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Validated All-in-One™ qPCR Primer for PER2(NM_022817.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene is a member of the Period family of genes and is expressed in a circadian pattern in the suprachiasmatic nucleus, the primary circadian pacemaker in the mammalian brain. Genes in this family encode components of the circadian rhythms of locomotor activity, metabolism, and behavior. Circadian expression in the suprachiasmatic nucleus continues in constant darkness, and a shift in the light/dark cycle evokes a proportional shift of gene expression in the suprachiasmatic nucleus. The specific function of this gene is not yet known. [provided by RefSeq].
Gene References into function
- The circadian gene Period2 plays an important role in tumor suppression and DNA damage response in vivo.
- Polymorphism of the PER2 casein kinase I epsilon binding region is unlikely to play an important role in the development of bipolar disorder.
- Circadian oscillations of Per1, Per2, and Per3 mRNA expression were observed in serum-stimulated normal human fibroblasts.
- Transcripts of hPer2 underwent circadian oscillation. The mRNA levels reached a maximum at 4 h and minimal levels at 12 h.
- disturbances in PER gene expression may result in disruption of the control of the normal circadian clock, thus benefiting the survival of cancer cells and promoting carcinogenesis
- Per2 levels were reduced in lymphoma cell lines and in acute myeloid leukemia (AML) patient samples
- per2 gene is associated with diurnal sleep preference.
- Point mutations in the prion protein, period 2, and the prepro-hypocretin/orexin gene have been found as the cause of a few sleep disorders.
- Evening exposure to blue light stimulates the expression of the clock gene PER2.
- Phosphorylation at Serine 662 leads to increased PER2 transcription and suggest that phosphorylation at another site leads to PER2 degradation.
- We have examined the circadian expression of clock genes in human leukocytes and found that Per2 mRNA showed weak rhythm.
- A clear circadian rhythm was shown for hPer1, hPer2, and hCry2 expression in CD34(+) cells and for hPer1 in the whole bone marrow, with maxima from early morning to midday.
- variations associated with seasonal affective disorder
- Per2, a core clock gene, links the circadian cycle to the ERalpha signaling network.
- a role for both Per1 and Per2 in normal breast function and show for the first time that deregulation of the circadian clock may be an important factor in the development of familial breast cancer
- The regulators of clock-controlled transcription PER2, CRY1 and CRY2 differ in their capacity to interact with each single component of the BMAL1-CLOCK heterodimer and, in the case of BMAL1, also in their interaction sites.
- The expression level of PER2 was decreased in hepatocellular carcinoma.
- The data support a model where heme-mediated oxidation triggers hPer2 degradation, thus controlling heterodimerization and ultimately gene transcription.
- Individual PER3 rhythms correlated significantly with sleep-wake timing and the timing of melatonin and cortisol, but those of PER2 and BMAL1 did not reach significance.
- These data support the hypothesis that circadian clock genes can control the cell cycle and cell survival signaling, and emphasize a central role of CK1epsilon and PERIOD2 in linking these systems.
- PER2 might have been influenced by positive selection, and offers preliminary insights into the evolution of this functional class of genes
- There was no significant age-related phase difference in PER1 or PER2 rhythm with respect to sleep timing; however, PER3 expression pattern was altered in the older subjects.
