cryptochrome/necrosis

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Circadian rhythms of factors involved in luteal regression are modified in p55 tumour necrosis factor receptor (TNFRp55)-deficient mice.

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The rhythm of factors involved in luteal regression is crucial in determining the physiological duration of the oestrous cycle. Given the role of tumour necrosis factor (TNF)-α in luteal function and circadian regulation and that most of the effects of TNF-α are mediated by p55 TNF receptor

Clock gene modulation by TNF-alpha depends on calcium and p38 MAP kinase signaling.

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A 24-h treatment with the cytokine tumor necrosis factor-alpha (TNF-alpha) suppresses transcription of E-box-driven clock genes (D-site albumin promoter binding protein, Dbp; Tyrotroph embryonic factor, Tef ; Hepatic leukemia factor, Hlf; Period homolog to Drosophila 1/2/3, Per1, Per2, and Per3) by

TNF-α modulates expression of the circadian clock gene Per2 in rheumatoid synovial cells.

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OBJECTIVE To study the effect of tumour necrosis factor (TNF)-α, responsible for the inflammation and circadian rhythm of rheumatoid arthritis (RA), on the expression of circadian clock genes in primary cultured human rheumatoid synovial cells. METHODS The expression of circadian clock genes,

The effects of Jiao-Tai-Wan on sleep, inflammation and insulin resistance in obesity-resistant rats with chronic partial sleep deprivation.

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BACKGROUND Jiao-Tai-Wan (JTW), composed of Rhizome Coptidis and Cortex Cinnamomi, is a classical traditional Chinese prescription for treating insomnia. Several in vivo studies have concluded that JTW could exert its therapeutical effect in insomnia rats. However, the specific mechanism is still

Overexpression of CRY1 protects against the development of atherosclerosis via the TLR/NF-κB pathway.

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It has been demonstrated that the circadian clock system could be a potential factor involved in inflammation and the progression of atherosclerosis. A previous study has reported that cryptochrome 1 (CRY1), which is a core clock component, is associated with regulating proinflammation. However,

Regulation of apoptosis by the circadian clock through NF-kappaB signaling.

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In mice and humans the circadian rhythm of many biochemical reactions, physiology, and behavior is generated by a transcriptional-translation feedback loop (TTFL) made up of the so-called core clock genes/proteins. The circadian system interfaces with most signaling pathways including those involved

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