Does TNF alpha cause apoptosis?
Does TNF alpha cause apoptosis?
Out of the almost 17 members of the TNF superfamily, TNF is probably the most potent inducer of apoptosis. TNF activates both cell-survival and cell-death mechanisms simultaneously.
What activates TRAIL?
TRAIL is a cytokine that is produced and secreted by most normal tissue cells. It causes apoptosis primarily in tumor cells, by binding to certain death receptors.
What is TRAIL protein?
TRAIL Protein, Recombinant human. Overview. Human TRAIL (TNF-Related Apoptosis Inducing Ligand), also called APO2 Ligand, is a cytotoxic protein which activates rapid apoptosis in tumor cells, but not in normal cells. TRAIL-induced apoptosis, is achieved through binding to two death-signaling receptors, DR4 and DR5.
What does TNF alpha do?
Tumour Necrosis Factor alpha (TNF alpha), is an inflammatory cytokine produced by macrophages/monocytes during acute inflammation and is responsible for a diverse range of signalling events within cells, leading to necrosis or apoptosis. The protein is also important for resistance to infection and cancers.
How does TRAIL cause apoptosis?
TRAIL induces apoptosis by binding to and activating signaling by trimeric death receptors in a manner that is similar to that of other “death ligands,― such as FasL or TNFα, which signal through the Fas receptor (CD95) and TNF receptor (TNFR1), respectively. TRAIL binds to five different receptors.
How does TRAIL induce apoptosis?
TRAIL has been shown to induce apoptosis through binding its respective receptors, DR4 and DR5. Ligation of TRAIL to its receptor results in trimerization of the receptor and clustering of the receptor’s intracellular DD, leading to the formation of the death-inducing signaling complex (DISC).
What is TRAIL treatment?
A cell protein that can attach to certain molecules in some cancer cells and may kill the cells. TRAIL is being studied in the treatment of cancer. Also called Apo-2L, TNF-related apoptosis-inducing ligand, and tumor necrosis factor-related apoptosis-inducing ligand.