Rabbit anti-RARA Polyclonal An

别名：兔抗RARA多克隆抗体A synthesized peptide derived from Human RARA(Accession P10276), corresponding to amino acid residues M1-Y24. WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000Store at -20 °C for one year. Avoid repeated freeze/thaw cyclesWB,IHC,ICC-IF,ELISA见优宁维官网RabbitHuman;Mouse;Rat

克隆性：见优宁维官网

产品描述：

Retinoids (vitamin A and its active retinoic acid derivatives) are non-steroid hormones that regulate cell proliferation, differentiation and apoptosis. Retinoic acid receptors (RARalpha, -beta and -gamma) and retinoid X receptors (RXRalpha, -beta and -gamma) are nuclear receptors that function as RAR-RXR heterodimers or RXR homodimers (1-2). In response to retinoid binding, these dimers control gene expression by binding to specific retinoic acid response elements, by recruiting cofactors and the transcriptional machinery, and by indirectly regulating chromatin structure. Finally, ligand binding and phosphorylation of RARalpha by JNK at Thr181, Ser445 and Ser461 controls the stability of RAR-RXR through the ubiquitin-proteasome pathway (3-4). At least four distinct genetic lesions affect RARalpha and result in acute promyelocytic leukemia (APL). The t(15;17) translocation that results in the PML-RARalpha fusion protein is responsible for more than 99% of APL cases, and the fusion protein inhibits PML-dependent apoptotic pathways in a dominant negative fashion. In addition PML-RARalpha inhibits transcription of retinoic acid target genes by recruiting co-repressors, attenuating myeloid differentiation (5-6).

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