Search Results for: Kevan Herold returned 12 results

NOD-scid
RRID:IMSR_JAX:001303
From Jackson Labs: Mice homozygous for the severe combined immune deficiency spontaneous mutation Prkdcscid, commonly referred to as scid, are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Prkdcscid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. In general, Prkdcscid leakiness is low on the NOD/ShiLtSz genetic background.

NOD
RRID:IMSR_JAX:001976
From Jackson Labs: The NOD/ShiLtJ strain (commonly called NOD) is a polygenic model for autoimmune type 1 diabetes. Diabetes in NOD mice is characterized by hyperglycemia and insulitis, a leukocytic infiltration of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. A 2017 phenotyping study found that 90% of females and 52% of males became diabetic by 30 weeks; median female incidence was 18 weeks. Immune phenotypes in the NOD background consist of defects in antigen presentation, T lymphocyte repertoire, NK cell function, macrophage cytokine production, wound healing, and C5 complement. These defects make the NOD background a common choice for immunodeficient mouse strains. Diabetes onset data is available.

MIP-GFP (line 1)
RRID:IMSR_JAX:006864
From Jackson Labs: These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the control of the mouse insulin 1 promoter. Fluorescence is detected in pancreatic beta-cells from embryonic day (E)13.5 through adulthood. This mutant mouse strain may be useful in studies of diabetes and pancreatic beta islet cell biology.

NOD.MIP-GFP
RRID:IMSR_JAX:005282
From Jackson Labs: These MIP-GFP mice express a transgene containing a fusion gene joining enhanced green fluorescent protein to a fragment of the human growth hormone 1. Homozygotes develop diabetes by 9 weeks of age.

Methylation profiling of insulin DNA in response to proinflammatory cytokines during the progression of autoimmune diabetes in NOD mice

B6 ob
RRID:IMSR_JAX:000632
From Jackson Labs: Mice homozygous for the obese spontaneous mutation, Lepob (commonly referred to as ob or ob/ob), exhibit obesity, hyperphagia, transient hyperglycemia, glucose intolerance, and elevated plasma insulin. They are also hypometabolic, hypothermic, and subfertile. Wound healing is impaired and hormone production from both pituitary and adrenal glands is increased. This strain is used to model phases I and II of diabetes type II and obesity. Obesity is characterized by an increase in the number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice.

Goat anti-Mouse IgM (Heavy chain) Cross-Adsorbed Secondary Antibody, Alexa Fluor™ 488
RRID:AB_2535711

Goat anti-Rabbit IgG (H+L) Cross-Adsorbed Secondary Antibody, Alexa Fluor™ 647
RRID:AB_2535812

GCK Polyclonal Antibody
RRID:AB_10863656

Goat Anti-Human Antibody
RRID:AB_2795643

Goat Anti-Mouse IgM Antibody
RRID:AB_92481

Anti-Citrulline Antibody
RRID:AB_305485
DISCONTINUED.

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