Phosphorylation of CLOCK, acetylation of BMAL1 (ARNTL) at target gene promoters

Stable Identifier
R-HSA-9931512
Type
Pathway
Species
Homo sapiens
ReviewStatus
5/5
General
SVG |   | PPTX  | SBGN
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After phosphorylated BMAL1:CLOCK heterodimers bind E-box elements in the promoters of target genes, CLOCK acetylates BMAL1 (inferred from mouse homologs in Hirayama et al. 2007) and becomes hyperphosphorylated through an incompletely characterized mechanism (inferred from the mouse homolog in Yoshitane et al. 2009, Robles et al. 2017). The hyperphosphorylation appears to both increase transcriptional activation activity and increase proteolytic degradation of CLOCK.
Literature References
PubMed ID Title Journal Year
19414601 Roles of CLOCK phosphorylation in suppression of E-box-dependent transcription

Yoshitane, H, Takao, T, Satomi, Y, Du, NH, Okano, T, Fukada, Y

Mol Cell Biol 2009
27818261 Phosphorylation Is a Central Mechanism for Circadian Control of Metabolism and Physiology

Robles, MS, Humphrey, SJ, Mann, M

Cell Metab 2017
18075593 CLOCK-mediated acetylation of BMAL1 controls circadian function

Hirayama, J, Sahar, S, Grimaldi, B, Tamaru, T, Takamatsu, K, Nakahata, Y, Sassone-Corsi, P

Nature 2007
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