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Clock rabbit pAb - ES2004

Clock rabbit pAb - ES2004

Regular price $207.20 CAD
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Clock rabbit pAb

Sizes: 50μL, 100μL

Catalogue Numbers: ES2004-50, ES2004-100

Citations, Manuals and MSDS Available upon request.

Background: The protein encoded by this gene plays a central role in the regulation of circadian rhythms. The protein encodes a transcription factor of the basic helix-loop-helix (bHLH) family and contains DNA binding histone acetyltransferase activity. The encoded protein forms a heterodimer with ARNTL (BMAL1) that binds E-box enhancer elements upstream of Period (PER1, PER2, PER3) and Cryptochrome (CRY1, CRY2) genes and activates transcription of these genes. PER and CRY proteins heterodimerize and repress their own transcription by interacting in a feedback loop with CLOCK/ARNTL complexes. Polymorphisms in this gene may be associated with behavioral changes in certain populations and with obesity and metabolic syndrome. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2014],

Alternate Name: CLOCK; BHLHE8; KIAA0334; Circadian locomoter output cycles protein kaput; hCLOCK; Class E basic helix-loop-helix protein 8; bHLHe8

Source: Rabbit

Applications: WB; IHC; IF; ELISA

Dilution: Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. ELISA: 1/20000. Not yet tested in other applications.

Reactivity: Human; Mouse; Rat

Immunogen: The antiserum was produced against synthesized peptide derived from human Clock. AA range:241-290

Storage and Stability: -20°C/1 year

Clonality: Polyclonal

Isotype: IgG

Concentration: 1 mg/ml

Observed Band (KD): 95kD

Human Gene ID: 9575

Human SWISS Prot NO: O15516

Subcellular Location: Nucleus. Cytoplasm. Cytoplasm, cytosol. Shuttling between the cytoplasm and the nucleus is under circadian regulation and is ARNTL/BMAL1-dependent. Phosphorylated form located in the nucleus while the nonphosphorylated form found only in the cytoplasm. Sequestered to the cytoplasm in the presence of ID2 (By similarity). Localizes to sites of DNA damage in a H2AX-independent manner.

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