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Akt is the main kinase mediating the embryonic specification of artery cells

ABSTRACT: This study aimed at understanding the function of Akt signaling in vascular development in Zebrafish.

ORGANISM(S): Danio rerio

PROVIDER: GSE252648 | GEO | 2024/01/10

REPOSITORIES: GEO

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Akt is the main kinase mediating the embryonic specification of artery cells

Project description:Akt is the main kinase mediating the embryonic specification of artery cells

| PRJNA1061565 | ENA

Akt is a mediator of artery specification during zebrafish development.

Project description: Not available

| S-EPMC11441982 | biostudies-literature

Real-time quantitative PCR analysis of WT and NOD1 knockout zebrafish (PI3K-AKT)

Project description:Zebrafish larvae from WT and NOD1-1IS-/- collected at 10 dpf were used for Zebrafish PI3K-AKT Signaling Pathway RT2 Profiler PCR Array.

2017-06-23 | GSE80622 | GEO

Aberrant AKT Activation Drives Ganglioneuroma and Can Be Therapeutically Targeted by mTOR Inhibitors

Project description:Peripheral sympathetic nervous system tumors are the most common extra-cranial pediatric tumors in children and include neuroblastoma, ganglioneuroma and intermixed ganglioneuroblastoma. Ganglioneuroma can be induced by activating mutations of the RET proto-oncogene or activated Ras in murine models, but the etiology and molecular pathogenesis of this disease is unknown for the majority of human ganglioneuromas. Surgery is the only effective therapy for ganglioneuroma which can be challenging due to tumor location and compression of surrounding structures. Thus, there is great potential benefit to the definition of presurgical therapies that can reduce the size and extent of these tumors, and therefore limit morbidity. We found high levels of phosphorylated AKT in most of human ganglioneuromas, but only in a small portion of human poorly differentiated neuroblastomas (p<0.0001, Fisher’s exact test). As a result, we created zebrafish transgenic for constitutively activated myr-Akt2 in the sympathetic nervous system. These zebrafish were found to develop benign ganglioneuroma without progression to neuroblastoma. Zebrafish tumors displayed high expression of phosphorylated Akt and the downstream Akt targets, phosphorylated mTOR, S6 and EIF4EBP1. Histopathological and comparative genomic analyses revealed that zebrafish ganglioneuroma highly resembles human ganglioneuroma. Inhibition of the downstream AKT target, mTOR, using clinically available inhibitors effectively reduced tumor burden in zebrafish embryos transplanted with primary ganglioneuroma. Our results implicate activated and phosphorylated AKT as a tumorigenic driver in ganglioneuroma, and propose inhibition of the AKT-target kinase mTOR as an ideal candidate to treat patients with ganglioneuroma.

2020-07-22 | GSE135682 | GEO

Study of Akt Inhibitor MK2206 in Patients With Relapsed Lymphoma

Project description:This phase II clinical trial studies how well Akt inhibitor MK2206 works in treating patients with relapsed lymphoma. Akt inhibitor MK2206 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

| 2099453 | ecrin-mdr-crc

Artery/vein specification is governed by opposing phosphatidylinositol-3 kinase and MAP kinase/ERK signaling.

Project description: Not available

| S-EPMC1930149 | biostudies-literature

PRMT5-mediated arginine methylation activates AKT kinase to govern tumorigenesis

Project description:AKT is involved in a number of key cellular processes including cell proliferation, apoptosis and metabolism. Hyperactivation of AKT is associated with many pathological conditions, particularly cancers. Emerging evidence indicates that arginine methylation is involved in modulating AKT signaling pathway. However, whether and how arginine methylation directly regulates AKT kinase activity remain unknown. Here we report that protein arginine methyltransferase 5 (PRMT5), but not other PRMTs, promotes AKT activation by catalyzing symmetric dimethylation of AKT1 at arginine 391 (R391). Mechanistically, AKT1-R391 methylation cooperates with phosphatidylinositol 3,4,5 trisphosphate (PIP3) to relieve the pleckstrin homology (PH)-in conformation, leading to AKT1 membrane translocation and subsequent activation by phosphoinositide-dependent kinase-1 (PDK1) and the mechanistic target of rapamycin complex 2 (mTORC2). As a result, deficiency in AKT1-R391 methylation significantly suppresses AKT1 kinase activity and tumorigenesis. Lastly, we show that PRMT5 inhibitor synergizes with AKT inhibitor or chemotherapeutic drugs to enhance cell death. Altogether, our study suggests that R391 methylation is an important step for AKT activation and its oncogenic function.

2022-02-17 | PXD026071 | Pride

A chemical screen in zebrafish embryonic cells establishes that Akt activation is required for neural crest development [RNA-seq]

Project description:The neural crest is a dynamic progenitor cell population that arises at the border of neural and non-neural ectoderm. The inductive roles of FGF, Wnt, and BMP at the neural plate border are well established, but the signals required for subsequent neural crest development remain poorly characterized. Here, we conducted a screen in primary zebrafish embryo cultures for chemicals that decrease neural crest formation, as read out by crestin:EGFP expression. We found that the natural product caffeic acid phenethyl ester (CAPE) disrupts neural crest gene expression, migration, and melanocytic differentiation by reducing Sox10 activity. CAPE inhibits PI3K/Akt signaling specifically in FGF-stimulated cells, and neural crest defects in CAPE-treated embryos are suppressed by constitutively active Akt1. Inhibition of Akt activity by constitutively active PTEN similarly decreases crestin expression and Sox10 activity. Our study has identified Akt as a novel intracellular pathway required for neural crest development.

2017-08-17 | GSE95814 | GEO

A chemical screen in zebrafish embryonic cells establishes that Akt activation is required for neural crest development [ATAC-seq]

2017-08-17 | GSE95813 | GEO

Akt Inhibitor MK2206 in Treating Patients With Advanced Gastric or Gastroesophageal Junction Cancer

Project description:This phase II clinical trial studies how well Akt inhibitor MK2206 works in treating patients with advanced gastric or gastroesophageal junction cancer. Akt inhibitor MK2206 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

| 2099584 | ecrin-mdr-crc

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