Rev-ErbA alpha
Rev-ErbA alpha also known as NR1D1 (nuclear receptor subfamily 1, group D, member 1), is a protein that in humans is encoded by the NR1D1 gene.
Rev-erb is a member of the Rev-ErbA family of nuclear receptors and is a transcriptional repressor. In mammals, Rev-erb is highly expressed in the liver, skeletal muscle, adipose tissue, and the brain, participating in the development and circadian regulation of these tissues.

# Gene and protein structure
Rev-erb is transcribed from the opposite strand of the thyroid receptor  (c-erbA) gene on chromosome 17, with a 269-nucleotide overlap between the two transcripts.  The other mammalian isoform of the receptor, Rev-erb is encoded by another gene on chromosome 3.  In addition, there is one non-mammalian homolog, the ecdysone-regulated gene E75, which is present in Drosophila and C. elegans.  The Rev-erb gene itself has multiple transcripts. Two promoters govern the expression of the Rev-erb gene in human and rat, generating two mRNA isoforms. The full-length isoform encodes a 614-amino acid protein, while a second isoform is generated from an internal promoter and produces a protein that is shorter by 106 amino acids. Both Rev-erb mRNA isoforms contain E-boxes as well as Rev-erb response elements, which means that they can be regulated in a circadian manner by the BMAL and Rev-erba proteins. In fact, both transcripts exhibit rhythmic expression in serum-synchronized fibroblasts.
The Rev-erb protein is structurally unique from other nuclear receptors, in that it lacks helix 12 (H12) in its ligand-binding domain, which is usually responsible for forming the ligand binding pocket in other nuclear receptors. In place of the missing H12, Rev-erb displays a hydrophobic interface that binds the corepressor N-CoR, making it a potent transcriptional repressor.  All members of the Rev-erb family bind heme, which may act as a ligand to regulate their transcriptional activity.

# Physiologic function
Rev-erb regulates gene transcription by directly binding to target response elements (RevREs), and comprises an A/T-rich flank followed by AGGTCA.  Rev-erb mediates repression by recruiting the corepressor N-CoR, which then activates the histone deacetylase (HDAC) 3.  A number of target genes have been identified for Rev-erb, including the lipoproteins ApoA1 and ApoCIII, hydratase dehydrogenase, the circadian factor BMAL, and the anti-fibrinolytic factor PAI-1. Many of these genes are coordinately regulated by Rev-erb and the RAR-related orphan receptor ROR, which share the same response elements but exert opposite effects on gene transcription. Crosstalk between Rev-erb and ROR likely acts to fine-tune their target physiologic networks, such as circadian rhythms, metabolic homeostasis, and inflammation.
Rev-erb mRNA is induced during adipogenesis and is highly expressed in adipose tissue. One study reported that overexpression of Rev-erb may enhance adipogenesis in cultured mouse adipocytes, but the mechanism of this effect remains to be elucidated. More recently, a study showed that the deletion of Rev-erb in mice alters glucose and lipid metabolism and leads to obesity.
Rev-erb expression is also regulated at the post-translational level: it is phosphorylated on the amino terminus by glycogen synthase kinase (GSK 3), which contributes to its protein stability. It has been shown that lithium, which inhibits GSK3, can de-stabilize Rev-erb protein and affect its function in the circadian clock. This may partly explain lithiums therapeutic effect on circadian diseases such as bipolar disorder.