Characterization of the human CREB3L2 gene promoter

Abstract

Abstract. CREB3L2 encodes a member of the CREB3 family of transcription factors. We characterized its promoter region, showing that it is asymmetrically bidirectional, also driving the expression of a variant of AKR1D1. It has a CRE binding site which is conserved among mammalians; removal or alteration of it resulted in reduced promoter activity. When transiently transfecting the HEK293 cell line with constructs with partially deleted promoter regions, 5' deletions beyond 1058-bp upstream of the transcription starting site resulted in successive reduction of the activity. The inclusion of the untranslated part of CREB3L2 exon 1 strongly inhibited the promoter activity. Forskolin resulted in a decreased reporter activity, whereas phorbol 12-myristate 13-acetate increased the promoter activity irrespective of the status of the CRE binding site. The presence of the CRE site indicates autoregulation of CREB3L2 and/or regulation via other members of the CREB3 family or a variety of bZIP transcription factors.

Exploring the binding of resveratrol to a promoter DNA sequence d(CCAATTGG)2 through multispectroscopic, nuclear magnetic resonance and molecular dynamics studies

“…This finding establishes that NF-Y recognizes the correct reading frame dyad symmetric CCAAT core motif [31]. Literature reveals that the CCAAT sequence is vital in many cellular processes that involve cell proliferation and cell integrity [32][33][34][35].…”

FUS-CREB3L2/L1–Positive Sarcomas Show a Specific Gene Expression Profile with Upregulation of CD24 and FOXL1

“…CRE binding sites in the HSPA5 promoter are normally bound directly by the CREB3L2/L1 proteins in the unfolded protein response, which acts to rescue the cell from ER stressinduced apoptosis (9). However, FUS-CREB3L2DTM was found to be the weakest activator through the cloned sites (13) and had no effect on the CREB3L2 promoter, which contains a conserved CRE site, whereas CREB3L2DTM did (24), suggesting a discrepancy in the regulatory actions of the wt and chimeric proteins. In the present study, HSPA5 and CREB3L2 were not differentially expressed in LGFMS tumor samples or in FC-HEK, suggesting that the regulation of these genes is not FUS-CREB3L2 dependent.…”

“…A total of 500 ng of pFLhRL construct were cotransfected with 100 ng or 1 mg of the pCR3.1-FUS-CREB3L2DTM, pCR3.1-CREB3L2DTM, or empty pCR3.1 expression plasmids. The plasmids pCR3.1-FUS-CREB3L2DTM and pCR3.1-CREB3L2DTM have been described before (24). The "DTM" proteins lack the transmembrane and COOH-terminal domains and thus correspond to the active, cleaved forms of the chimeric and wt, respectively, transcription factors which localize to the nucleus (13).…”

“…Gene expression array (cases [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19], IHC analyses (cases 1, 2, 10, 11, and 20-24), ICC (cases 5 and 6), and/or SNP array (cases 1-9) were carried out on 24 LGFMS cases listed in Table 1. The clinical, cytogenetic, and fusion transcript data on 20 of the cases have been published before (5)(6)(7)(8).…”

Comparative Analysis of CREB3 and CREB3L2 Protein Expression in HEK293 Cells

“…Tg treatment significantly upregulated full-length CREB3L2 in wt HEK293 cells and abolished the difference due to SEL1L deficiency ( Figure 2 C,E). Since the CREB3L2 promoter has only been characterized [ 38 ], further studies are needed to determine whether Tg or SEL1L deficiency increase the level of the CREB3L2 protein through a transcriptional and/or translational mechanism. Kondo et al reported that among the three canonical ER stress sensors, the PERK pathway does not contribute to Tg-induced CREB3L2 expression; however, the contributions of other ER stress sensors, ATF6 and IRE1, remain to be determined [ 3 , 6 , 28 , 29 ].…”