Results 241 to 250 of about 2,980,721 (284)

Fusion protein-mediated costimulation in engineered T cells: from intrinsic signaling to tumor microenvironment rewiring. [PDF]

Front Immunol
Toumi R, Guenette SJ, Oda SK.
europepmc   +1 more source

The signaling and regulatory functions of dying cells and cell corpses. [PDF]

Commun Biol
Zhang G, Liu J, Li W, Wang B, Feng H, Cui T, Pan T, Chen D, Xiong Y.   +8 more
europepmc   +1 more source

Apoptosis induced by death receptors

Pharmaceutica Acta Helvetiae, 2000
Death receptors belong to the TNF receptor family and are characterised by an intracellular death domain that serves to recruit adapter proteins such as TRADD and FADD and cysteine proteases such as Caspase-8. Activation of Caspase-8 on the aggregated receptor leads to apoptosis. Triggering of death receptors is mediated through the binding of specific
Pascal Schneider, J Tschopp
exaly   +5 more sources

Death Receptors: Signaling and Modulation

Science, 1998
REVIEW Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival. Certain cells have unique sensors, termed death receptors, on their surface.
Vishva Dixit, Avi Ashkenazi
exaly   +4 more sources

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Homomeric and heteromeric interactions of the extracellular domains of death receptors and death decoy receptors

Biochemical and Biophysical Research Communications, 2005
Death receptors (DRs) can induce apoptosis by oligomerization with TRAIL, whereas death decoy receptors (DcRs) cannot, due to their lack of functional intracellular death domains. However, it is not known whether DRs and DcRs can interact with one another to form oligomeric complexes prior to TRAIL binding.
Myung-Hee Kwon, Yong-Sung Kim
exaly   +3 more sources

The Death Receptors

1999
In recent years apoptosis, also called programmed cell death, has been recognized to be the physiological way for a nucleated animal cell to die. Apoptosis takes care of unwanted, injured or virus-infected cells (Farber 1994; Collins 1995). Autoreactive T and B cells that are produced by the immune system by the millions every day are also eliminated ...
Peter, M. E., Scaffidi, C., Medema, J. P., Kischkel, F., Krammer, P. H.   +4 more
openaire   +4 more sources

Death Receptors and Apoptosis

Dermatologic Clinics, 2007
Interactions between death receptors from the tumor necrosis factor superfamily and their ligands play a crucial role in the development and the integrity of the epidermis. The major consequence resulting from death receptor targeting is apoptosis.
Contassot E, Gaide O, French LE
openaire   +3 more sources

Death receptors

Essays in Biochemistry, 2003
Death receptors [Fas/Apo-1/CD95, TNF-R1 [tumour necrosis factor (TNF) receptor 1], DR3 [death receptor 3], TRAIL-R1 [TNF-related apoptosis-inducing ligand receptor 1], TRAIL-R2, DR6, p75-NGFR [p75-nerve growth factor receptor], EDAR [ectodermal dysplasia receptor]] form a subgroup of the TNF-R superfamily that can induce apoptosis (programmed cell ...
openaire   +2 more sources

Death Receptor Ligands in Tumors

Journal of Immunotherapy, 2002
Activation of apoptosis via death receptors is a tightly regulated event, and the death pathway itself is open to interference on the part of soluble or membrane-bound decoy receptors. The aggregation state of the death-inducing ligand is a crucial factor, particularly when these molecules are used as recombinant drugs against tumors.
Paola, Cappello, Francesco, Novelli, Guido, Forni, Mirella, Giovarelli   +3 more
openaire   +2 more sources

Targeting TRAIL death receptors

Current Opinion in Pharmacology, 2008
The natural occurring tumor necrosis factor related apoptosis-inducing ligand (TRAIL) induces apoptosis following binding to the two TRAIL death receptors (DRs). Its recombinant form and monoclonal antibodies against the TRAIL DRs induce cell death in a wide variety of tumor cell lines and xenografts without causing toxicity to normal cells and are ...
C N A M, Oldenhuis, J H, Stegehuis, A M E, Walenkamp, S, de Jong, E G E, de Vries   +4 more
openaire   +2 more sources