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.
We have isolated a novel member of the TNFR family, designated TAJ, that is highly expressed during embryonic development. TAJ possesses a unique cytoplasmic domain with no sequence homology to the previously characterized members of the TNFR family. TAJ interacts with the TRAF family members and activates the JNK pathway when overexpressed in mammalian cells. Although it lacks a death domain, TAJ is capable of inducing apoptosis by a caspase-independent mechanism. Based on its unique expression profile and signaling properties, TAJ may play an essential role in embryonic development.
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Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593, USA.
Jasmin
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Kumar
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Sharma
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Chaudhary
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D000595:Amino Acid Sequence; D000818:Animals; D020169:Caspases / Q000378:metabolism*; D016923:Cell Death; D002460:Cell Line; D003001:Cloning, Molecular; D005314:Embryonic and Fetal Development; D005260:Female; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases; D008297:Male; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008969:Molecular Sequence Data; D009928:Organ Specificity; D018124:Receptors, Tumor Necrosis Factor / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism*; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid
D018124:Receptors, Tumor Necrosis Factor; C409471:Tnfrsf19 protein, mouse; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D020169:Caspases