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Your search keyword '"Van Seuningen, I."' showing total 268 results
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268 results on '"Van Seuningen, I."'

1. Metabolite biomarker discovery for pancreatic neuroendocrine tumors using metabolomic approach

Author

Jannin, A., primary, Dessein, A.F., additional, Dabo, S., additional, Descat, A., additional, Vantyghem, M.C., additional, Chevalier, B., additional, Cardot-Bauters, C., additional, El Amrani, M., additional, Dominguez, S., additional, Marciniak, C., additional, Van Seuningen, I., additional, Do Cao, C., additional, Jonckheere, N., additional, and Coppin, L., additional

Published
2023
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3. Analysis of the proximal promoter of the human colon-specific B4GALNT2 (Sda synthase) gene:B4GALNT2 is transcriptionally regulated by ETS1

Author

Wavelet-Vermuse, C. (Cindy), Groux, S. (Sophie), Vicogne, D. (Dorothee), Cogez, V. (Virginie), Venturi, G. (Giulia), Trinchera, M. (Marco), Brysbaert, G. (Guillaume), Krzewinski, M-A. (Marie-Ange), Hadj Bachir, E. (Elsa), Schulz, C. (Celine), Vincent, A. (Audrey), Van Seuningen, I. (Isabelle), Harduin Lepers, A. (Anne), Université de Lille, CNRS, Unité de Glycobiologie Structurale et Fonctionnelle (UGSF) - UMR 8576, Miniaturisation pour la Synthèse, l'Analyse et la Protéomique (MSAP) - USR 3290, and Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]

Subjects
Transcriptional regulation, Core promoter, ETS1, Colon, B4GALNT2
Abstract

Background: The Sda antigen and corresponding biosynthetic enzyme B4GALNT2 are primarily expressed in normal colonic mucosa and are down-regulated to a variable degree in colon cancer tissues. Although their expression profile is well studied, little is known about the underlying regulatory mechanisms. Methods: To clarify the molecular basis of Sda expression in the human gastrointestinal tract, we investigated the transcriptional regulation of the human B4GALNT2 gene. The proximal promoter region was delineated using luciferase assays and essential trans-acting factors were identified through transient overexpression and silencing of several transcription factors. Results: A short cis-regulatory region restricted to the −72 to +12 area upstream of the B4GALNT2 short-type transcript variant contained the essential promoter activity that drives the expression of the human B4GALNT2 regardless of the cell type. We further showed that B4GALNT2 transcriptional activation mostly requires ETS1 and to a lesser extent SP1. Conclusions: Results presented herein are expected to provide clues to better understand B4GALNT2 regulatory mechanisms. 1864;11-12

Published
2021

18. Gènes MUC : une superfamille de gènes ? Vers une classification fonctionnelle des apomucines humaines

Author

Séverine Nollet, Pierre Degand, Nicole Porchet, J.P. Aubert, Pascal Pigny, Marie-Pierre Buisine, Anne Laine, Jean-Luc Desseyn, Nicolas Moniaux, and Van Seuningen I

Subjects
Genetics, Gene isoform, chemistry.chemical_classification, Aging, Mucin, Nucleic acid sequence, Cell Biology, Biology, Homology (biology), chemistry, Gene expression, Human genome, Glycoprotein, Gene
Abstract

The MUC genes encode epithelial mucins. Eight different human genes have been well characterized, and two others identified more recently. Among them, a family of four genes, expressed in the respiratory and digestive tracts, is clustered to chromosome 11p15.5; and these genes encode gel-forming mucins which are structurally related to the superfamily of cystine-knot growth factors. A second group is composed of three independent genes encoding various isoforms of mucins including membrane-bound mucins associated to carcinomas. In this second group, MUC3 and MUC4 encode large apomucins containing EGF-like domains.

Published
1999
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19. Involvement of a Signal Transduction Mechanism in ATP-induced Mucin Release from Cultured Airway Goblet Cells

Author

Van-Seuningen I, K C Kim, Zheng Qx, and University of Maryland, school of pharmacy

Subjects
Male, Pulmonary and Respiratory Medicine, [SDV]Life Sciences [q-bio], Inositol Phosphates, Clinical Biochemistry, Biology, Pertussis toxin, 03 medical and health sciences, chemistry.chemical_compound, Adenosine Triphosphate, 0302 clinical medicine, GTP-Binding Proteins, Cricetinae, Extracellular, medicine, Animals, Inositol, Phosphatidylinositol, Molecular Biology, ComputingMilieux_MISCELLANEOUS, Cells, Cultured, 030304 developmental biology, 0303 health sciences, Goblet cell, Mesocricetus, Phospholipase C, Mucin, Mucins, Receptors, Purinergic, Cell Biology, 3. Good health, Cell biology, Enzyme Activation, Trachea, medicine.anatomical_structure, chemistry, Biochemistry, Type C Phospholipases, 030220 oncology & carcinogenesis, Signal transduction, Signal Transduction
Abstract

Release of mucins from cultured airway surface epithelial cells can be stimulated by extracellular ATP via a P2-purinergic receptor-mediated mechanism (K. C. Kim and B. C. Lee. 1991. Br. J. Pharmacol. 103:1053-1056). In this report, we studied the mechanism by which extracellular ATP induces the mucin release. We found that: (1) ATP increased both mucin release and generation of inositol phosphates in a dose-dependent fashion, and their dose-effect relationships were almost superimposed; (2) the increases in both mucin release and the phosphatidylinositol phosphate (PI) turnover by extracellular ATP were partially, but almost equally, blocked by the pretreatment with pertussis toxin (42% for mucin release and 44% for PI turnover). We conclude that in cultured airway goblet cells extracellular ATP stimulates mucin release by a signal transduction mechanism, which seems to involve coupling of ATP-activated P2 purinoceptors with phospholipase C, at least in part, via pertussis toxin-sensitive GTP-binding proteins. This may be an important finding in understanding the regulation of mucin release by airway goblet cells, since a number of agents present in the airway could influence this signal transduction pathway and subsequently modulate the mucin secretion.

