Cross-reacts with Human, Rat and Pig. May cross react with Mouse.

Thyroid hormone receptors (TRs) are ligand dependent members of the steroid/retinoic acid superfamily of transcription factors. The two genes encoding TRs identified to date, TR alpha and TR Beta, have been mapped to human chromosomes 17 and 3, respectively. TRs bind to thyroid hormone response elements (TREs) with half site binding motifs in the orientation of palindromes, direct repeats, or inverted palindromes. The affinities of binding are both variable and influenced differentially by 3,5,3 -triiodo-L-thyronine (T-3).

Gorilla, Gibbon, Marmoset. Predicted cross-reactivity based on sequence identity: Panda (94%), Elephant (89%), Bat (89%), Opossum (89%).

Rev-erbA alpha, a NR1 Thyroid Hormone-Like Receptor, is encoded by the same genomic locus as, but transcribed from the opposite strand of, Thyroid Hormone Receptor Alpha (TR Alpha). Rev-erbA alpha is a target of Nuclear Receptor ROR Alpha (Delerive et al. 2002), and a transcription regulator that has been shown to affect myocyte differentiation, adipogenesis, and lipoprotein metabolism. Recently Reb-erbA alpha has been shown to affect circadian rhythms by regulating cyclic Bmal1 transcription (Preitner et al. 2002, Ueda et al. 2002). Mice lacking Rev-erbA alpha show abnormal postnatal cerebellar development. Rev-erbA alpha expression has been documented in human skeletal muscle and a variety of mouse and rat tissues. ESTs have been isolated from human tissue libraries, including cancerous adrenal, blood, brain, breast, colon, duodenum, fetus, head/neck, kidney, lung, skeletal muscle, skin, synovium, and uterus, and normal brain, breast, colon, eye, heart, pancreas, pituitary, rostate, skeletal muscle, skin, testis, and thyroid.