Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
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JAK/STAT pathway dysregulation in tumors: a Drosophila perspectiveNotch and Mef2 synergize to promote proliferation and metastasis through JNK signal activation in DrosophilaAmyloid Precursor Proteins Are Dynamically Trafficked and Processed during Neuronal Development.Quantitative proteomic analysis of Parkin substrates in Drosophila neurons.How to take autophagy and endocytosis up a notch.miR-125b can enhance skin tumor initiation and promote malignant progression by repressing differentiation and prolonging cell survivalDe-regulation of JNK and JAK/STAT signaling in ESCRT-II mutant tissues cooperatively contributes to neoplastic tumorigenesis.Drosophila Vps4 promotes Epidermal growth factor receptor signaling independently of its role in receptor degradation.Vps4A functions as a tumor suppressor by regulating the secretion and uptake of exosomal microRNAs in human hepatoma cellsAt the crossroads of polarity, proliferation and apoptosis: the use of Drosophila to unravel the multifaceted role of endocytosis in tumor suppression.Rabaptin-5 and Rabex-5 are neoplastic tumour suppressor genes that interact to modulate Rab5 dynamics in Drosophila melanogaster.Coordination of membrane events during autophagy by multiple class III PI3-kinase complexes.Developmental and cellular functions of the ESCRT machinery in pluricellular organisms.ESCRT proteins and cell signalling.Shaping development with ESCRTs.Functional ESCRT machinery is required for constitutive recycling of claudin-1 and maintenance of polarity in vertebrate epithelial cellsReciprocal signals between microglia and neurons regulate α-synuclein secretion by exophagy through a neuronal cJUN-N-terminal kinase-signaling axisElevated expression of the V-ATPase C subunit triggers JNK-dependent cell invasion and overgrowth in a Drosophila epithelium.Cellular VPS4 is required for efficient entry and egress of budded virions of Autographa californica multiple nucleopolyhedrovirus.Drosophila endocytic neoplastic tumor suppressor genes regulate Sav/Wts/Hpo signaling and the c-Jun N-terminal kinase pathway.All roads lead to the vacuole-autophagic transport as part of the endomembrane trafficking network in plants.An intracellular activation of Smoothened that is independent of Hedgehog stimulation in Drosophila.Modelling Cooperative Tumorigenesis in Drosophila.Molecular Genetics of Frontotemporal Dementia Elucidated by Drosophila Models-Defects in Endosomal⁻Lysosomal Pathway.
P2860
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P2860
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
description
2009 nî lūn-bûn
@nan
2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
@ast
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
@en
type
label
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
@ast
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
@en
prefLabel
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
@ast
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
@en
P2093
P2860
P50
P1433
P1476
Disruption of Vps4 and JNK function in Drosophila causes tumour growth.
@en
P2093
Catherine Sem-Jacobsen
Franz Wendler
Jean-Paul Vincent
Karine Lindmo
Lina M Rodahl
P2860
P356
10.1371/JOURNAL.PONE.0004354
P407
P577
2009-02-04T00:00:00Z