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**cAMP responsive element-binding protein-like 2 (CREBL2)** is a member of the basic leucine zipper (bZIP) family of transcription factors related to CREB, sharing a conserved domain involved in DNA binding and protein dimerization[1][2][3][6]. CREBL2 is implicated as a transcriptional regulator linking energy and nutrient sensing to metabolic gene expression, and is a direct phosphorylation target of AMPK and acts downstream of mTORC1, especially influencing metabolism in muscle and liver cells[1][4]. Its expression is upregulated during adipogenic differentiation and it promotes lipogenesis via control of key transcription factors such as PPARγ and C/EBPα[1]. Genomic deletions in CREBL2 are found in various cancers, suggesting a tumor suppressor role[1][2][6], and its mRNA is modulated by regulatory RNAs such as miR-1246[1]. Disease associations include Temtamy syndrome, Cantu syndrome, and a potential impact on the gene expression profiles in hematological malignancies and metabolic dysregulation[2]. There is no documented evidence of direct therapeutic targeting by drugs or of its use as a biomarker or known safety concerns in therapy to date.
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