Martinon, F., Hofmann, K. & Tschopp, J. The Pyrin domain: a possible member of the death domain-fold family implicated in apoptosis and inflammation. Curr. Biol. 10, R118-R120
University of Lausanne, Lausanne, Vaud, Switzerland Current Biology
(Impact Factor: 9.57).
03/2001; 11(4):R118-20. DOI: 10.1016/S0960-9822(01)00056-2
Available from: Fabio Martinon
- "Cloning of NALP1 and Pycard was described previously (Martinon et al., 2001). "
- "The locus for familial vitiligo on chromosome 17 was recently demonstrated to harbor the gene coding for NALP1. NALP1(NACHT-LRR-PYD- containing protein- 1), together with the related protein NALP2, has been identified by Martinon et al. in a databank search for proteins containing a pyrin domain. The protein contains a NACHT domain, an LRR domain (leucine-rich repeat), and a pyrin domain. "
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ABSTRACT: Vitiligo is an acquired autoimmune disease of unknown etiology showing depigmentation of the skin due to the absence of melanocytes. Familial vitiligo suggests a genetic origin to this disease. Chromosome 17 was recently demonstrated to harbor the gene coding for NALP1.
A total of 18 patients of vitiligo were selected on the basis of clinical history. Group 1 (N=8) showing segmental or localized vitiligo with one or two macules on the body. Group 2 (N=10) with generalized or whole body vitiligo. A control group of 10 healthy individuals were selected from our laboratory persons with no history or any infections or skin disease. NALP1 gene expression was studied using RT-PCR assay and the bands quantitated as intensity using volume as measurement and comparison of results was done using SPSS 16 version for statistical analysis. NALP1 gene expression was observed in vitiligo patients with different intensities.
Greater reduction in the intensity was seen in Group I, which was inversely proportional to the volume of the band. The intensity of the NALP1 and the GAPDH gene expression was more in Group 2 patients than that shown by Group 1.
This study shows expression of NALP1 gene in patients as well as normals. NALP1 is widely expressed at low levels but is expressed at high levels in immune cells, particularly T cells and Langerhans cells, in which different patterns are seen that are consistent with the particular involvement of NALP1 in skin autoimmunity.
Available from: Petr Broz
- "The adaptor ASC (also known as PYCARD) has an N-terminal PYD that facilitates interactions with the PYD domain of NLRs, and a C-terminal CARD domain that recruits caspase-1 through CARD-CARD interactions (Martinon et al., 2001). Interestingly, besides its role as an adaptor, ASC is required to induce autoproteolysis of pro-caspase-1 in the inflammasome complex, a prerequirement for efficient cytokine processing (Broz et al., 2010b). "
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ABSTRACT: Francisella tularensis is an intracellular pathogen that can cause severe disease in a wide range of mammalian hosts. Primarily residing in host macrophages, F. tularensis escapes phagosomal degradation, and replicates in the macrophage cytosol. The macrophage uses a series of pattern recognition receptors to detect conserved microbial molecules from invading pathogens, and initiates an appropriate host response. In the cytosol, F. tularensis is recognized by the inflammasome, a multiprotein complex responsible for the activation of the cysteine protease caspase-1. Caspase-1 activation leads to processing and release of proinflammatory cytokines and host cell death. Here we review recent work on the molecular mechanisms of inflammasome activation by F. tularensis, and its consequences both in vitro and in vivo. Finally, we discuss the coordination between the inflammasome and other cytosolic host responses, and the evidence for F. tularensis virulence factors that suppress inflammasome activation.
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