Single-cell quantification of Bax activation and mathematical modelling suggest pore formation on minimal mitochondrial Bax accumulation.
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Small molecules, big effects: the role of microRNAs in regulation of cardiomyocyte deathBuilding blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosisCharge profile analysis reveals that activation of pro-apoptotic regulators Bax and Bak relies on charge transfer mediated allosteric regulationSystems analysis of apoptosis protein expression allows the case-specific prediction of cell death responsiveness of melanoma cells.From computational modelling of the intrinsic apoptosis pathway to a systems-based analysis of chemotherapy resistance: achievements, perspectives and challenges in systems medicine.Modeling the TNFα-induced apoptosis pathway in hepatocytes.Programming biological models in Python using PySBIntra- and interdimeric caspase-8 self-cleavage controls strength and timing of CD95-induced apoptosis.Partial acceptor photobleaching-based quantitative FRET method completely overcoming emission spectral crosstalks.Ma-PbFRET: multiple acceptors FRET measurement based on partial acceptor photobleaching.Role of mitochondrial Bax, caspases, and MAPKs for ceramide-induced apoptosis in renal proximal tubular cells.Artemisinin induces A549 cell apoptosis dominantly via a reactive oxygen species-mediated amplification activation loop among caspase-9, -8 and -3.Measuring and modeling apoptosis in single cells.Glucose metabolism determines resistance of cancer cells to bioenergetic crisis after cytochrome-c release.Multi-parametric analysis of cell death pathways using live-cell microscopy.Quantitative FRET measurement using emission-spectral unmixing with independent excitation crosstalk correction.Proteasome inhibition can impair caspase-8 activation upon submaximal stimulation of apoptotic tumor necrosis factor-related apoptosis inducing ligand (TRAIL) signaling.Wide-field microscopic FRET imaging using simultaneous spectral unmixing of excitation and emission spectra.A simplified Bcl-2 network model reveals quantitative determinants of cell-to-cell variation in sensitivity to anti-mitotic chemotherapeutics.Overexpression of DCF1 inhibits glioma through destruction of mitochondria and activation of apoptosis pathway.Death ligand concentration and the membrane proximal signaling module regulate the type 1/type 2 choice in apoptotic death signaling.Monte carlo study elucidates the type 1/type 2 choice in apoptotic death signaling in healthy and cancer cells.Regulation of ceramide channels by Bcl-2 family proteins.The secrets of the Bcl-2 family.Bax assembly into rings and arcs in apoptotic mitochondria is linked to membrane pores.The indirect activation model of mitochondrial outer membrane permeabilisation (MOMP) initiation requires a trade-off between robustness in the absence of and sensitivity in the presence of stress.Pan-BH3 mimetic S1 exhibits broad-spectrum antitumour effects by cooperation between Bax and Bak.An Autoinhibited Dimeric Form of BAX Regulates the BAX Activation Pathway.Bcl-2 inhibits apoptosis by increasing the time-to-death and intrinsic cell-to-cell variations in the mitochondrial pathway of cell death.A novel BH3 mimetic S1 potently induces Bax/Bak-dependent apoptosis by targeting both Bcl-2 and Mcl-1.Bax exists in a dynamic equilibrium between the cytosol and mitochondria to control apoptotic primingHow can we kill cancer cells: Insights from the computational models of apoptosis.BAX insertion, oligomerization, and outer membrane permeabilization in brain mitochondria: role of permeability transition and SH-redox regulation.Boolean network-based model of the Bcl-2 family mediated MOMP regulation.Bax, Bak and beyond - mitochondrial performance in apoptosis.Multichannel wide-field microscopic FRET imaging based on simultaneous spectral unmixing of excitation and emission spectra.Nerve growth factor protects retinal ganglion cells against injury induced by retinal ischemia-reperfusion in rats.Bax retrotranslocation potentiates Bcl-xL's antiapoptotic activity and is essential for switch-like transitions between MOMP competency and resistance.High PGAM5 expression induces chemoresistance by enhancing Bcl-xL-mediated anti-apoptotic signaling and predicts poor prognosis in hepatocellular carcinoma patientsThe Problem of Antigen Affinity Discrimination in B-Cell Immunology
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P2860
Single-cell quantification of Bax activation and mathematical modelling suggest pore formation on minimal mitochondrial Bax accumulation.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
@zh
2009年學術文章
@zh-hant
name
Single-cell quantification of ...... itochondrial Bax accumulation.
@en
Single-cell quantification of ...... itochondrial Bax accumulation.
@nl
type
label
Single-cell quantification of ...... itochondrial Bax accumulation.
@en
Single-cell quantification of ...... itochondrial Bax accumulation.
@nl
prefLabel
Single-cell quantification of ...... itochondrial Bax accumulation.
@en
Single-cell quantification of ...... itochondrial Bax accumulation.
@nl
P2093
P2860
P50
P356
P1476
Single-cell quantification of ...... mitochondrial Bax accumulation
@en
P2093
C G Concannon
S Anguissola
P2860
P2888
P304
P356
10.1038/CDD.2009.123
P577
2009-09-11T00:00:00Z