We have updated our privacy policy. If you have any question, contact us at privacy@scicrunch.org. Dismiss and don't show again

Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-kappaB pathway.

Immunity | Dec 6, 1997

Death receptor 4 (DR4) is a recently described receptor for the cytotoxic ligand TRAIL that reportedly uses a FADD-independent pathway to induce apoptosis and does not activate the NF-kappaB pathway. We have isolated a new member of the tumor necrosis factor receptor (TNFR) family, designated DR5, which bears a high degree of sequence homology to DR4. However, contrary to the previous reports, both DR4- and DR5-induced apoptosis can be blocked by dominant-negative FADD, and both receptors can activate NF-kappaB using a TRADD-dependent pathway. Finally, both receptors can interact with FADD, TRADD, and RIP. Thus, both DR5 and DR4 use FADD, TRADD, and RIP in their signal transduction pathways, and FADD is the common mediator of apoptosis by all known death domain-containing receptors.

Pubmed ID: 9430227 RIS Download

Mesh terms: Adaptor Proteins, Signal Transducing | Amino Acid Sequence | Animals | Apoptosis | Base Sequence | Carrier Proteins | Caspase 8 | Caspase 9 | Caspases | Cell Line | Cloning, Molecular | Cricetinae | Cysteine Endopeptidases | DNA, Complementary | Fas-Associated Death Domain Protein | Humans | Molecular Sequence Data | NF-kappa B | Proteins | Receptor-Interacting Protein Serine-Threonine Kinases | Receptors, TNF-Related Apoptosis-Inducing Ligand | Receptors, Tumor Necrosis Factor | Receptors, Tumor Necrosis Factor, Member 25 | Sequence Analysis, DNA | TNF Receptor-Associated Factor 1 | Tissue Distribution | Tumor Cells, Cultured

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants


Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.