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Example sentences for: cru
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Calmodulin PDEs (CaM-PDEs) are sensitive to calmodulin and calcium up regulation [ 54 ] . cAMP can then affect cell signaling via interactions with the regulatory subunits of cAMP activated kinases, including protein kinase A, leading to their subsequent activation, and via binding of cAMP response element binding proteins (CREBs) to cAMP response elements (CREs) or cAMP response units (CRU) consisting of CREs.
The cAMP-regulated formation of a 31-kDa USF1 isoform may also play a role in formation of the RIIβ CRU.
C/EBP is previously reported to be an important accessory factor for transactivation by several other transcription factors [ 26 ] . C/EBPβ was shown to transactivate the α1-acid glycoprotein gene promoter even when mutated in the DNA-binding domain, and this activation appeared to depend on protein-protein interaction with glucocorticoid receptor through the leucine zipper region [ 27 ] . Recently, a conserved domain in C/EBPα and C/EBPβ was shown to mediate cAMP responsiveness, strengthening the fact that C/EBP may be characterized as a cAMP-responsive nuclear regulator [ 28 29 ] . On the COX-2 promoter in granulosa cells, cAMP-mediated regulation was shown to be mediated primarily by an E-box that bind USF1 and USF2 isoforms in a manner resembling the RIIβ E-box in Sertoli cells [ 30 ] . Transactivation of the COX-2 gene in skin carcinoma cells is highly dependent on this E-box together with a C/EBP binding site that bind C/EBPβ and C/EBPδ [ 31 ] . These data strengthens a model of formation of a cAMP-responsive unit (CRU) containing USF and C/EBP.
The Pck1 promoter can thus exist in altered states of cAMP responsiveness, depending on the transcription factors bound to CRU elements [ 55 ] . In hepatocytes, SREBP-1c can block transcriptional induction of cAMP on PEPCK-C metabolic action [ 56 ] .
In the liver, cAMP regulates Pck1 transcription via the binding of CREB, as well as CCAAT/enhancer binding protein (C/EBP), to the CRU.
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