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2025
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| Online Access: | https://doi.org/10.5281/zenodo.17986921 |
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| _version_ | 1866901105903927296 |
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| author | Mamoor, Shahan |
| author_facet | Mamoor, Shahan |
| contents | <p>We describe here NLRP7 activation (and in some cases silencing) as a signature event in circumstances of sudden change in speed of cell cycle (rapid cycling induced by tumor suppressor deletion), as a direct transcriptional consequence of expression of chronic disease susceptibility genes like NOD2, and in the steady state in nature, in chronic human diseases including multiple sclerosis and IBD (CD). NLRP7 activation or silencing in resistance models suggests that this NLR possesses an advanced alarm or change signal triggered by large changes in cellular or microenvironment (i.e., cancer metastasis). We describe what appears to be a signature event in the etiology of human disease likely in relation to cell cycle alteration recently described as a signature feature found in cells following expression of a chronic disease-associated susceptibility gene, with etiologic significance following activity in the nucleus like oncogene expression early in disease development or transformation. Co-regulation with TIGIT and BATF suggests involvement of exhaustion signaling or NLRP7 activity during periods of senescence or interactions with exhausted cells.</p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_17986921 |
| institution | Zenodo |
| language | |
| publishDate | 2025 |
| publisher | Zenodo |
| record_format | zenodo |
| spellingShingle | NLRP7 engagement in transformation and etiology of chronic disease. Mamoor, Shahan <p>We describe here NLRP7 activation (and in some cases silencing) as a signature event in circumstances of sudden change in speed of cell cycle (rapid cycling induced by tumor suppressor deletion), as a direct transcriptional consequence of expression of chronic disease susceptibility genes like NOD2, and in the steady state in nature, in chronic human diseases including multiple sclerosis and IBD (CD). NLRP7 activation or silencing in resistance models suggests that this NLR possesses an advanced alarm or change signal triggered by large changes in cellular or microenvironment (i.e., cancer metastasis). We describe what appears to be a signature event in the etiology of human disease likely in relation to cell cycle alteration recently described as a signature feature found in cells following expression of a chronic disease-associated susceptibility gene, with etiologic significance following activity in the nucleus like oncogene expression early in disease development or transformation. Co-regulation with TIGIT and BATF suggests involvement of exhaustion signaling or NLRP7 activity during periods of senescence or interactions with exhausted cells.</p> |
| title | NLRP7 engagement in transformation and etiology of chronic disease. |
| url | https://doi.org/10.5281/zenodo.17986921 |