The antiserum was produced against synthesized peptide derived from human Period Circadian Protein 2 around the phosphorylation site of Ser662. AA range:636-685

Phospho-PER2 (S662) Polyclonal Antibody detects endogenous levels of PER2 protein only when phosphorylated at S662.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):AEsVA

PER2

Period circadian protein homolog 2

PER2 ;
KIAA0347 ;
Period circadian protein homolog 2 ;
hPER2 ;
Circadian clock protein PERIOD 2

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. This gene is upregulated by CLOCK/ARNTL heterodimers but then represses this upregulation in a feedback loop using PER/CRY heterodimers to interact with CLOCK/ARNTL. Polymorphisms in this gene may increase the risk of getting certain cancers and have been linked to sleep disorders. [provided by RefSeq, Jan 2014],

Disease:Defects in PER2 are a cause of familial advanced sleep-phase syndrome (FASPS) [MIM:604348]. FASPS is characterized by very early sleep onset and offset. Individuals are 'morning larks' with a 4 hours advance of the sleep, temperature and melatonin rhythms.,Function:Component of the circadian clock mechanism which is essential for generating circadian rhythms. Negative element in the circadian transcriptional loop. Influences clock function by interacting with other circadian regulatory proteins and transporting them to the nucleus. Negatively regulates CLOCK|NPAS2-BMAL1|BMAL2-induced transactivation.,induction:Serum-induced levels in fibroblasts show circadian oscillations. Maximum levels after 1 hour stimulation, minimum levels after 12 hours. Another peak is then observed after 24 hours.,PTM:Phosphorylated by CSNK1E and CSNK1D. Phosphorylation results in PER2 protein degradation.,similarity:Contains 1 PAC (PAS-associated C-terminal) domain.,similarity:Contains 2 PAS (PER-ARNT-SIM) domains.,subcellular location:Mainly nuclear. Nucleocytoplasmic shuttling is effected by interaction with other circadian core oscillator proteins and/or by phosphorylation. Retention of PER1 in the cytoplasm occurs through PER1-PER2 heterodimer formation or by interaction with CSNK1E and/or phosphorylation which appears to mask the PER nuclear localization signal. Also translocated to the nucleus by CRY1 or CRY2.,subunit:Component of the circadian core oscillator, which includes the CRY proteins, CLOCK or NPAS2, BMAL1 or BMAL2, CSNK1D and/or CSNK1E, TIMELESS, and the PER proteins. Interacts directly with PER1 and PER3, and through a C-terminal domain, with CRY1 and CRY2. Interaction with CSNK1D or CSNK1E promotes nuclear location of PER proteins. Interacts, via its second PAS domain, with TIMELESS in vitro. Interacts with NFIL3.,tissue specificity:Widely expressed. Found in heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas. High levels in skeletal muscle and pancreas. Low level in lung.,

[Isoform 1]: Nucleus . Cytoplasm . Cytoplasm, perinuclear region . Nucleocytoplasmic shuttling is effected by interaction with other circadian core oscillator proteins and/or by phosphorylation. Translocate to the nucleus after phosphorylation by CSNK1D or CSNK1E. Also translocated to the nucleus by CRY1 or CRY2. PML regulates its nuclear localization. .; [Isoform 2]: Nucleus, nucleolus .

>>Circadian rhythm ;
>>Circadian entrainment ;
>>Transcriptional misregulation in cancer ;
>>Acute myeloid leukemia