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Mouse models of diabetic nephropathy.
TLDR
This interim report and an online supplement detail the progress made toward a complete murine model of human diabetic kidney disease and the critical analysis of existing murine models, which substantially enhances the understanding of this disease process. Expand
B lymphocytes are critical antigen-presenting cells for the initiation of T cell-mediated autoimmune diabetes in nonobese diabetic mice.
TLDR
B lymphocytes appear to contribute to IDDM in NOD mice as APC with a preferential ability to present certain beta cell Ags such as GAD to autoreactive T cells. Expand
Hyperproinsulinaemia in obese fat/fat mice associated with a carboxypeptidase E mutation which reduces enzyme activity
TLDR
The fat mutation represents the first demonstration of an obesity–diabetes syndrome elicited by a genetic defect in a prohormone processing pathway. Expand
The NOD mouse model of type 1 diabetes: As good as it gets?
TLDR
The authors re-examine the value of this mouse model as a tool for understanding human diabetes and for testing potential therapies, reviewing both strengths and weaknesses. Expand
The family of toxin‐related ecto‐ADP‐ribosyltransferases in humans and the mouse
TLDR
The position‐sensitive iterative database search program PSI‐BLAST connected the mammalian ARTs with most known bacterial ADP‐ribosylating toxins, suggesting that the two enzyme families that catalyze reversible mono‐ADP‐ ribosylation either were lost from the genomes of these nonchordata eucaryotes or were subject to horizontal gene transfer between kingdoms. Expand
B lymphocytes are essential for the initiation of T cell-mediated autoimmune diabetes: analysis of a new "speed congenic" stock of NOD.Ig mu null mice
TLDR
B lymphocytes play a heretofore unrecognized role that is essential for the initial development and/or activation of beta cell autoreactive T cells in NOD mice. Expand
Interleukin 4 reverses T cell proliferative unresponsiveness and prevents the onset of diabetes in nonobese diabetic mice
TLDR
The ability of rIL-4 to reverse completely the NOD thymic and peripheral T cell proliferative defect in vitro and protect against diabetes in vivo provides further support for a causal relationship between this T cell Proliferative unresponsiveness and susceptibility to diabetes in NOD mice. Expand
NIT-1, a pancreatic beta-cell line established from a transgenic NOD/Lt mouse.
TLDR
Northern-blot analysis confirmed high levels of insulin mRNA but only trace glucagon mRNA and undetectable somatostatin mRNA and IFN-gamma induction of intercellular adhesion molecule 1 (Icam-1) transcripts was not accompanied by demonstrable cell surface expression of ICAM-1 antigen. Expand
The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency.
TLDR
It is proposed that the unusual features of T-cell ontogeny characteristic of the NOD inbred strain synergize with the scid-imparted block in thymocyte development, leading to activation of theNOD-unique Emv-30 to initiate thymomagenesis. Expand
Use of recombinant congenic and congenic strains of NOD mice to identify a new insulin-dependent diabetes resistance gene
TLDR
This analysis shows the utility of RCS and congenic stocks for the identification and isolation of non-MHC genes with strong antidiabetogenic functions in NOD/Lt mice. Expand
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