NOD.CB17-Prkdc-scid/J Mouse

Known as: NOD.SCID, NOD/LtSz-Prkdc-scid/J, NOD SCID 
Originally derived by Prochazka et al (1992) at Jackson Laboratories, by crossing a C.B-17 congenic background mouse with the scid mutation to a… (More)
National Institutes of Health

Papers overview

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Highly Cited
2011
Highly Cited
2011
Highly Cited
2011
RATIONALE Transgenic Notch reporter mice express enhanced green fluorescent protein in cells with C-promoter binding factor-1… (More)
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Highly Cited
2008
Highly Cited
2008
OBJECTIVES To investigate a B-cell-depleting strategy to reverse diabetes in naïve NOD mice. RESEARCH DESIGN AND METHODS We… (More)
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Highly Cited
2008
Highly Cited
2008
OBJECTIVE Glucagon-like peptide-1 (GLP-1) and gastrin promote pancreatic beta-cell function, survival, and growth. Here, we… (More)
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2008
2008
Studies have suggested a correlation between the decline in infectious diseases and increase in the incidence of type 1 diabetes… (More)
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2006
2006
On the basis of on the marked inhibitory activity of the vitamin D receptor agonist Elocalcitol on basal and growth factor… (More)
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Highly Cited
2005
Highly Cited
2005
Internal tandem duplication mutations of the FLT3 gene (FLT3/ITD mutations) are the most frequent molecular abnormality in acute… (More)
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Highly Cited
2003
Highly Cited
2003
Vascular endothelial growth factor (VEGF) and its receptors (VEGFR) have been implicated in promoting solid tumor growth and… (More)
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Highly Cited
2001
Highly Cited
2001
An increasing number of studies have documented the central role of T cell costimulation in autoimmunity. Here we show that the… (More)
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Highly Cited
1995
Highly Cited
1995
The scid mutation was backcrossed ten generations onto the NOD/Lt strain background, resulting in an immunodeficient stock (NOD… (More)
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