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Mice, Inbred NOD

Inbred NOD (non-obese diabetic) mice are a widely used animal model for type 1 diabetes research.
These mice spontaneously develop autoimmune diabetes, making them a valuable tool for studying the immunological and genetic factors involved in disease pathogenesis.
The NOD mouse strain is characterized by progressive insulitis, leading to destruction of pancreatic beta cells and the onset of hyperglycemia.
Researchers leverage these mice to investigate novel therapeutic interventions, as well as to explore the underlying mechanisms of autoimmune processes.
This MeSH term provides a concise overview of the key features and applications of inbred NOD mice in biomedical research.

Most cited protocols related to «Mice, Inbred NOD»

Differentiation and Characterization of Midbrain Dopaminergic Neurons

Human ESC (H9, H1) and iPSC lines (2C6 and SeV6) were subjected to a modified dual SMAD-inhibition^{13 (link)} based FP induction^{12 (link)} protocol. Exposure to SHH C25II, Purmorphamine, FGF8 and CHIR99021 were optimized for midbrain FP and DA neuron yield (see Figure 1d). Following FP induction, further maturation was carried out in Neurobasal/B27 medium supplemented with AA, BDNF, GDNF, TGFβ3 and dbcAMP (see full methods for details). The resulting DA neurons were subjected to extensive phenotypic characterization via immunocytochemistry, qRT-PCR, gene expression profiling, HPLC analysis for DA and in vitro electrophysiological recordings. In vivo studies were performed in 6-hydroxydopamine lesioned, hemiparkinsonian rodents (adult NOD-SCID IL2Rgc mice and Sprague Dawley rats) as well as in two adult rhesus monkeys treated with carotid injections of MPTP. DA neurons were injected stereotactically in the striata of the animals (150 × 10³ cells in mice, 250 × 10³ cells in rats) and a total of 7.5 × 10⁶ cells (distributed in 6 tracts; 3 on each side of brain) in monkeys. Behavioral assays were performed at monthly intervals post grafting, including amphetamine mediated rotational analysis as well as a test for focal akinesia (“stepping test”) and forelimb use (cylinder test). Rats and mice were sacrificed at 18–20 weeks and the primates at 1 month post grafting. Characterization of the grafts was performed via stereological analyses of cell numbers and graft volumes and comprehensive immunohistochemistry.

Kriks S., Shim J.W., Piao J., Ganat Y.M., Wakeman D.R., Xie Z., Carrillo-Reid L., Auyeung G., Antonacci C., Buch A., Yang L., Beal M.F., Surmeier D.J., Kordower J.H., Tabar V, & Studer L. (2011). Floor plate-derived dopamine neurons from hESCs efficiently engraft in animal models of PD. Nature, 480(7378), 547-551.

Publication 2011

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Adult Amphetamine Animals Biological Assay Brain Bucladesine Carotid Arteries Cells Chir 99021 FGF8 protein, human Forelimb Glial Cell Line-Derived Neurotrophic Factor Grafts High-Performance Liquid Chromatographies Homo sapiens Hydroxydopamine Immunocytochemistry Immunohistochemistry Induced Pluripotent Stem Cells Macaca mulatta Mesencephalon Mice, Inbred NOD Monkeys Mus Neurons Phenotype Primates purmorphamine Rats, Sprague-Dawley Rattus Rodent SCID Mice Step Test Striatum, Corpus

