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Relevant bibliographies by topics / DHCR24/Seladin-1

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Journal articles

Academic literature on the topic 'DHCR24/Seladin-1'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "DHCR24/Seladin-1"

1

Kuehnle, Katrin, Arames Crameri, Roland E. Kälin, et al. "Prosurvival Effect of DHCR24/Seladin-1 in Acute and Chronic Responses to Oxidative Stress." Molecular and Cellular Biology 28, no. 2 (2007): 539–50. http://dx.doi.org/10.1128/mcb.00584-07.

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ABSTRACT DHCR24/seladin-1, a crucial enzyme in sterol synthesis, is of lower abundance in brain areas affected by Alzheimer's disease. While high levels of DHCR24/seladin-1 exert antiapoptotic function by conferring resistance against oxidative stress, the molecular mechanism for this protective effect is not fully understood. Here we show that DHCR24/seladin-1 expression is up-regulated in an acute response and down-regulated in a chronic response to oxidative stress. High levels of DHCR24/seladin-1 were associated with elevated cholesterol concentrations and a general increase in cholesterol

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2

Battista, Marie-Claude, Claude Roberge, Antoine Martinez, and Nicole Gallo-Payet. "24-Dehydrocholesterol Reductase/Seladin-1: A Key Protein Differentially Involved in Adrenocorticotropin Effects Observed in Human and Rat Adrenal Cortex." Endocrinology 150, no. 9 (2009): 4180–90. http://dx.doi.org/10.1210/en.2009-0410.

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Abstract DHCR24 (24-dehydrocholesterol reductase), or seladin-1, is one of the most expressed genes in the adrenal gland. Because the rat and human adult adrenal cortex differ in their respective functional properties, the aim of the present study was to verify whether seladin-1 may be differentially involved in basal and ACTH-stimulated steroidogenesis and oxidative stress management. Seladin-1 expression was predominantly observed in both human and rat zona fasciculata, with a predominant cytoplasmic localization in human cells and a nucleo-cytoplasmic distribution in rat cells. In human fas

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3

Battista, Marie-Claude, Marie-Odile Guimond, Claude Roberge, et al. "Inhibition of DHCR24/Seladin-1 impairs cellular homeostasis in prostate cancer." Prostate 70, no. 9 (2010): 921–33. http://dx.doi.org/10.1002/pros.21126.

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4

Martiskainen, Henna, Kaisa M. A. Paldanius, Teemu Natunen, et al. "DHCR24 exerts neuroprotection upon inflammation-induced neuronal death." Journal of Neuroinflammation 14, no. 1 (2017): 215. https://doi.org/10.1186/s12974-017-0991-6.

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<strong>Background: </strong>DHCR24, involved in the de novo synthesis of cholesterol and protection of neuronal cells against different stress conditions, has been shown to be selectively downregulated in neurons of the affected brain areas in Alzheimer's disease.<strong>Methods: </strong>Here, we investigated whether the overexpression of DHCR24 protects neurons against inflammation-induced neuronal death using co-cultures of mouse embryonic primary cortical neurons and BV2 microglial cells upon acute neuroinflammation. Moreover, the effects of DHCR24 overexpression on dendritic spine densit

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5

Fuller, Peter J., Maria Alexiadis, Tom Jobling, and Jane McNeilage. "Seladin-1/DHCR24 expression in normal ovary, ovarian epithelial and granulosa tumours." Clinical Endocrinology 63, no. 1 (2005): 111–15. http://dx.doi.org/10.1111/j.1365-2265.2005.02308.x.

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6

Bonaccorsi, Lorella, Paola Luciani, Gabriella Nesi, et al. "Androgen receptor regulation of the seladin-1/DHCR24 gene: altered expression in prostate cancer." Laboratory Investigation 88, no. 10 (2008): 1049–56. http://dx.doi.org/10.1038/labinvest.2008.80.

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7

Zerenturk, Eser J., Ika Kristiana, Saloni Gill, and Andrew J. Brown. "The endogenous regulator 24(S),25-epoxycholesterol inhibits cholesterol synthesis at DHCR24 (Seladin-1)." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1821, no. 9 (2012): 1269–77. http://dx.doi.org/10.1016/j.bbalip.2011.11.009.

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8

Cecchi, C., F. Rosati, A. Pensalfini та ін. "Seladin-1/DHCR24 protects neuroblastoma cells against Aβ toxicity by increasing membrane cholesterol content". Journal of Cellular and Molecular Medicine 12, № 5b (2008): 1990–2002. http://dx.doi.org/10.1111/j.1582-4934.2008.00216.x.

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9

Giannini, S., S. Benvenuti, P. Luciani, et al. "Intermittent high glucose concentrations reduce neuronal precursor survival by altering the IGF system: the involvement of the neuroprotective factor DHCR24 (Seladin-1)." Journal of Endocrinology 198, no. 3 (2008): 523–32. http://dx.doi.org/10.1677/joe-07-0613.

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The exposure of neurons to high glucose concentrations is considered a determinant of diabetic neuropathy, whereas members of the IGF system are neurotropic factors. Here, we investigated the effects of constant and intermittent high glucose concentrations on IGF1 and IGF-binding proteins (IGFBPs) in human neuroblast long-term cell cultures fetal neuroepithelial cells (FNC). These cells express the IGF1 receptor, and express and release in the culture medium IGFBP2, IGFBP4, and IGF1. The release of IGF1 was significantly increased by 17β-estradiol (10 nM). IGF1 (100 nM) treatment determined a

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10

Wang, Yongjun, Pamela M. Rogers, Keith R. Stayrook, et al. "The Selective Alzheimer's Disease Indicator-1 Gene (Seladin-1/DHCR24) Is a Liver X Receptor Target Gene." Molecular Pharmacology 74, no. 6 (2008): 1716–21. http://dx.doi.org/10.1124/mol.108.048538.

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