Preparing your results

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

X
Forgot Password

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

The death domain kinase RIP mediates the TNF-induced NF-kappaB signal.

Immunity | Mar 16, 1998

http://www.ncbi.nlm.nih.gov/pubmed/9529147

The death domain serine/threonine kinase RIP interacts with the death receptors Fas and tumor necrosis receptor 1 (TNFR1). In vitro, RIP stimulates apoptosis, SAPK/JNK, and NF-kappaB activation. To define the physiologic role(s) that RIP plays in regulating apoptosis in vivo, we introduced a rip null mutation in mice through homologous recombination. RIP-deficient mice appear normal at birth but fail to thrive, displaying extensive apoptosis in both the lymphoid and adipose tissue and dying at 1-3 days of age. In contrast to a normal thymic anti-Fas response, rip-/- cells are highly sensitive to TNFalpha-induced cell death. Sensitivity to TNFalpha-mediated cell death in rip-/- cells is accompanied by a failure to activate the transcription factor NF-kappaB.

Pubmed ID: 9529147 RIS Download

Mesh terms: Adipose Tissue | Animals | Antigens, CD95 | Apoptosis | Calcium-Calmodulin-Dependent Protein Kinases | Cytokines | Failure to Thrive | Genes, Lethal | JNK Mitogen-Activated Protein Kinases | Lymphoid Tissue | Mice | Mice, Mutant Strains | Mitogen-Activated Protein Kinases | NF-kappa B | Protein-Serine-Threonine Kinases | Proteins | Receptor-Interacting Protein Serine-Threonine Kinases | Tumor Necrosis Factor-alpha

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

None

Mouse Genome Informatics (Data, Gene Annotation)

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.