Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma - Wikidata - awgldk - TriplyDB

Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma

Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma

http://www.wikidata.org/entity/Q40514814

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Anaplastic lymphoma kinase: signalling in development and disease Research progresses in the pathogenesis of anaplastic large cell lymphoma.Ablation of Akt2 induces autophagy through cell cycle arrest, the downregulation of p70S6K, and the deregulation of mitochondria in MDA-MB231 cells.Expression of serine 194-phosphorylated Fas-associated death domain protein correlates with proliferation in B-cell non-Hodgkin lymphomas.The ALK inhibitor ASP3026 eradicates NPM-ALK⁺ T-cell anaplastic large-cell lymphoma in vitro and in a systemic xenograft lymphoma model.Activity of the heat shock protein 90 inhibitor ganetespib in melanoma Functional validation of the anaplastic lymphoma kinase signature identifies CEBPB and BCL2A1 as critical target genes.Tumorigenic polyploid cells contain elevated ROS and ARE selectively targeted by antioxidant treatment.Identification of NVP-TAE684, a potent, selective, and efficacious inhibitor of NPM-ALK.Constitutive activation of Akt contributes to the pathogenesis and survival of mantle cell lymphoma.Autocrine release of interleukin-9 promotes Jak3-dependent survival of ALK+ anaplastic large-cell lymphoma cells.Pathobiology of ALK+ anaplastic large-cell lymphoma.ALK+ anaplastic large cell lymphoma exhibits phosphatidylinositol-3 kinase/Akt activity with retained but inactivated PTEN--a report from the Children's Oncology Group.What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?Anaplastic lymphoma kinase and its signalling molecules as novel targets in lymphoma therapy.SUMOylation Confers Posttranslational Stability on NPM-ALK Oncogenic Protein.Increasing cisplatin sensitivity by schedule-dependent inhibition of AKT and Chk1.Constitutive control of AKT1 gene expression by JUNB/CJUN in ALK+ anaplastic large-cell lymphoma: a novel crosstalk mechanism.Molecular and functional characterizations of the association and interactions between nucleophosmin-anaplastic lymphoma kinase and type I insulin-like growth factor receptor.Thioredoxin reductase 1 suppresses adipocyte differentiation and insulin responsiveness Mammalian target of rapamycin (mTOR) pathway signalling in lymphomas.IGF-IR tyrosine kinase interacts with NPM-ALK oncogene to induce survival of T-cell ALK+ anaplastic large-cell lymphoma cells.Crosstalk between the IGF-1R/AKT/mTORC1 pathway and the tumor suppressors p53 and p27 determines cisplatin sensitivity and limits the effectiveness of an IGF-1R pathway inhibitor.ALK-positive cancer: still a growing entity.TrkA is a binding partner of NPM-ALK that promotes the survival of ALK+ T-cell lymphoma.RPPA-based protein profiling reveals eIF4G overexpression and 4E-BP1 serine 65 phosphorylation as molecular events that correspond with a pro-survival phenotype in chronic lymphocytic leukemia.Amplification at 7q22 targets cyclin-dependent kinase 6 in T-cell lymphoma.Activation of mammalian target of rapamycin signaling promotes cell cycle progression and protects cells from apoptosis in mantle cell lymphoma.Activation of mammalian target of rapamycin signaling pathway contributes to tumor cell survival in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.Expression of Akt (protein kinase B) and its isoforms in malignant lymphomas.The miR-106a~363Xpcl1 miRNA cluster induces murine T cell lymphoma despite transcriptional activation of the p27Kip1 cell cycle inhibitor.The IGF-1R/AKT pathway determines cell fate in response to p53.Ablation of oncogenic ALK is a viable therapeutic approach for anaplastic large-cell lymphomas.NPM-ALK: The Prototypic Member of a Family of Oncogenic Fusion Tyrosine Kinases.Stabilization and activation of p53 downregulates mTOR signaling through AMPK in mantle cell lymphoma.Insights into the Pathogenesis of Anaplastic Large-Cell Lymphoma through Genome-wide DNA Methylation Profiling.Leukotriene B4 receptor inhibitor LY293111 induces cell cycle arrest and apoptosis in human anaplastic large-cell lymphoma cells via JNK phosphorylation.Ectopic expression of transcription factor BATF3 induces B-cell lymphomas in a murine B-cell transplantation model.PI3K/AKT pathway-mediated regulation of p27(Kip1) is associated with cell cycle arrest and apoptosis in cervical cancer.

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Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma

http://www.wikidata.org/entity/Q40514814

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2004 nî lūn-bûn

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2004年论文

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Inhibition of Akt increases p2 ...... anaplastic large cell lymphoma

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Inhibition of Akt increases p2 ...... anaplastic large cell lymphoma

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P2093

Coralyn Atwell

http://www.w3.org/2001/XMLSchema#string

Francois-Xavier Claret

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George Z Rassidakis

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Hesham M Amin

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Ioannis Grammatikakis

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L Jeffrey Medeiros

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Marianna Feretzaki

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Quan Lin

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Raymond Lai

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P2860

Cloning of p27Kip1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals

Akt-dependent phosphorylation of p27Kip1 promotes binding to 14-3-3 and cytoplasmic localization

Cytoplasmic relocalization and inhibition of the cyclin-dependent kinase inhibitor p27(Kip1) by PKB/Akt-mediated phosphorylation in breast cancer

Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma

p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21

The phosphatidylinositol 3-Kinase AKT pathway in human cancer

Role of the ubiquitin-proteasome pathway in regulating abundance of the cyclin-dependent kinase inhibitor p27

PKB/Akt mediates cell-cycle progression by phosphorylation of p27(Kip1) at threonine 157 and modulation of its cellular localization.

Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy.

Translocations involving anaplastic lymphoma kinase (ALK).

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8339386

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15374880

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1382060

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