| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
Many members of the nucleotide-binding and oligomerization domain (NOD) and leucine-rich-repeat (LRR)-containing protein (NLR) family play important roles in pathogen recognition and inflammation. We identified PYNOD/NLRP10, one of the member of this family that lacks LRR, and found that PYNOD inhibit inflammatory signal mediated by caspase-1 and ASC. To further investigate physiological function of PYNOD, we have established PYNOD-deficient mice. PYNOD-deficient mice exhibited no obvious gross abnormalities, no evidence of autoimmunity and spontaneous tumor formation, and normal innate immune responses.
However, we have found that PYNOD is highly expressed in stomach of gastric cancer mouse model (Gan mice), in which inflammatory COX-2/PGE2 pathway and Wnt signaling are activated simultaneously in gastric mucosa. Furthermore, we also detected high PYNOD expression in tumor region containing papillary type adenocarcinoma from gastric cancer patients.
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