Akt requires glucose metabolism to suppress puma expression and prevent apoptosis of leukemic T cells. - Test2 - elhamkhani - TriplyDB

Akt requires glucose metabolism to suppress puma expression and prevent apoptosis of leukemic T cells.

Akt requires glucose metabolism to suppress puma expression and prevent apoptosis of leukemic T cells.

http://www.wikidata.org/entity/Q34568683

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Metabolic regulation of regulatory T cell development and function Nitric Oxide Synthase 2 Improves Proliferation and Glycolysis of Peripheral γδ T Cells ROS signaling under metabolic stress: cross-talk between AMPK and AKT pathway.Concurrent inhibition of PI3K and mTORC1/mTORC2 overcomes resistance to rapamycin induced apoptosis by down-regulation of Mcl-1 in mantle cell lymphoma.AMPK-regulated and Akt-dependent enhancement of glucose uptake is essential in ischemic preconditioning-alleviated reperfusion injury Inhibition of an NAD⁺ salvage pathway provides efficient and selective toxicity to human pluripotent stem cells.Inhibition of AKT2 enhances sensitivity to gemcitabine via regulating PUMA and NF-κB signaling pathway in human pancreatic ductal adenocarcinoma.Transformation with oncogenic Ras and the simian virus 40 T antigens induces caspase-dependent sensitivity to fatty acid biosynthetic inhibition Metabolic pathways in T cell fate and function.Dysfunction of the TP53 tumor suppressor gene in lymphoid malignancies.Multiple myeloma exhibits novel dependence on GLUT4, GLUT8, and GLUT11: implications for glucose transporter-directed therapy.Intracellular expression of Tat alters mitochondrial functions in T cells: a potential mechanism to understand mitochondrial damage during HIV-1 replication Metabolic stress in autophagy and cell death pathways Acidosis promotes Bcl-2 family-mediated evasion of apoptosis: involvement of acid-sensing G protein-coupled receptor Gpr65 signaling to Mek/Erk.Discovery of a Novel Inhibitor of the Protein Tyrosine Phosphatase Shp2.Glucose starvation induces mutation and lineage-dependent adaptive responses in a large collection of cancer cell lines.Matched and mismatched metabolic fuels in lymphocyte function.Epidermal growth factor regulates hematopoietic regeneration after radiation injury Metabolic regulation of T lymphocytes.Maternal supplementation of diabetic mice with thymoquinone protects their offspring from abnormal obesity and diabetes by modulating their lipid profile and free radical production and restoring lymphocyte proliferation via PI3K/AKT signaling.The role of E3 ubiquitin ligase Cbl proteins in interleukin-2-induced Jurkat T-cell activation.Overexpressed CISD2 has prognostic value in human gastric cancer and promotes gastric cancer cell proliferation and tumorigenesis via AKT signaling pathway.Akt1 is the principal Akt isoform regulating apoptosis in limiting cytokine concentrations.Hypoxia and classical activation limits Mycobacterium tuberculosis survival by Akt-dependent glycolytic shift in macrophages.Activated lymphocytes as a metabolic model for carcinogenesis.miR-125b regulates differentiation and metabolic reprogramming of T cell acute lymphoblastic leukemia by directly targeting A20.The Role of p53 in Metabolic Regulation Regulatory T cells, mTOR kinase, and metabolic activity.The fourth dimension in immunological space: how the struggle for nutrients selects high-affinity lymphocytes.The Many Unknowns Concerning the Bioenergetics of Exhaustion and Senescence during Chronic Viral Infection.Targeting glutamine metabolism in multiple myeloma enhances BIM binding to BCL-2 eliciting synthetic lethality to venetoclax.The PI3K pathway in B cell metabolism Glucose transporter 1-mediated glucose uptake is limiting for B-cell acute lymphoblastic leukemia anabolic metabolism and resistance to apoptosis.Metabolic Regulation of Apoptosis in Cancer.Low-glucose conditions of tumor microenvironment enhance cytotoxicity of tetrathiomolybdate to neuroblastoma cells.Akt-dependent glucose metabolism promotes Mcl-1 synthesis to maintain cell survival and resistance to Bcl-2 inhibition.Coordinated repression of BIM and PUMA by Epstein-Barr virus latent genes maintains the survival of Burkitt lymphoma cells.Metabolism and autophagy in the immune system: immunometabolism comes of age.Comparison of spheroids formed by rat glioma stem cells and neural stem cells reveals differences in glucose metabolism and promising therapeutic applications.Pkb/Akt1 mediates Wnt/GSK3β/β-catenin signaling-induced apoptosis in human cord blood stem cells exposed to organophosphate pesticide monocrotophos.

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Akt requires glucose metabolism to suppress puma expression and prevent apoptosis of leukemic T cells.

http://www.wikidata.org/entity/Q34568683

description

2010 nî lūn-bûn

@nan

2010 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

@ast

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

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Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

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type

label

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

@ast

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

@en

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

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prefLabel

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

@ast

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

@en

Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

@nl

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JBC.M110.179101

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Journal of Biological Chemistry

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Akt requires glucose metabolis ...... apoptosis of leukemic T cells.

@en

P2093

Amanda N Nichols

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Brian J Altman

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Emily F Mason

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Gerard P Zambetti

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Jeffrey C Rathmell

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Jessica A Wofford

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Jonathan L Coloff

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Olga Ilkayeva

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Sarah R Jacobs

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Sean P Garrison

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P2860

PUMA induces the rapid apoptosis of colorectal cancer cells

PUMA, a novel proapoptotic gene, is induced by p53

Evidence that Ser87 of BimEL is phosphorylated by Akt and regulates BimEL apoptotic function

Growth factors can influence cell growth and survival through effects on glucose metabolism

Phosphorylation of Puma modulates its apoptotic function by regulating protein stability

Glucose metabolism attenuates p53 and Puma-dependent cell death upon growth factor deprivation

FOXO3a-dependent regulation of Puma in response to cytokine/growth factor withdrawal

Puma cooperates with Bim, the rate-limiting BH3-only protein in cell death during lymphocyte development, in apoptosis induction

On the Origin of Cancer Cells

The Noxa/Mcl-1 axis regulates susceptibility to apoptosis under glucose limitation in dividing T cells

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5921-5933

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scholarly article

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10.1074/JBC.M110.179101

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7

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286

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2010-12-15T00:00:00Z

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21159778

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