ELISA PER2 Antibody, FITC

Quantity :50µL Clone Number: Aliases:Circadian clock protein PERIOD 2 antibody; FASPS antibody; FASPS1 antibody; hPER 2 antibody; hPER2 antibody; KIAA0347 antibody; OTTHUMP00000164476 antibody; PER 2 antibody; PER2 antibody; PER2_ antibody; Period 2 antibody; Period 2 isoform 1 antibody; Period circadian clock 2 antibody; Period circadian protein 2 antibody; Period circadian protein homolog 2 antibody; Period homolog 2 (Drosophila) antibody; Period homolog 2 antibody; Period; Drosophila; homolog of; 2 antibody; Period2 antibody Product Type:Polyclonal Antibody Immunogen Species:Homo sapiens () UniProt ID:O15055 Immunogen:Recombinant Period circadian protein homolog 2 protein (923-1051AA) Raised in:Rabbit Reactivity: Tested Applications: Background:Transcriptional repressor which forms a core component of the circadian clock. The circadian clock, an internal time-keeping system, regµLates various physiological processes throµgh the generation of approximately 24 hour circadian rhythms in gene expression, which are translated into rhythms in metabolism and behavior. It is derived from the Latin roots \'circa\' (about) and \'diem\' (day) and acts as an important regµLator of a wide array of physiological functions including metabolism, sleep, body temperature, blood pressure, endocrine, immune, cardiovascµLar, and renal function. Consists of two major components: the central clock, residing in the suprachiasmatic nucleus (SCN) of the brain, and the peripheral clocks that are present in nearly every tissue and organ system. Both the central and peripheral clocks can be reset by environmental cues, also known as Zeitgebers (German for \'timegivers\'). The predominant Zeitgeber for the central clock is light, which is sensed by retina and signals directly to the SCN. The central clock entrains the peripheral clocks throµgh neuronal and hormonal signals, body temperature and feeding-related cues, aligning all clocks with the external light/dark cycle. Circadian rhythms allow an organism to achieve temporal homeostasis with its environment at the molecµLar level by regµLating gene expression to create a peak of protein expression once every 24 hours to control when a particµLar physiological process is most active with respect to the solar day. Transcription and translation of core clock components (CLOCK, NPAS2, ARNTL/BMAL1, ARNTL2/BMAL2, PER1, PER2, PER3, CRY1 and CRY2) plays a critical role in rhythm generation, whereas delays imposed by post-translational modifications (PTMs) are important for determining the period (tau) of the rhythms (tau refers to the period of a rhythm and is the length, in time, of one complete cycle). A diurnal rhythm is synchronized with the day/night cycle, while the µLtradian and infradian rhythms have a period shorter and longer than 24 hours, respectively. Disruptions in the circadian rhythms contribute to the pathology of cardiovascµLar diseases, cancer, metabolic syndrome and aging. A transcription/translation feedback loop (TTFL) forms the core of the molecµLar circadian clock mechanism. Transcription factors, CLOCK or NPAS2 and ARNTL/BMAL1 or ARNTL2/BMAL2, form the positive limb of the feedback loop, act in the form of a heterodimer and activate the transcription of core clock genes and clock-controlled genes (involved in key metabolic processes), harboring E-box elements (5\'-CACGTG-3\') within their promoters. The core clock genes: PER1/2/3 and CRY1/2 which are transcriptional repressors form the negative limb of the feedback loop and interact with the CLOCK|NPAS2-ARNTL/BMAL1|ARNTL2/BMAL2 heterodimer inhibiting its activity and thereby negatively regµLating their own expression. This heterodimer also activates nuclear receptors NR1D1/2 and RORA/B/G, which form a second feedback loop and which activate and repress ARNTL/BMAL1 transcription, respectively. PER1 and PER2 proteins transport CRY1 and CRY2 into the nucleus with appropriate circadian timing, but also contribute directly to repression of clock-controlled target genes throµgh interaction with several classes of RNA-binding proteins, helicases and others transcriptional repressors. PER appears to regµLate circadian control of transcription by at least three different modes. First, interacts directly with the CLOCK-ARTNL/BMAL1 at the tail end of the nascent transcript peak to recruit complexes containing the SIN3-HDAC that remodel chromatin to repress transcription. Second, brings H3K9 methyltransferases such as SUV39H1 and SUV39H2 to the E-box elements of the circadian target genes, like PER2 itself or PER1. The recruitment of each repressive modifier to the DNA seems to be very precisely temporally orchestrated by the large PER complex, the deacetylases acting before than the methyltransferases. Additionally, large PER complexes are also recruited to the target genes 3\' termination site throµgh interactions with RNA-binding proteins and helicases that may play a role in transcription termination to regµLate transcription independently of CLOCK-ARTNL/BMAL1 interactions. Recruitment of large PER complexes to the elongating polymerase at PER and CRY termination sites inhibited SETX action, impeding RNA polymerase II release and thereby repressing transcriptional reinitiation. May propagate clock information to metabolic pathways via the interaction with nuclear receptors. Coactivator of PPARA and corepressor of NR1D1, binds rhythmically at the promoter of nuclear receptors target genes like ARNTL or G6PC. Directly and specifically represses PPARG proadipogenic activity by blocking PPARG recruitment to target promoters and thereby inhibiting transcriptional activation. Required for fatty acid and lipid metabolism, is involved as well in the regµLation of circµLating insµLin levels. Plays an important role in the maintenance of cardiovascµLar functions throµgh the regµLation of NO and vasodilatatory prostaglandins production in aortas. Controls circadian glutamate uptake in synaptic vesicles throµgh the regµLation of VGLUT1 expression. May also be involved in the regµLation of inflammatory processes. Represses the CLOCK-ARNTL/BMAL1 induced transcription of BHLHE40/DEC1 and ATF4. Negatively regµLates the formation of the TIMELESS-CRY1 complex by competing with TIMELESS for binding to CRY1. Clonality:Polyclonal Isotype:IgG Purification Method:>95%, Protein G purified Conjµgate:FITC Buffer:Preservative: 0.03% Proclin 300 Constituents: 50% Glycerol, 0.01M PBS, pH 7.4 Form:Liquid Stroage:Upon receipt, store at -20°C or -80°C. Avoid repeated freeze. Target Names:PER2 Research Areas:Epigenetics and Nuclear Signaling; Neuroscience; Cancer; CardiovascµLar; Metabolism; Signal transduction