Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2. - sprookjes - yvandenbroek - TriplyDB

Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

http://www.wikidata.org/entity/Q30418605

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mTORC1 inhibition delays growth of neurofibromatosis type 2 schwannoma.Emerging Putative Associations between Non-Coding RNAs and Protein-Coding Genes in Neuropathic Pain: Added Value from Reusing Microarray Data A novel small molecule HSP90 inhibitor, NXD30001, differentially induces heat shock proteins in nervous tissue in culture and in vivo Temporal Phosphoproteome Dynamics Induced by an ATP Synthase Inhibitor Citreoviridin.Single nucleotide polymorphisms of HSP90AA1 gene influence response of SLE patients to glucocorticoids treatment.HSP90AB1: Helping the good and the bad.The efficacy of lapatinib and nilotinib in combination with radiation therapy in a model of NF2 associated peripheral schwannoma.CNS Tumors in Neurofibromatosis.[Pathogenesis and molecular pathology of vestibular schwannoma].Update from the 2013 International Neurofibromatosis Conference.Combined Inhibition of NEDD8-Activating Enzyme and mTOR Suppresses NF2 Loss-Driven Tumorigenesis.Traditional and systems biology based drug discovery for the rare tumor syndrome neurofibromatosis type 2.

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Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

http://www.wikidata.org/entity/Q30418605

description

2013 nî lūn-bûn

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2013 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2013 թվականի մայիսին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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name

Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

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Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

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type

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Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

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Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

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Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

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Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

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1078-0432.CCR-12-3167

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Clinical Cancer Research

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Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2

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Allan E Rubenstein

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Ascia Eskin

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Cory H White

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Fabrice Chareyre

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Jan Manent

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Karo Tanaka

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Marco Giovannini

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Michiko Niwa-Kawakita

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Ruihong Chen

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Stanley F Nelson

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P2860

Merlin/NF2 suppresses tumorigenesis by inhibiting the E3 ubiquitin ligase CRL4(DCAF1) in the nucleus

Suppression of the mTOR-raptor signaling pathway by the inhibitor of heat shock protein 90 geldanamycin

Alteration in a new gene encoding a putative membrane-organizing protein causes neuro-fibromatosis type 2

Merlin, a "magic" linker between extracellular cues and intracellular signaling pathways that regulate cell motility, proliferation, and survival

The NF2 tumor suppressor gene product, merlin, mediates contact inhibition of growth through interactions with CD44

High-content, high-throughput analysis of cell cycle perturbations induced by the HSP90 inhibitor XL888

Conditional biallelic Nf2 mutation in the mouse promotes manifestations of human neurofibromatosis type 2.

Mice heterozygous for a mutation at the Nf2 tumor suppressor locus develop a range of highly metastatic tumors

HSP90 and the chaperoning of cancer

ERM proteins and merlin: integrators at the cell cortex

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3856-3870

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10.1158/1078-0432.CCR-12-3167

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14

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Walter J Jessen

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2013-05-28T00:00:00Z

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23714726

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