Published
1993
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22. Mucin muc2 deficiency and weaning influences the expression of the innate defense genes reg3ß, reg3¿ and angiogenin-4

Author

Burger-van Paassen, N., Loonen, L.M.P., Witte-Bouma, J., Korteland-van Male, A.M., de Bruijn, A.C., van der Sluis, M., Lu, P., van Goudoever, J.B., Wells, J., Dekker, J., van Seuningen, I., Renes, I.B., Burger-van Paassen, N., Loonen, L.M.P., Witte-Bouma, J., Korteland-van Male, A.M., de Bruijn, A.C., van der Sluis, M., Lu, P., van Goudoever, J.B., Wells, J., Dekker, J., van Seuningen, I., and Renes, I.B.

Abstract

Background Mucin Muc2 is the structural component of the intestinal mucus layer. Absence of Muc2 leads to loss of this layer allowing direct bacterial-epithelial interactions. We hypothesized that absence of the mucus layer leads to increased expression of innate defense peptides. Specifically, we aimed to study the consequence of Muc2 deficiency (Muc2-/-) on the expression of regenerating islet-derived protein 3 beta (Reg3ß), regenerating islet-derived protein 3 gamma (Reg3¿), and angiogenin-4 (Ang4) in the intestine shortly before and after weaning. Methods Intestinal tissues of Muc2-/- and wild-type (WT) mice were collected at postnatal day 14 (P14, i.e. pre-weaning) and P28 (i.e. post-weaning). Reg3ß, Reg3¿, and Ang4 expression was studied by quantitative real-time PCR, Western-blot, in situ hybridization, and immunohistochemistry. Results Reg3ß and Reg3¿ were expressed by diverging epithelial cell types; namely enterocytes, Paneth cells, and goblet cells. Additionally, Ang4 expression was confined to Paneth cells and goblet cells. Expression of Reg3ß, Reg3¿, and Ang4 differed between WT and Muc2-/- mice before and after weaning. Interestingly, absence of Muc2 strongly increased Reg3ß and Reg3¿ expression in the small intestine and colon. Finally, morphological signs of colitis were only observed in the distal colon of Muc2-/- mice at P28, where and when expression levels of Reg3ß, Reg3¿, and Ang4 were the lowest. Conclusions Expression of Reg3 proteins and Ang4 by goblet cells point to an important role for goblet cells in innate defense. Absence of Muc2 results in up-regulation of Reg3ß and Reg3¿ expression, suggesting altered bacterial-epithelial signaling and an innate defense response in Muc2-/- mice. The inverse correlation between colitis development and Reg3ß, Reg3¿, and Ang4 expression levels might point toward a role for these innate defense peptides in regulating intestinal inflammation

Published
2012

23. Transcript profiling of Elf5+/- mammary glands during pregnancy identifies novel targets of Elf5.

Author

Whitsett, JA, Rogers, RL, Van Seuningen, I, Gould, J, Hertzog, PJ, Naylor, MJ, Pritchard, MA, Whitsett, JA, Rogers, RL, Van Seuningen, I, Gould, J, Hertzog, PJ, Naylor, MJ, and Pritchard, MA

Abstract

BACKGROUND: Elf5, an epithelial specific Ets transcription factor, plays a crucial role in the pregnancy-associated development of the mouse mammary gland. Elf5(-/-) embryos do not survive, however the Elf5(+/-) mammary gland displays a severe pregnancy-associated developmental defect. While it is known that Elf5 is crucial for correct mammary development and lactation, the molecular mechanisms employed by Elf5 to exert its effects on the mammary gland are largely unknown. PRINCIPAL FINDINGS: Transcript profiling was used to investigate the transcriptional changes that occur as a result of Elf5 haploinsufficiency in the Elf5(+/-) mouse model. We show that the development of the mouse Elf5(+/-) mammary gland is delayed at a transcriptional and morphological level, due to the delayed increase in Elf5 protein in these glands. We also identify a number of potential Elf5 target genes, including Mucin 4, whose expression, is directly regulated by the binding of Elf5 to an Ets binding site within its promoter. CONCLUSION: We identify novel transcriptional targets of Elf5 and show that Muc4 is a direct target of Elf5, further elucidating the mechanisms through which Elf5 regulates proliferation and differentiation in the mammary gland.

Published
2010

24. P003 Selective inhibition of eIF2alpha dephosphorylation prevents colitis and shows therapeutic potential in a new model of ulcerative colitis

Author

Treton, X., primary, Pedruzzi, E., additional, Guichard, C., additional, Vallee, M., additional, Sedghi, S., additional, Ladeiro, Y., additional, Montcuquet, N., additional, Freund, J.N., additional, Van Seuningen, I., additional, Barreau, F., additional, Hugot, J.P., additional, Cazals-Hatem, D., additional, Daniel, F., additional, OgierDenis, E., additional, and Bouhnik, Y., additional

Published
2013
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