A novel method to develop highly specific models for regulatory units detects a new LTR in GenBank which contains a functional promoter

Frech, Kornelie; Danescu-Mayer, Joana; Werner, Thomas

doi:10.1006/jmbi.1997.1140

Cited by 97 publications

(59 citation statements)

References 43 publications

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“…The identification of specific frameworks of transcription factor binding sites linked to gene coregulation remains challenging, as the characteristics of such frameworks cannot be defined by sequence homology. It is now widely accepted that position weight matrices defining the specific order, spacing, distance, and orientation for transcription factors allow the best in silico characterization of promoter motifs (11,18). Systematic promoter module analysis of the proximal promoter regions of upregulated known NF-B-dependant genes identified a NF-B module (NFKB_IRFF_01) associated with progression of DN.…”

Section: Discussionmentioning

confidence: 99%

Modular Activation of Nuclear Factor-κB Transcriptional Programs in Human Diabetic Nephropathy

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Modular Activation of Nuclear Factor-κB Transcriptional Programs in Human Diabetic Nephropathy

et al. 2006

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“…A threshold of 100% genes containing the module, a distance of 5 -200 bp and an intersite variability of 15 bp or less were permitted between TFBSs. The software ModelInspector (Genomatix) was used with the default settings to identify the previously characterized TF binding modules in additional promoter regions of the Genomatix Human Promoter Database (Version Eldorado 12-2012) (Frech et al 1997). …”

Section: Comparative Promoter Analysismentioning

confidence: 99%

Human intestine luminal ACE2 and amino acid transporter expression increased by ACE-inhibitors

et al. 2014

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Sodium-dependent neutral amino acid transporter B(0)AT1 (SLC6A19) and imino acid (proline) transporter SIT1 (SLC6A20) are expressed at the luminal membrane of small intestine enterocytes and proximal tubule kidney cells where they exert key functions for amino acid (re)absorption as documented by their role in Hartnup disorder and iminoglycinuria, respectively. Expression of B(0)AT1 was shown in rodent intestine to depend on the presence of the carboxypeptidase angiotensin-converting enzyme 2 (ACE2). This enzyme belongs to the renin-angiotensin system and its expression is induced by treatment with ACE-inhibitors (ACEIs) or angiotensin II AT1 receptor blockers (ARBs) in many rodent tissues. We show here in the Xenopus laevis oocyte expression system that human ACE2 also functionally interacts with SIT1. To investigate in human intestine the potential effect of ACEIs or ARBs on ACE2, we analysed intestinal biopsies taken during routine gastroduodenoscopy and ileocolonoscopy from 46 patients of which 9 were under ACEI and 13 ARB treatment. Analysis of transcript expression by real-time PCR and of proteins by immunofluorescence showed a co-localization of SIT1 and B(0)AT1 with ACE2 in the brush-border membrane of human small intestine enterocytes and a distinct axial expression pattern of the tested gene products along the intestine. Patients treated with ACEIs displayed in comparison with untreated controls increased intestinal mRNA levels of ACE2, peptide transporter PEPT1 (SLC15A1) and AA transporters B(0)AT1 and PAT1 (SLC36A1). This study unravels in human intestine the localization and distribution of intestinal transporters involved in amino acid absorption and suggests that ACEIs impact on their expression. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64

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“…Sites were computationally predicted with predefined transcription factor binding modules 45,46 in the Promoter Module Library (Genomatix).…”

Section: In Silico Promoter Analysismentioning

confidence: 99%

Sp1‐Mediated Nonmuscle Myosin Light Chain Kinase Expression and Enhanced Activity in Vascular Endothelial Growth Factor–Induced Vascular Permeability

et al. 2015

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Despite the important role played by the nonmuscle isoform of myosin light chain kinase (nmMLCK) in vascular barrier regulation and the implication of both nmMLCK and vascular endothelial growth factor (VEGF) in the pathogenesis of acute respiratory distress syndrome (ARDS), the role played by nmMLCK in VEGF-induced vascular permeability is poorly understood. In this study, the role played by nmMLCK in VEGF-induced vascular hyperpermeability was investigated. Human lung endothelial cell barrier integrity in response to VEGF is examined in both the absence and the presence of nmMLCK small interfering RNAs. Levels of nmMLCK messenger RNA (mRNA), protein, and promoter activity expression were monitored after VEGF stimulation in lung endothelial cells. nmMYLK promoter activity was assessed using nmMYLK promoter luciferase reporter constructs with a series of nested deletions. nmMYLK transcriptional regulation was further characterized by examination of a key transcriptional factor. nmMLCK plays an important role in VEGFinduced permeability. We found that activation of the VEGF signaling pathway in lung endothelial cells increases MYLK gene product at both mRNA and protein levels. Increased nmMLCK mRNA and protein expression is a result of increased nmMYLK promoter activity, regulated in part by binding of the Sp1 transcription factor on triggering by the VEGF signaling pathway. Taken together, these findings suggest that MYLK is an important ARDS candidate gene and a therapeutic target that is highly influenced by excessive VEGF concentrations in the inflamed lung.

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A novel method to develop highly specific models for regulatory units detects a new LTR in GenBank which contains a functional promoter

Cited by 97 publications

References 43 publications

Modular Activation of Nuclear Factor-κB Transcriptional Programs in Human Diabetic Nephropathy

Modular Activation of Nuclear Factor-κB Transcriptional Programs in Human Diabetic Nephropathy

Human intestine luminal ACE2 and amino acid transporter expression increased by ACE-inhibitors

Sp1‐Mediated Nonmuscle Myosin Light Chain Kinase Expression and Enhanced Activity in Vascular Endothelial Growth Factor–Induced Vascular Permeability

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