HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells - Test2 - elhamkhani - TriplyDB

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

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Contribution of chaperones to STAT pathway signaling.Multifaceted intervention by the Hsp90 inhibitor ganetespib (STA-9090) in cancer cells with activated JAK/STAT signaling Elucidating the CXCL12/CXCR4 signaling network in chronic lymphocytic leukemia through phosphoproteomics analysis Apoptosis in response to heat stress is positively associated with heat-shock protein 90 expression in chicken myocardial cells in vitro Advances in the pathophysiology and treatment of relapsed/refractory Hodgkin's lymphoma with an emphasis on targeted therapies and transplantation strategies Heat shock protein 90 inhibitors repress latent membrane protein 1 (LMP1) expression and proliferation of Epstein-Barr virus-positive natural killer cell lymphoma.Macrocyclic inhibitors of hsp90 Heat-shock protein 90 alpha (HSP90α) modulates signaling pathways towards tolerance of oxidative stress and enhanced survival of hepatocytes of Mugil cephalus.The heat shock protein 90 inhibitor BIIB021 suppresses the growth of T and natural killer cell lymphomas.Tumor-specific HSP90 inhibition as a therapeutic approach in JAK-mutant acute lymphoblastic leukemias.Targetable molecular pathways in classical Hodgkin's lymphoma.Cellular and molecular mechanisms in cancer immune escape: a comprehensive review.Update on salvage options in relapsed/refractory hodgkin lymphoma after autotransplant.Myocyte-Derived Hsp90 Modulates Collagen Upregulation via Biphasic Activation of STAT-3 in Fibroblasts during Cardiac Hypertrophy.Constitutive activation of STAT3 in Sézary syndrome is independent of SHP-1.Combination of JAK2 and HSP90 inhibitors: an effective therapeutic option in drug-resistant chronic myelogenous leukemia.JAK Inhibitors and other Novel Agents in Myeloproliferative Neoplasms: Are We Hitting the Target?Drug sensitivity profiling identifies potential therapies for lymphoproliferative disorders with overactive JAK/STAT3 signaling.Multiplexed Proteome Dynamics Profiling Reveals Mechanisms Controlling Protein Homeostasis.Analysis of dynamic tyrosine phosphoproteome in LFA-1 triggered migrating T-cells.

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P2860

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

http://www.wikidata.org/entity/Q42562350

description

2009 nî lūn-bûn

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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2009年论文

@zh

2009年论文

@zh-cn

name

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

@en

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

@nl

type

label

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

@en

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

@nl

prefLabel

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

@en

HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

@nl

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Cell Communication and Signaling

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HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

@en

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Dieter Kube

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

Frederike von Bonin

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

Lorenz Trümper

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

Nils Schoof

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

P2860

The heat shock protein 90-CDC37 chaperone complex is required for signaling by types I and II interferons

The activity of hsp90 alpha promoter is regulated by NF-kappa B transcription factors

Aberrant expression of the Th2 cytokine IL-21 in Hodgkin lymphoma cells regulates STAT3 signaling and attracts Treg cells via regulation of MIP-3alpha

Nuclear factor kappaB-dependent gene expression profiling of Hodgkin's disease tumor cells, pathogenetic significance, and link to constitutive signal transducer and activator of transcription 5a activity

Specific function of STAT3, SOCS1, and SOCS3 in the regulation of proliferation and survival of classical Hodgkin lymphoma cells.

A potential role for HSP90 inhibitors in the treatment of JAK2 mutant-positive diseases as demonstrated using quantitative flow cytometry.

Pharmacologic activation of p53-dependent and p53-independent apoptotic pathways in Hodgkin/Reed-Sternberg cells.

JAK1 and Tyk2 activation by the homologous polycythemia vera JAK2 V617F mutation: cross-talk with IGF1 receptor.

Constitutive activation of STAT proteins in the HDLM-2 and L540 Hodgkin lymphoma-derived cell lines supports cell survival.

STAT3 is constitutively activated in Hodgkin cell lines.

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17

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scholarly article

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10.1186/1478-811X-7-17

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7

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2009-07-16T00:00:00Z

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1033316645

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19607667

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2714310

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