2004
DOI: 10.1016/j.cellimm.2004.05.001
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Enhanced pro-inflammatory cytokine production in Gαi2-deficient mice on colitis prone and colitis resistant 129Sv genetic backgrounds

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Cited by 14 publications
(9 citation statements)
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“…Mice with intestinal inflammation manifesting increased transcript levels of proinflammatory cytokines therefore also demonstrate higher levels of systemic DNA damage to various cell types. Increased blood and stool cytokine levels of proinflammatory cytokines have similarly been reported in IL‐10 –/– mice with colitis,26–28 in Gαi2 –/– mice29–31 and in DSS‐induced colitis in wildtype mice,13, 18 supporting our observations.…”
Section: Resultssupporting
confidence: 89%
“…Mice with intestinal inflammation manifesting increased transcript levels of proinflammatory cytokines therefore also demonstrate higher levels of systemic DNA damage to various cell types. Increased blood and stool cytokine levels of proinflammatory cytokines have similarly been reported in IL‐10 –/– mice with colitis,26–28 in Gαi2 –/– mice29–31 and in DSS‐induced colitis in wildtype mice,13, 18 supporting our observations.…”
Section: Resultssupporting
confidence: 89%
“…Subsequent QRT-PCR studies also confirmed that TNFα levels following a LPS challenge were significantly greater in Gαi2-deficient cells. This is consistent with the published data from Gαi2 (−/−) mice [26], [54].…”
Section: Discussionsupporting
confidence: 93%
“…Gαi2 has been reported to inhibit the activities of types I, V, and VI adenylyl cyclase isoforms directly [17]. As Gαi2 appears to be involved in a complex pattern of signaling [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27], insight into its function was sought by silencing the Gαi2 transcript. In addition, the Gβ2 subunits released upon activation of the heterotrimeric G protein activate specific effectors, and previous studies have shown it to be the primary beta subunit for certain Gαi signaling pathways in macrophage cells [5], [6].…”
Section: Resultsmentioning
confidence: 99%
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“…Gαi2‐deficient C57BL/6 (B6) mice are relatively resistant to colitis, whereas Gαi2‐deficient 129 mice develop IBD earlier and with greater frequency and severity 7. Linkage analysis has identified a locus on mouse chromosome 3 termed Gpdc1 , which confers colitogenic susceptibility in the Gα i 2‐deficient mouse 8.…”
mentioning
confidence: 99%