John F. Öhd
Lund University
18 Papers
142 Citations
John F. Öhd is an academic researcher from Lund University. The author has contributed to research in topics: Receptor & Apoptosis. The author has an hindex of 10, co-authored 18 publications. Previous affiliations of John F. Öhd include Malmö University.
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Papers
The leukotriene receptor CysLT1 and 5-lipoxygenase are upregulated in colon cancer.
Christian Kamp-Nielsen,John F. Öhd,Katarina Wikström,Ramin Massoumi,Sailaja Paruchuri,Maria Juhas,Anita Sjölander +6 more
- 01 Jan 2003
TL;DR: The results demonstrate that these leukotrienes can suppress the NS-398 induced apoptosis in intestinal cells and this effect could be prevented by LTD4 or LTB4.
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The Leukotriene Receptor CYSLT1 And 5- Lipoxygenase Are Upregulated In Colon Cancer
Christian Kamp Nielsen,John F. Öhd,Katarina Wikström,Ramin Massoumi,Sailaja Paruchuri,Maria Juhas,Anita Sjölander +6 more
TL;DR: In this article, leukotrienes were used to suppress the NS-398 induced apoptosis in colon cancer cells, which was shown to suppress colorectal cancer cells.
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Regulation of leukotriene-dependent induction of cyclooxygenase-2 and Bcl-2.
TL;DR: It is found that LTD(4) induced a 3-fold elevation of COX-2 transcription in Int 407 cells and a 2-fold equivalent in colon cancer cells, Caco-2, and this was mediated through a pertussis toxin sensitive G-protein and the MAP kinase Erk-1/2 pathway, which pointed towards the existence of negative feedback regulation.
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Leukotriene D4-Induced Activation and Translocation of the G-Protein αi3-Subunit in Human Epithelial Cells
TL;DR: Findings imply that the Gi3-protein is the pertussis-toxin-sensitive G-protein previously found to mediate several downstream LTD4-stimulated signalling events, and indicate that the cytoskeleton might participate in the signalling process of human epithelial cells.
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Pro-inflammatory mediator leukotriene D4 induces transcriptional activity of potentially oncogenic genes.
TL;DR: It is demonstrated that following LTD4 stimulation, beta-catenin is translocated to the nucleus, triggering the transcriptional activity of the TCF (T-cell factor)/LEF (lymphoid enhancer factor) family of transcription factors, dependent on phosphoinositide-3 kinase activation and glycogen synthase kinase inhibition.
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