|Other Names||Retinoic acid-induced protein 1, RAI1, KIAA1820|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP6237a was selected from the C-term region of human RAI1 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Transcriptional regulator of the circadian clock components: CLOCK, ARNTL/BMAL1, ARNTL2/BMAL2, PER1/3, CRY1/2, NR1D1/2 and RORA/C. Positively regulates the transcriptional activity of CLOCK a core component of the circadian clock. Regulates transcription through chromatin remodeling by interacting with other proteins in chromatin as well as proteins in the basic transcriptional machinery. May be important for embryonic and postnatal development. May be involved in neuronal differentiation.|
|Cellular Location||Cytoplasm. Nucleus. Note=In neurons, localized to neurites.|
|Tissue Location||Expressed in all tissues examined with higher expression in the heart and brain. No expression was seen in the corpus callosum of the brain.|
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The gene for Rai1 is located within the Smith-Magenis syndrome region on chromosome 17. It is highly similar to its mouse counterpart and is expressed at high levels mainly in neuronal tissues. The protein encoded by this gene includes a polymorphic polyglutamine tract in the N-terminal domain. Expression of the mouse counterpart in neurons is induced by retinoic acid. This gene is associated with both the severity of the phenotype and the response to medication in schizophrenic patients.
Toulouse, A., et al., Genomics 82(2):162-171 (2003).Slager, R.E., et al., Nat. Genet. 33(4):466-468 (2003).Bi, W., et al., Genome Res. 12(5):713-728 (2002).Seranski, P., et al., Genomics 56(1):1-11 (1999).Seranski, P., et al., Gene 270 (1-2), 69-76 (2001).
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