be involved in the development of central nervous system (CNS) metastasis from breast cancer. Accordingly, herein we explored whether single nucleotide polymorphisms (SNPs) of this pathway are associated with altered risk of CNS metastasis formation in metastatic breast cancer patients. Methods: The GENEOM study (NCT00959556) included blood sample collection from breast cancer patients treated in the neoadjuvant, adjuvant or metastatic setting. We identified patients with CNS metastases for comparison with patients without CNS metastasis, defined as either absence of neurological symptoms or normal brain magnetic resonance imaging (MRI) before death or during 5-year follow-up. Eighty-eight SNPs of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian (or mechanistic) target of rapamycin (mTOR) pathway genes were selected for analysis: AKT1 (17 SNPs), AKT2 (4), FGFR1 (2), mTOR (7), PDK1 (4), PI3KR1 (11), PI3KCA (20), PTEN (17), RPS6KB1 (6). Results: Of 342 patients with metastases, 207 fulfilled the inclusion criteria: One-hundred-and-seven patients remained free of CNS metastases at last follow-up or date of death whereas 100 patients developed CNS metastases. Among clinical parameters, hormonal and human epidermal growth factor receptor-2 (HER2) status as well as vascular tumour emboli was associated with risk of CNS metastasis. Only PI3KR1-rs706716 was associated with CNS metastasis in univariate analysis after Bonferroni correction (p < 0.00085). Multivariate analysis showed associations between AKT1-rs3803304, AKT2-rs3730050, PDK1-rs11686903 and PI3KR1-rs706716 and CNS metastasis. Conclusion: PI3KR1-rs706716 may be associated with CNS metastasis in metastatic breast cancer patients and could be included in a predictive composite score to detect early CNS metastasis irrespective of breast cancer subtype. (C) 2017 Elsevier Ltd. All rights reserved.

Reduced insulin action in muscle of high fat diet rats over the diurnal cycle is not associated with defective insulin signaling


Authors: Small, Lewin; Brandon, Amanda E.; Parker, Benjamin L.; Deshpande, Vinita; Samsudeen, Azrah F.; Kowalski, Greg M.; Reznick, Jane; Wilks, Donna L.; Preston, Elaine; Bruce, Clinton R.; James, David E.; Turner, Nigel; Cooney, Gregory J.

Objective: Energy metabolism and insulin action follow a diurnal rhythm. It is therefore important that investigations into dysregulation of these pathways are relevant to the physiology of this diurnal rhythm. Methods: We examined glucose uptake, markers of insulin action, and the phosphorylation of insulin signaling intermediates in muscle of chow and high fat, high sucrose (HFHS) diet-fed rats over the normal diurnal cycle. Results: HFHS animals displayed hyperinsulinemia but had reduced systemic glucose disposal and lower muscle glucose uptake during the feeding period. Analysis of gene expression, enzyme activity, protein abundance and phosphorylation revealed a clear diurnal regulation of substrate oxidation pathways with no difference in Akt signaling in muscle. Transfection of a constitutively active Akt2 into the muscle of HFHS rats did not rescue diet-induced reductions in insulin-stimulated glucose uptake. Conclusions: These studies suggest that reduced glucose uptake in muscle during the diurnal cycle induced by short-term HFHS-feeding is not the result of reduced insulin signaling. (C) 2019 The Authors. Published by Elsevier GmbH.

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