Proteomic Profiling of TCGA Tumor Samples

All tumor samples for the current study were obtained through the TCGA Biospecimen Core Resource (BCR) as described previously^{6 (link)}. No other selection criteria other than availability were applied for this study. Patient-derived xenograft tumors from established Basal and Luminal-B breast cancer intrinsic subtypes ^{37 (link), 38 (link)} were raised subcutaneously in 8 week old NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice (Jackson Labs, Bar Harbor, Maine) as previously described^{39 (link), 40 (link)}. Normal colon biopsies were obtained from screening colonoscopies performed between July 2006 and October 2010 under Vanderbilt University IRB approval #061096.
Tissue proteins were extracted and tryptic peptide digests were analyzed by multidimensional liquid chromatography-tandem mass spectrometry. Xenograft QC samples were run after every 5 colorectal tumor samples. Raw data were processed for peptide identification by database and spectral library searching and identified peptides were assembled as proteins and mapped to gene identifiers for proteogenomic comparisons. Quantitative proteomic comparisons were based on spectral count data. Detailed descriptions of the samples, LC-MS/MS analysis, and data analysis methods can be found in Supplementary Methods. All of the primary mass spectrometry data on TCGA tumor samples are deposited at the CPTAC Data Coordinating Center as raw and mzML files and complete protein assembly datasets for public access (https://cptac-data-portal.georgetown.edu).

Zhang B., Wang J., Wang X., Zhu J., Liu Q., Shi Z., Chambers M.C., Zimmerman L.J., Shaddox K.F., Kim S., Davies S.R., Wang S., Wang P., Kinsinger C.R., Rivers R.C., Rodriguez H., Townsend R.R., Ellis M.J., Carr S.A., Tabb D.L., Coffey R.J., Slebos R.J, & Liebler D.C. (2014). Proteogenomic characterization of human colon and rectal cancer. Nature, 513(7518), 382-387.

Publication 2014

Biopsy Breast Carcinoma cDNA Library Colon Colonoscopy Colorectal Neoplasms Heterografts Liquid Chromatography Mass Spectrometry Mice, Inbred NOD Neoplasms Patients Peptides Phenobarbital Proteins Tandem Mass Spectrometry Tissues Trypsin

Lineage Tracing of Pancreatic Tumor Models

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Publication 2012

Abdomen Alleles Animals Anophthalmia with pulmonary hypoplasia Ascites Carcinoma Cells Ceruletide Dehydration Dexamethasone Disease Progression fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether Hypertrophy Mice, Inbred NOD Mice, Laboratory Neoplasms Pancreas Pancreatitis Pathologists PDX1 protein, human SCID Mice Strains Sulfoxide, Dimethyl Transplantation

Generation of FoxP3-GFP-hCre BAC Transgenic Mice

The GFP-hCre cDNA fragment was inserted immediately downstream of the FoxP3 ATG translational start site by homologous recombination into a 188-kb mouse BAC (from the C57BL/6 genome; clone RP23-143D8) carrying the intact FoxP3 gene, as previously described (29 (link)). We used a codon-optimized “humanized” Cre (hCre) to improve translational efficiency in eukaryotic cells. An EGFP-hcre-Frt-Neo-Frt cassette was provided by N. Killeen (UCSF, San Francisco, CA). The modified BAC was purified using cesium chloride gradient ultracentrifugation and microinjected by the UCSF Transgenic/Targeted Mutagenesis Core Facility into the pronuclei of nonobese diabetic mouse embryos to generate FoxP3-GFP-hCre BAC Tg mice. Mice carrying the GFP-hCre transgene were screened by FACS analysis using peripheral blood cells. Several founder mice were generated and screened for GFP expression and lack of functional FoxP3 protein, as indicated by an inability of the transgene to rescue the FoxP3 KO mice. Dicer^lox/lox (14 (link)) mice and ROSA26R-YFP reporter mice (16 (link)) have been previously described. All mice were housed and bred under specific pathogen-free conditions at the UCSF Animal Barrier Facility. All animal experiments were approved by the Institutional Animal Care and Use Committee of UCSF.

Zhou X., Jeker L.T., Fife B.T., Zhu S., Anderson M.S., McManus M.T, & Bluestone J.A. (2008). Selective miRNA disruption in T reg cells leads to uncontrolled autoimmunity. The Journal of Experimental Medicine, 205(9), 1983-1991.

