Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis (Q44246409)

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scientific article published in December 2002

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English	Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis	scientific article published in December 2002

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scholarly article

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Europe PubMed Central

PubMed publication ID

1 December 2017

Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis (English)

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PubMed publication ID

1 December 2017

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Jeffrey L. Browning

2

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1 December 2017

author name string

Wilson CA

1

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Europe PubMed Central

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1 December 2017

publication date

1 December 2002

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1 December 2017

Cell Death & Differentiation

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1 December 2017

9

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Europe PubMed Central

PubMed publication ID

1 December 2017

12

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Europe PubMed Central

PubMed publication ID

1 December 2017

1321-1333

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Europe PubMed Central

PubMed publication ID

1 December 2017

More than one way to die: apoptosis, necrosis and reactive oxygen damage

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The biochemistry of apoptosis

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Tumor necrosis factor receptor and Fas signaling mechanisms.

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Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule

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Necrotic death pathway in Fas receptor signaling

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Resistance to the cytotoxic effects of tumor necrosis factor alpha can be overcome by inhibition of a FADD/caspase-dependent signaling pathway

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Induction of cell death by tumour necrosis factor (TNF) receptor 2, CD40 and CD30: a role for TNF-R1 activation by endogenous membrane-anchored TNF.

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TWEAK can induce cell death via endogenous TNF and TNF receptor 1.

1 reference

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Four deaths and a funeral: from caspases to alternative mechanisms.

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Caspase-independent programmed cell death with necrotic morphology

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Caspase-independent apoptotic pathways in T lymphocytes: a minireview

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Regulation of lymphocyte proliferation and death by FLIP.

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Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death

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Signaling through the lymphotoxin beta receptor induces the death of some adenocarcinoma tumor lines

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A cell-killing monoclonal antibody (anti-Fas) to a cell surface antigen co-downregulated with the receptor of tumor necrosis factor

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Interferon-gamma modulates a p53-independent apoptotic pathway and apoptosis-related gene expression

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TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis

1 reference

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The lymphotoxin-beta receptor is necessary and sufficient for LIGHT-mediated apoptosis of tumor cells

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Recombinant human tumor necrosis factor-alpha: effects on proliferation of normal and transformed cells in vitro.

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Lymphokines and monokines in anti-cancer therapy

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TAJ, a novel member of the tumor necrosis factor receptor family, activates the c-Jun N-terminal kinase pathway and mediates caspase-independent cell death

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Wengen, a member of the Drosophila tumor necrosis factor receptor superfamily, is required for Eiger signaling

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Absorptive and mucus-secreting subclones isolated from a multipotent intestinal cell line (HT-29) provide new models for cell polarity and terminal differentiation

1 reference

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Dual signaling of the Fas receptor: initiation of both apoptotic and necrotic cell death pathways

1 reference

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Caspase structure, proteolytic substrates, and function during apoptotic cell death

1 reference

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Cytokine-induced apoptosis in epithelial HT-29 cells is independent of nitric oxide formation. Evidence for an interleukin-13-driven phosphatidylinositol 3-kinase-dependent survival mechanism

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DNA fragmentation and cytotoxicity caused by tumor necrosis factor is enhanced by interferon-gamma

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Tumour necrosis factor-induced necrosis versus anti-Fas-induced apoptosis in L929 cells.

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Reduction in mitochondrial potential constitutes an early irreversible step of programmed lymphocyte death in vivo.

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Reactive Oxygen Species Regulate Activation-Induced T Cell Apoptosis

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The p75 neurotrophin receptor mediates neuronal apoptosis and is essential for naturally occurring sympathetic neuron death

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A novel function of CD40: induction of cell death in transformed cells

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T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors

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CD27, a member of the tumor necrosis factor receptor family, induces apoptosis and binds to Siva, a proapoptotic protein

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The cytoplasmic domain of the lymphotoxin-beta receptor mediates cell death in HeLa cells

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A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis

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Supraoptimal peptide-major histocompatibility complex causes a decrease in bc1-2 levels and allows tumor necrosis factor alpha receptor II-mediated apoptosis of cytotoxic T lymphocytes

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Caspase-independent cell killing by Fas-associated protein with death domain

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The caspase-8 inhibitor FLIP promotes activation of NF-kappaB and Erk signaling pathways

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Apoptosis inducing factor (AIF): a phylogenetically old, caspase-independent effector of cell death

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Condensed matter in cell death.

1 reference

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Interferon-gamma-induced differentiation and apoptosis of HT29 cells: dissociation of (glucosyl)ceramide signaling

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Signal transduction by the JNK group of MAP kinases

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Modulation of life and death by the TNF receptor superfamily

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Lymphotoxin-beta receptor signaling complex: role of tumor necrosis factor receptor-associated factor 3 recruitment in cell death and activation of nuclear factor kappaB

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Signal transduction by tumor necrosis factor and its relatives

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Selective depletion of heat shock protein 70 (Hsp70) activates a tumor-specific death program that is independent of caspases and bypasses Bcl-2.

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Heat-shock protein 70 antagonizes apoptosis-inducing factor

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Preparation and characterization of soluble recombinant heterotrimeric complexes of human lymphotoxins alpha and beta.

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Early redistribution of plasma membrane phosphatidylserine is a general feature of apoptosis regardless of the initiating stimulus: inhibition by overexpression of Bcl-2 and Abl

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Target cell lysis by CTL granule exocytosis is independent of ICE/Ced-3 family proteases

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Apoptotic death in epithelial cells: cleavage of DNA to 300 and/or 50 kb fragments prior to or in the absence of internucleosomal fragmentation.

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Aspartate-based inhibitor of interleukin-1 beta-converting enzyme prevents antitumor agent-induced apoptosis in human myeloid leukemia U937 cells

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Caspase independent/dependent regulation of K(+), cell shrinkage, and mitochondrial membrane potential during lymphocyte apoptosis

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7 January 2021

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Inhibition of caspase activity induces a switch from apoptosis to necrosis

1 reference

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TNF-alpha activates at least two apoptotic signaling cascades

1 reference

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7 January 2021

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Overexpression of bcl-2 enhances LIGHT- and interferon-gamma -mediated apoptosis in Hep3BT2 cells

1 reference

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10.1038/SJ.CDD.4401107

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Europe PubMed Central

PubMed publication ID

1 December 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

1 December 2017

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