Overview:

Members of the cAMP responsive element binding protein (CREB) family are critical mediators of gene expression in response to extracellular signals. Thus, they are essential regulators of adaptive behavior and long-term memory formation (1). A variety of protein kinases including protein kinase A (PKA), mitogen-activated protein kinases (MAPKs), and Ca2+/calmodulin dependent protein kinases (CAMKs) phosphorylate CRE1B at Ser133, which is required for CREB-mediated transcription (2,3). Activation of CREB1 has been implicated in the survival of mammalian cells. Mice that do not express CREB in the central nervous system display extensive apoptosis of postmitotic neurons during development (4). CREB can bind promoters containing CRE and activator protein 1 (AP-1) sites either as homo- and heterodimers to control gene expression.

References:

1. Valverde, O. et al: Modulation of anxiety-like behavior and morphine dependene in CREB-deficient mice. Neuropsychopharmacology. 2004 Jun;29(6):1122-33.

2. Johannessen, M. et al: What turns CREB on? Cellular Signalling 2004 16:1211-1227.

3. Kornhauser, J M. et al: CREB transcriptional activity in neurons is regulated by multiple, calcium-specific phosphorylation events. Neuron 2002 34:221-233.

4. Mantamadiotis, T. et al: Disruption of CREB function in brain leads to neurodegeneration. Nat genet. 2002 May; 31(1): 47-54.