Identification of three novel mRNA splice variants of GITR

@article{Nocentini2000IdentificationOT,
  title={Identification of three novel mRNA splice variants of GITR},
  author={Giuseppe Nocentini and Simona Ronchetti and Andrea Bartoli and Stefania Spinicelli and Domenico Vittorio Delfino and Luigi Brunetti and Graziella Migliorati and Carlo Riccardi},
  journal={Cell Death and Differentiation},
  year={2000},
  volume={7},
  pages={408-410}
}
GITR is a gene belonging to the nerve growth factor-tumor necrosis factor receptor (NGF/TNFR) family that is preferentially expressed in lymphoid tissues, is overexpressed following dexamethasone treatment or T cell receptor (TCR) stimulation and is able to modulate T cell apoptosis. Like other members of the NGF/TNFR family, GITR is composed of an intracellular domain, a transmembrane domain and an extracellular domain that is crucial for the binding with the specific ligand. In particular… Expand
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References

SHOWING 1-6 OF 6 REFERENCES
LARD: a new lymphoid-specific death domain containing receptor regulated by alternative pre-mRNA splicing.
  • G. Screaton, X. Xu, +4 authors J. Bell
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1997
TLDR
The expression of LARD is more tightly regulated than that of either Fas or TNF-R1 as it is found predominantly on lymphocytes but not on macrophages or a number of transformed lymphocyte cell lines. Expand
Tumor necrosis factor ligand superfamily: involvement in the pathology of malignant lymphomas.
TLDR
TNF superfamily ligands show for the immune response an involvement in the induction of cytokine secretion and the upregulation of adhesion molecules, activation antigens, and costimulatory proteins, all known to amplify stimulatory and regulatory signals. Expand
A new member of the tumor necrosis factor/nerve growth factor receptor family inhibits T cell receptor-induced apoptosis.
TLDR
GITR is a new member of tumor necrosis factor/nerve growth factor receptor family involved in the regulation of T cell receptor-mediated cell death. Expand
An antagonist decoy receptor and a death domain-containing receptor for TRAIL.
TLDR
Ectopic expression of TRID protected mammalian cells from TRAIL-induced apoptosis, which is consistent with a protective role. Expand
Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule.
TLDR
Levels of soluble Fas were elevated in patients with systemic lupus erythematosus, and mice injected with soluble Fas displayed autoimmune features. Expand
Comparison of the exonic structure of GITR and its alternative splicings (exon
  • J. Biol. Chem
  • 1992