Publication 2008

Animals Animals, Transgenic Blood Cells cesium chloride Clone Cells Codon DNA, Complementary Embryo Eukaryotic Cells Genes Genome Homologous Recombination Institutional Animal Care and Use Committees Mice, Inbred NOD Mice, Laboratory Mutagenesis Protein Biosynthesis Proteins Specific Pathogen Free Transgenes Ultracentrifugation

Passive Transfer Arthritis Model in Mice

Mice carrying the KRN T cell receptor transgene (25 (link)) on the C57BL/6 genetic background were mated with NOD mice to obtain KRN transgene-positive offsprings on the C57BL/6 × NOD F1 genetic background (K/B×N mice) as well as their transgene-negative (B×N) littermates. The presence of the transgene was determined by flow cytometry as well as by looking for visible signs of arthritis in the K/B×N mice. Blood was taken by retroorbital bleeding and sera from transgene-positive and transgene-negative mice were pooled separately.
Arthritis was induced by intraperitoneal injection of 400 µl of arthritogenic (K/B×N) or control serum into WT or PLCγ2^−/− bone marrow chimeras or intact (nonchimeric) mice, followed by daily assessment of arthritis development for 2 wk. Visible clinical signs of arthritis were scored on a 0–10 scale by two investigators blinded for the origin and treatment of the mice. Ankle thickness was measured by a spring-loaded caliper (Kroeplin). For histological analysis, mice were killed 4 d after serum transfer and their ankle joints were fixed in formalin (Sigma-Aldrich). The joints were then decalcified, embedded in paraffin, sectioned, and stained with hematoxylin and eosin (Histopathology Llc.). Photomicrographs were taken on a microscope (DMI 6000B; Leica).
To assess articular function, mice were placed on a custom-made wire grid (Charles River Laboratories) with identical wire thickness and spacing to a regular wire cage lid. The wire grid was flipped upside down and the length of time the mice held on to the grid was recorded. This test was performed three times daily during the period of 8–12 d after the serum injection. The obtained data were combined into holding-on curves similar to Kaplan-Meier survival curves.

Jakus Z., Simon E., Frommhold D., Sperandio M, & Mócsai A. (2009). Critical role of phospholipase Cγ2 in integrin and Fc receptor-mediated neutrophil functions and the effector phase of autoimmune arthritis. The Journal of Experimental Medicine, 206(3), 577-593.

Publication 2009

ARID1A protein, human Arthritis BLOOD Bone Marrow Chimera Eosin Flow Cytometry Formalin Genetic Background Injections, Intraperitoneal Joints Joints, Ankle Lanugo Mice, Inbred NOD Mice, Laboratory Mice, Transgenic Microscopy Paraffin Embedding Phospholipase C gamma 2 Photomicrography Rivers Serum T-Cell Receptor Transgenes

Most recents protocols related to «Mice, Inbred NOD»

LXR Agonist Inhibits Breast Cancer Growth

Not available on PMC !

Example 23

We have demonstrated that LXR agonists inhibit in vitro cancer progression phenotypes in breast cancer, pancreatic cancer, and renal cancer. To investigate if LXR agonist treatment inhibits breast cancer primary tumor growth in vivo, mice injected with MDA-468 human breast cancer cells were treated with either a control diet or a diet supplemented with LXR agonist GW3965 2 (FIG. 36).

To determine the effect of orally delivered GW3965 2 on breast cancer tumor growth, 2×106 MDA-468 human breast cancer cells were resuspended in 50 μL PBS and 50 μL matrigel and the cell suspension was injected into both lower memory fat pads of 7-week-old Nod Scid gamma female mice. The mice were assigned to a control diet treatment or a GW3965-supplemented diet treatment (75 mg/kg/day) two days prior to injection of the cancer cells. The GW3965 2 drug compound was formulated in the mouse chow by Research Diets, Inc. Tumor dimensions were measured using digital calipers, and tumor volume was calculated as (small diameter)²×(large diameter)/2.

Treatment with GW3965 resulted in significant reduction in breast cancer tumor size in vivo (FIG. 36).

US11865094B2. Treatment and diagnosis of melanoma (2024-01-09). The Rockefeller University [US]. Inventors: Sohail Tavazoie [US], Nora Pencheva [US].

