Recombinant Human PER2 protein (ab112382)

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.

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.

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.

Contains 1 PAC (PAS-associated C-terminal) domain.
Contains 2 PAS (PER-ARNT-SIM) domains.

Phosphorylated by CSNK1E and CSNK1D. Phosphorylation results in PER2 protein degradation.

Nucleus. Cytoplasm. 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.