TNF-alpha induction by LPS is regulated posttranscriptionally via a TpI2/ERK-dependent pathway
Article Abstract:
Research demonstrates that the antimicrobial immunity in mice is manifested through TpI2/ERK pathway in that the mutant mice show decreased levels of tissue necrosis factor-alpha (TNF) due to a defect in its induction. Data further indicate that mutation leads to resistance to LPS/D-Galactosamine-induced pathology and inhibition of TNF-alpha mRNA transport.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2000
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CD30 antigen, a marker for Hodgkin's lymphoma, is a receptor whose ligand defines an emerging family of cytokines with homology to TNF
Article Abstract:
The cDNA cognate from the murine T cell clone 7B9 was expression cloned by using a chimeric probe with the extracellular region of CD30 linked to branched immunoglobulin heavy chains. Sequence homology to members of the tumor necrosis factor (TNF) receptor super family can be observed in CD30, which is a surface marker for neoplastic cells of Hodgkin's lymphoma. The C-terminal region of the encoded protein reveals a marked homology to TNF-alpha, TNF-beta and the CD40L, the protein being a 239 amino acid type II membrane protein. The recombinant human ligand promotes the growth of CD3-stimulated T cells, but causes varied reactions, such as cell death, in many CD30+ lymphoma-derived clones.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1993
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Loss of neurofibromin results in neurotrophin-independent survival of embryonic sensory and sympathetic neurons
Article Abstract:
Analysis of the function of neurofibromin in the generation of neurotrophin dependence in embryonic neurons through observations of the neurofibromatosis 1 (NF1) gene in mice shows that neurofibromin acts as a negative regulator of neurotrophin-mediated signalling for the survival of peripheral embryonic cells. The significant way peripheral neurons are affected by the loss of neurofibromas suggests the neurons' possible function in the etiology of the disease.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
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