Patent 2024

agonists Breast Carcinoma Breast Neoplasm Cancer of Kidney Cardiac Arrest Cells Diet Disease Progression Drug Compounding Fingers Gamma Rays GW 3965 Malignant Neoplasm of Breast Malignant Neoplasms Mammary Carcinoma, Human matrigel Memory Mice, Inbred NOD Mus Neoplasms Pad, Fat Pancreatic Cancer Phenotype SCID Mice Woman

GABA Enhances IL-2 Reversal of T1D

Not available on PMC !

Example 5

Cotreatment with GABA Enhances the Ability of IL-2 to Reverse T1D.

Treatment with IL-2 has been shown to have a modest ability to reverse hyperglycemia in newly diabetic NOD mice. We now have data showing that administration of IL-2 with GABA can enhance its therapeutic effect, and more efficiently reverse hyperglycemia. In the FIG. 11, only one of three newly diabetic NOD mice treated with IL-2 became normoglycemic (blood glucose below 250 mgs/dl) (individual mice represented by black symbols). In contrast two of two newly diabetic mice treated with IL-2+GABA became normoglycemic (open symbols).

It is understood that the examples and embodiments described herein are for illustrative purposes only and that various modifications or changes in light thereof will be suggested to persons skilled in the art and are to be included within the spirit and purview of this application and scope of the appended claims. All publications, patents, and patent applications cited herein are hereby incorporated by reference in their entirety for all purposes.

US11872200B2. GABA agonists in the treatment of disorders associated with metabolic syndrome and GABA combinations in treatment or prophylaxis of type I diabetes (2024-01-16). The Regents of the University of California [US]. Inventors: Daniel L Kaufman [US], Jide Tian [US].

Patent 2024

Blood Glucose Combined Modality Therapy GABA Agonists gamma Aminobutyric Acid Hyperglycemia Light Metabolic Syndrome X Mice, Inbred NOD Mus Therapeutic Effect

Cryptosporidium parvum Infection Model

Not available on PMC !

Example 51

The NOD SCID gamma mouse model of chronic, asymptomatic C. parvum infection was used to test in vivo compound efficacy. NOD SCID gamma mice were infected with ˜1×10⁵C. parvum oocysts by oral gavage 5-7 days after weaning. The infected animals begin shedding oocysts in the feces 1 week after infection, which is measured by quantitative PCR (qPCR). Based on experience with the positive control compound paromomycin, four mice are required per experimental group to achieve 80% power to detect an 80% percent reduction in parasite shedding after four days of drug compound. In additional to the experimental drug regimen groups, additional negative (gavage with DMSO/methylcellulose carrier) and positive (paromomycin 2000 mg/kg once daily) control groups are included in each experiment. Mice are infected 5-7 days after weaning (day −6), infection is confirmed 1 week later (day 0), and experimental compounds are dosed by oral gavage on days 1-4. The dosing frequency was as indicated. Treatment efficacy was assessed by measurement of fecal oocyst shedding by qPCR on day 5.

US11866441B2. Compounds and methods for the treatment of parasitic diseases (2024-01-09). THE BROAD INSTITUTE, INC. [US], PRESIDENT AND FELLOWS OF HARVARD COLLEGE [US]. Inventors: Eamon Comer [US], Nobutaka Kato [US], Marshall Morningstar [US], Bruno Melillo [US].

Patent 2024

Animals Asymptomatic Infections Biological Assay Chronic Infection Drug Compounding Feces Gamma Rays Infection Investigational New Drugs Methylcellulose Mice, Inbred NOD Mus Oocysts Parasites Paromomycin SCID Mice Sulfoxide, Dimethyl Treatment Protocols Tube Feeding

