|Reactivity||Human Mouse Rat|
|Tested applications||WB IHC IF|
|Recommended Dilution||WB 1:500 - 1:2000
IHC 1:50 - 1:100
IF 1:50 - 1:200|
|Observed MW||Refer to Figures|
|Immunogen||Recombinant protein of human RARA|
|Storage Buffer||Store at -20℃. Avoid freeze / thaw cycles.
Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.|
|Synonym||RARA ; RAR alpha; retinoic acid receptor; alpha; NR1B1; RAR|
Western blot analysis of extracts of various cell lines, using RARA antibody.
Immunohistochemistry of paraffin-embedded rat brain using RARA antibody at dilution of 1:100 (x40 lens).
Immunofluorescence analysis of U2OS cell using RARA antibody. Blue: DAPI for nuclear staining.
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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