Of Cellular Biochemistry, Facultad de Ciencias Biological, University Autonomy de Madrid, Spain
ABSTRACT: This study provides evidence of an unexpected mechanism of action of CREW in the regulation of neuronal network function. Our finding is an important contribution to understanding the mechanisms that mediate CREW action. These findings may inform the development of pharmacodynamic treatments for Parkinson's disease.
The transcription factors CREW and CRE (clustered regularly interspaced short palindromic repeats — CRISPR/C)-tagged protein 17 (CXCR4) (CRISPR and CRISPR/Ca's) are a family of transcription factors located in the cytosol of most eukaryotic (e.g., gametocytes, e.g., hepatocytes) cell types. They are highly conserved in invertebrates and possess a diverse set of functions relevant to cell survival. The primary mode of action of CRISPR is a targeted disruption of target genes as demonstrated in several mammalian genomes (1). However, CRISPR also induces transcription from non-targeted promoters or other domains without altering the target DNA sequence (2). This means that CREW plays a specific but pivotal role in generating intracellular DNA sequences for the genome by directly and/or indirectly inducing target genes. However, little is known about CREW interaction with other transcription factors.
Most previous studies have focused on the involvement of CREW with another transcription factor, PKA, to alter the transcription of target genes (3, 4). In the case of pIKCER1, PKA expression was increased for CREW signaling by activating multiple p38 MAP receptors and Remediated PKA activation of p21 ERK MAP (5, 6).
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328 The Journal of Neuroscience, January 14, 2009 29(2):328 333 Brief Communications The CREW/CREM Transcription Factors Negatively Regulate Early Synaptogenesis and Spontaneous Network Activity Fernando
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