Papers using
Gli3
antibodies
Papers on
Gli3
Monogenic causes of inflammatory disease in rheumatology.Verbsky, Milwaukee, United States. In Curr Opin Rheumatol, Sep 2012
Further study of well defined monogenic causes of inflammatory diseases, such as FMF, PAPA, TRAPS, and HIDS, has elucidated the pathophysiology of these diseases leading to targeted immunotherapy with anticytokine biological medications.
Interleukin-1, inflammasomes, autoinflammation and the skin.French et al., Zürich, Switzerland. In Swiss Med Wkly, 2011
In mouse models recapitulating mutations observed in CAPS, neutrophilic inflammation of the skin is a cardinal feature, in a manner similar to several autoinflammatory diseases with skin involvement such as PAPA (pyoderma gangrenosum, acne and pyogenic arthritis) and Schnitzler's syndrome, in which IL-1β very probably plays a pathogenic role.
[Autoinflammatory diseases as cause of wound healing defects].Eming et al., Köln, Germany. In Hautarzt, 2011
In this article we will focus on the review of those autoinflammatory diseases that often display ulcerative cutaneous and aphthous lesions including pyoderma gangrenosum, Behçet disease, PAPA syndrome and hyperimmunoglobulinemia D with periodic fever syndrome (HIDS).
mRNA expression signature of Gleason grade predicts lethal prostate cancer.Mucci et al., Boston, United States. In J Clin Oncol, 2011
METHODS: Using the complementary DNA-mediated annealing, selection, extension, and ligation assay, we measured the mRNA expression of 6,100 genes in prostate tumor tissue in the Swedish Watchful Waiting cohort (n = 358) and Physicians' Health Study (PHS; n = 109).
[Inflammasomes and related diseases].Saito, Kyoto, Japan. In Nihon Rinsho Meneki Gakkai Kaishi, 2010
Genetic disorder of inflammasome-IL-1 system cause autoinflammatory diseases such as cryopyrin-associated autoinflammatory disease, familial Mediterranean fever, deficiency of IL-1 receptor antagonist, and PAPA syndrome.
Free radical-mediated oxidative DNA damage in the mechanism of thalidomide teratogenicity.Wells et al., Toronto, Canada. In Nat Med, 1999
Although the mechanism of teratogenesis and determinants of risk remain unclear, related teratogenic xenobiotics are bioactivated by embryonic prostaglandin H synthase (PHS) to a free-radical intermediates that produce reactive oxygen species (ROS), which cause oxidative damage to DNA and other cellular macromolecules.