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Study shows abnormal circadian locomotor rhythms and Per1 and Per 2 gene expression in six-month-old triple transgenic mice model of Alzheimer's disease.
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hippocampal Per1 is critical for long-term memory formation.
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Period genes not only orchestrate dynamic changes in metabolic activity, but also regulate homeostatic self-renewal of hepatocytes through Mkp1-Erk1/2 signaling pathway.
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Results show that Per1 expression is associated with a short period and Per2 expression is associated with a long period and, that Per1 and Per2 cooperatively confine the range of circadian period length to approximately 24-h.
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This vitro data suggests that basal activity of autophagy seems to be modulated by PER1, and confirms the in vivo data by showing that the autophagic machinery is depressed in Per1-/--hippocampal neurons.
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These findings indicate that the expressions of two key clock genes, Per1 and Bmal1, in the SCN are regulated in such a way that they may adopt different phases and free-running periods relative to each other and are respectively associated with the expression of activity onset and offset.
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we elucidate the dual functions of PER as repressor and de-repressor in a context-dependent manner.
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Atxn2(-/-) mice showed an unstable rhythmicity of locomotor activity, but the level of PER1 and PER2 IR in the SCN did not differ between genotypes.
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In hippocampal neurons of wild-type mice, pP90RSK translocates into the nucleus upon stimulation with forskolin (left), whereas in Period1-knockout (Per1(-/-) ) mice (right) the kinase is trapped at the nuclear periphery
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beta-amyloid protein (31-35) altered the expression of the Per1 and Per2 in the suprachiasmatic nucleus, hippocampus and heart. These findings provide experimental evidence for circadian rhythm disturbances in patients with Alzheimer's disease.
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In vivo knockdown of Rfk, Riboflavin (vitamin B2) kinase essential for FAD synthesis, altered the expression rhythms of CRY1, CRY2, and PER1
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these data support an important role for the circadian clock protein PER1 in the modulation of blood pressure in a high salt/mineralocorticoid model of hypertension
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Per1 knockdown leads to JNK phosphorylation, CCL2 production and allodynia.
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Deletion of Per1 alleviated the inhibitory effect of PPAR-gamma on CC chemokine receptor 2 expression, resulting in enhanced macrophage recruitment into the liver.
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Rate-limiting mitochondrial enzymes that process lipids and carbohydrates accumulate in a diurnal manner and are dependent on the clock proteins PER1/2. Diurnal regulation of mitochondrial respiration was blunted in PER1/2 knockout mice.
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that the presence of a depressive state around the early active phase of activity may be related to impairment of rhythmicity and expression levels of Per1 and Per2 genes under abnormal light-dark conditions
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Study demonstrated that transiently and selectively reducing the levels of the clock gene Period1 decreases electrical activity in the mouse suprachiasmatic nucleus
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measured gene expression of Fos, Per1 and Sgk1 45 min after exposure to brief cold swim stress in male and female mice; stress induced a stronger increase in Fos and Per1 expression in females than males
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Histone monoubiquitination by Clock-Bmal1 complex marks Per1 and Per2 genes for circadian feedback.
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In mice, food intake stimulates oxyntomodulin secretion from the gut, which resets liver transcription rhythms via induction of the core clock genes Per1 and 2.
