Human AKT1 blocking peptide (CDBP0364)

Synthetic Human AKT1 blocking peptide for BL

Product Overview
AKT ( C - term ) peptide ( human )
Species Reactivity
1 mg/ml
50 μg
PBS with 0.02% sodium azide
0.02% Sodium Azide
Upon Receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
The serine-threonine protein kinase encoded by the AKT1 gene is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Mutations in this gene have been associated with the Proteus syndrome. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jul 2011]
14-3-3 protein binding; ATP binding; ATP binding; enzyme binding; identical protein binding; kinase activity; nitric-oxide synthase regulator activity; phosphatidylinositol-3,4,5-trisphosphate binding; phosphatidylinositol-3,4-bisphosphate binding; protei
AKT1; v-akt murine thymoma viral oncogene homolog 1; AKT; PKB; RAC; CWS6; PRKBA; PKB-ALPHA; RAC-ALPHA; RAC-alpha serine/threonine-protein kinase; PKB alpha; RAC-PK-alpha; proto-oncogene c-Akt; protein kinase B alpha; rac protein kinase alpha;


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Identification of the BRAF V600E mutation in a patient with sclerosing pneumocytoma: A case report


Authors: Jiang, Guanming; Zhang, Min; Tan, Qinquan; Lin, Shunhuan; Zeng, Yihong; Liu, Chun; Chen, Rongrong; Zhou, Jianping

Objectives: Sclerosing pneumocytoma (sclerosing hemangioma, SP) is a rare benign tumor of the lung with a low risk of recurrence. The genomic profile of SP is not well-known. Here we report gene mutation findings in a 17year-old girl with SP. Materials and methods: Immunohistochemistry (IHC), next-generation sequencing (NGS), and sanger sequencing were performed on the tumor tissue of this patient for pathological diagnosis and gene mutation analysis. Results and conclusion: Two mutations were identified in the tumor tissue by NGS and sanger sequencing: AKT1 E17K and BRAF (B-Raf proto-oncogene, serine/threonine kinase) V600E. This is the first case report of a BRAF V600E mutation in a patient with SP. This discovery extends our understanding of the pathogenesis of SP, and suggests the need for future testing of BRAF V600E in this rare tumor type.

KLF4 Acts as a wt-CFTR Suppressor through an AKT-Mediated Pathway


Authors: Sousa, Luis; Pankonien, Ines; Clarke, Luka A.; Silva, Iris; Kunzelmann, Karl; Amaral, Margarida D.

Cystic Fibrosis (CF) is caused by >2000 mutations in the CF transmembrane conductance regulator (CFTR) gene, but one mutation-F508del-occurs in similar to 80% of patients worldwide. Besides its main function as an anion channel, the CFTR protein has been implicated in epithelial differentiation, tissue regeneration, and, when dysfunctional, cancer. However, the mechanisms that regulate such relationships are not fully elucidated. Kruppel-like factors (KLFs) are a family of transcription factors (TFs) playing central roles in development, stem cell differentiation, and proliferation. Herein, we hypothesized that these TFs might have an impact on CFTR expression and function, being its missing link to differentiation. Our results indicate that KLF4 (but not KLF2 nor KLF5) is upregulated in CF vs. non-CF cells and that it negatively regulates wt-CFTR expression and function. Of note, F508del-CFTR expressing cells are insensitive to KLF4 modulation. Next, we investigated which KLF4-related pathways have an effect on CFTR. Our data also show that KLF4 modulates wt-CFTR (but not F508del-CFTR) via both the serine/threonine kinase AKT1 (AKT) and glycogen synthase kinase 3 beta (GSK3 beta) signaling. While AKT acts positively, GSK3 beta is a negative regulator of CFTR. This crosstalk between wt-CFTR and KLF4 via AKT/ GSK3 beta signaling, which is disrupted in CF, constitutes a novel mechanism linking CFTR to the epithelial differentiation.

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