Effects of ENU dosage on mouse strains

Justice, Monica J.; Carpenter, Donald A.; Favor, Jack; Neuhäuser-Klaus, A.; Angelis, Martin Hrabé de; Soewarto, Dian; Moser, Amy R.; Cordes, Sabine P.; Miller, Darla R.; Chapman, Verne M.; Weber, John; Rinchik, Eugene M.; Hunsicker, Patricia R.; Russell, William D.; Bode, Vernon C.

doi:10.1007/s003350010094

Cited by 132 publications

(79 citation statements)

References 23 publications

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“…A total of 71 mice have been injected by this procedure, and 61 of them have survived. This rate compares favorably with what has been reported in the literature for this procedure (Justice et al, 2000). We had proposed to inject 180 mice over the 3-year period of the grant, and we therefore have one-third of this number now available.…”

Section: Bodysupporting

confidence: 81%

A Search for Mutations that Affect Susceptibility to Breast Cancer

Gasser¹

2002

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Section: Bodysupporting

confidence: 81%

A Search for Mutations that Affect Susceptibility to Breast Cancer

Gasser¹

2002

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“…Mouse mutagenesis, screening, and mapping G3 animals were generated according to the protocol of Justice et al (14). Blood samples were collected from all G3 animals and samples were stained for the expression of cell surface markers characteristic of T cell, B cell, monocyte, and neutrophil lineages.…”

Section: Methodsmentioning

confidence: 99%

A Novel Mutation in CD83 Results in the Development of a Unique Population of CD4+ T Cells

Garcı́a-Martı́nez

Appleby

Staehling‐Hampton

et al. 2004

The Journal of Immunology

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Using a mouse mutagenesis screen, we have identified CD83 as being critical for the development of CD4+ T cells and for their function postactivation. CD11c+ dendritic cells develop and function normally in mice with a mutated CD83 gene but CD4+ T cell development is substantially reduced. Additionally, we now show that those CD4+ cells that develop in a CD83 mutant animal fail to respond normally following allogeneic stimulation. This is at least in part due to an altered cytokine expression pattern characterized by an increased production of IL-4 and IL-10 and diminished IL-2 production. Thus, in addition to its role in selection of CD4+ T cells, absence of CD83 results in the generation of cells with an altered activation and cytokine profile.

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“…A-T base pair substitutions and/or small intragenic lesions. Many of the mutant offspring produced by ENU-treated mice will, therefore, be hypomorph (partial loss of function), although gain-of-function as well as complete lossof-function mutants can also be expected (57,58). Several studies have demonstrated that the number of induced mutations depends on the dosage of ENU administered (59,60) and on the number of exons and length of coding sequences (61).…”

Section: Mutagenesis Screenmentioning

confidence: 99%

EJE Prize 2013: Regulation of aldosterone secretion: from physiology to disease

Beuschlein

2013

European Journal of Endocrinology

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Arterial hypertension is a major cardiovascular risk factor that affects between 10 and 40% of the population in industrialized countries. Primary aldosteronism (PA) is the most common form of secondary hypertension with an estimated prevalence of around 10% in referral centers and 4% in a primary care setting. Despite its high prevalence until recently, the underlying genetic and molecular basis of this common disease had remained largely obscure. Over the past decade, a number of insights have been achieved that have relied on in vitro cellular systems, wild-type and genetically modified in vivo models, as well as clinical studies in well-characterized patient populations. This progress has been made possible by a number of independent technical developments including that of specific hormone assays that allow measurement in small sample volumes as well as genetic techniques that enable high-throughput sequencing of a large number of samples. Furthermore, animal models have provided important insights into the physiology of aldosterone regulation that have served as a starting point for investigation of mechanisms involved in autonomous aldosterone secretion. Finally, national and international networks that have built up registries and biobanks have been instrumental in fostering translational research endeavors in PA. Therefore, it is to be expected that in the near future, further pathophysiological mechanisms that result in autonomous aldosterone secretion will be unraveled. European Journal of Endocrinology 168 R85-R93

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Effects of ENU dosage on mouse strains

Cited by 132 publications

References 23 publications

A Search for Mutations that Affect Susceptibility to Breast Cancer

A Search for Mutations that Affect Susceptibility to Breast Cancer

A Novel Mutation in CD83 Results in the Development of a Unique Population of CD4+ T Cells

EJE Prize 2013: Regulation of aldosterone secretion: from physiology to disease

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