Csk-deficient boundary cells are eliminated from normal Drosophila epithelia by exclusion, migration, and apoptosis.
about
Non-autonomous overgrowth by oncogenic niche cells: Cellular cooperation and competition in tumorigenesisTraversing the basement membrane in vivo: a diversity of strategiesEpithelial homeostasisThe interplay between obesity and cancer: a fly viewElimination of unfit cells maintains tissue health and prolongs lifespanPolychaetoid controls patterning by modulating adhesion in the Drosophila pupal retinaInteraction with surrounding normal epithelial cells influences signalling pathways and behaviour of Src-transformed cells.Cellular behavior in the developing Drosophila pupal retinaParvin overexpression uncovers tissue-specific genetic pathways and disrupts F-actin to induce apoptosis in the developing epithelia in DrosophilaThe Drosophila GIPC homologue can modulate myosin based processes and planar cell polarity but is not essential for development.Drosophila as a model for context-dependent tumorigenesis.Rho1 regulates apoptosis via activation of the JNK signaling pathway at the plasma membrane.A role for the epithelial microenvironment at tumor boundaries: evidence from Drosophila and human squamous cell carcinomas.GLYAT regulates JNK-mediated cell death in DrosophilaDrosophila Abelson kinase mediates cell invasion and proliferation through two distinct MAPK pathways.The HIV-1 Vpu protein induces apoptosis in Drosophila via activation of JNK signalingAbnormalities in cell proliferation and apico-basal cell polarity are separable in Drosophila lgl mutant clones in the developing eye.c-Src drives intestinal regeneration and transformation.Oncogenic Ras/Src cooperativity in pancreatic neoplasia.The orthologous Tbx transcription factors Omb and TBX2 induce epithelial cell migration and extrusion in vivo without involvement of matrix metalloproteinasesSds22/PP1 links epithelial integrity and tumor suppression via regulation of myosin II and JNK signalingIncreased H⁺ efflux is sufficient to induce dysplasia and necessary for viability with oncogene expression.Modeling tumor invasion and metastasis in DrosophilaERK1/2 and p38α/β signaling in tumor cell quiescence: opportunities to control dormant residual disease.Chimaerin and Rac regulate cell number, adherens junctions, and ERK MAP kinase signaling in the Drosophila eye.The Notch-mediated hyperplasia circuitry in Drosophila reveals a Src-JNK signaling axis.C-terminal Src Kinase Gates Homeostatic Synaptic Plasticity and Regulates Fasciclin II Expression at the Drosophila Neuromuscular Junction.Cooperation of the BTB-Zinc finger protein, Abrupt, with cytoskeletal regulators in Drosophila epithelial tumorigenesis.A novel link between FMR gene and the JNK pathway provides clues to possible role in malignant pleural mesothelioma.Catenins: keeping cells from getting their signals crossed.Caspase signalling in the absence of apoptosis drives Jnk-dependent invasion.Mechanisms of cell competition: themes and variations.In Drosophila, RhoGEF2 cooperates with activated Ras in tumorigenesis through a pathway involving Rho1-Rok-Myosin-II and JNK signallingRegulation of tumor cell dormancy by tissue microenvironments and autophagy.Pattern formation in the Drosophila eyeRemodeling the model organism: matrix metalloproteinase functions in invertebratesChemical genetic discovery of targets and anti-targets for cancer polypharmacology.Transcriptional profiling of Drosophila S2 cells in early response to Drosophila C virusTransformed Drosophila cells evade diet-mediated insulin resistance through wingless signalingSilencing by small RNAs is linked to endosomal trafficking.
P2860
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P2860
Csk-deficient boundary cells are eliminated from normal Drosophila epithelia by exclusion, migration, and apoptosis.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年学术文章
@wuu
2006年学术文章
@zh
2006年学术文章
@zh-cn
2006年学术文章
@zh-hans
2006年学术文章
@zh-my
2006年学术文章
@zh-sg
2006年學術文章
@yue
2006年學術文章
@zh-hant
name
Csk-deficient boundary cells a ...... ion, migration, and apoptosis.
@en
Csk-deficient boundary cells a ...... ion, migration, and apoptosis.
@nl
type
label
Csk-deficient boundary cells a ...... ion, migration, and apoptosis.
@en
Csk-deficient boundary cells a ...... ion, migration, and apoptosis.
@nl
prefLabel
Csk-deficient boundary cells a ...... ion, migration, and apoptosis.
@en
Csk-deficient boundary cells a ...... ion, migration, and apoptosis.
@nl
P1433
P1476
Csk-deficient boundary cells a ...... ion, migration, and apoptosis.
@en
P2093
David E Larson
Ross L Cagan
P356
10.1016/J.DEVCEL.2005.11.007
P407
P50
P577
2006-01-01T00:00:00Z