Assessing PRDM16 Impact on Pancreatic Cancer

For the soft agar assay, cell culture dishes (p60) were first prepared using complete DMEM media containing 0.6% agarose (#16500500; Thermo Fisher Scientific) and allowed to solidify at room temperature for 2 h. Then, cells suspended in complete DMEM media containing 0.3% agarose were added to the dishes preloaded with the 0.6% agarose layer. PANC-1 and BxPC-3 stably expressing control or PRDM16 gRNA were plated at a density of 1,000 cells per dish and grown for ∼2 mo. Within this time frame, PANC-1 isogenic cell lines developed small but similar colonies in size, whereas neither of the BXPC-3 isogenic cell lines developed colonies. Colonies were visualized and counted using an Olympus CKX53 microscope with the UPlanFL N 4×/0.13 iPC objective.
For the cell proliferation assay, isogenic PANC-1 (50,000 cells/well) and BxPC-3 (100,000 cells/well) cell lines stably expressing control or PRDM16 gRNA were inoculated into 6-well plates. Three (for PANC-1) and six (for BxPC-3) days after inoculation, cells were trypsinized and mixed with equal volumes of trypan blue (#T10282; Invitrogen) before being counted using an automatic cell counter (#AMQAF2000; Invitrogen Countess 3 FL). Each well was counted twice and averaged to ensure accurate cell counts were obtained.
For the in vivo growth assay, NOD scid gamma (NSG) mice were injected subcutaneously with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA (106 cells) under septic conditions. During the observation period of ∼2 mo, mice were maintained in sterile conditions and sacrificed if they displayed any symptoms of illness. At the end of the observation period, tumors were dissected, weighted, and imaged using a 12-megapixel f/1.8 aperture camera.

Hurwitz E., Parajuli P., Ozkan S., Prunier C., Nguyen T.L., Campbell D., Friend C., Bryan A.A., Lu T.X., Smith S.C., Razzaque M.S., Xu K, & Atfi A. (2023). Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer. The Journal of Cell Biology, 222(4), e202203036.

Publication 2023

Agar Biological Assay Cell Culture Techniques Cell Lines Cell Proliferation Cells Gamma Rays Hyperostosis, Diffuse Idiopathic Skeletal MEL1S protein, human Mice, Inbred NOD Microscopy Mus Neoplasms Reading Frames SCID Mice Sepharose Sepsis Sterility, Reproductive Trypan Blue Vaccination

Generation of HNSCC Patient-Derived Xenografts

To generate the HNSCC PDX, the human HNSCC tissues were obtained without patient information from the Peking University School and Hospital of Stomatology. The tumor tissues were cut into small pieces, followed by implantation into the flanks of NOD-SCID mice (6 weeks old), according to a previously described method [8 (link)]. HNSCC specimens from 60 patients were obtained from the Peking University School and Hospital of Stomatology from September 2012 to October 2016. The inclusion criteria were as follows: 1) the tumor was in the tongue; 2) there was no distant metastasis; 3) removal of the primary carcinoma and neck dissection without preoperative radiotherapy or chemotherapy; and 4) patients who underwent postoperative follow-up for at least five years. Without conducting a pathological study, the clinical TNM staging approach was used to classify the tumor size and clinical stage for the 40 HNSCC samples among the 60 samples: 1) tumor size limited in T2 and T3; 2) clinically negative cervical lymph node (cN0); and 3) no distant metastasis (M0). Based on the histopathologic evaluation of the lymph nodes, these 40 patients were split into lymph node-negative and positive groups. These experiments were approved by the Institutional Review Board of the Peking University School and Hospital of Stomatology and all samples were obtained from patients who signed informed consent forms approving the use of their tissues for research purposes after surgery (Approval number: PKUSSIRB-2012010). The tissues were snap-frozen and placed at −80 °C until analysis.

Qin Z., Zhang W., Liu S., Wang Y., Peng X, & Jia L. (2023). PVT1 inhibition stimulates anti-tumor immunity, prevents metastasis, and depletes cancer stem cells in squamous cell carcinoma. Cell Death & Disease, 14(3), 187.

Publication 2023

Carcinoma Ethics Committees, Research Freezing Homo sapiens Mice, Inbred NOD Neck Neck Dissection Neoplasm Metastasis Neoplasms Nodes, Lymph Ovum Implantation Patients Pharmacotherapy Radiotherapy SCID Mice Squamous Cell Carcinoma of the Head and Neck Tissues Tongue

Top products related to «Mice, Inbred NOD»

Nod scid mice by Charles River Laboratories

Sourced in China, Japan, United States, Italy, Germany, France, Canada, United Kingdom

NOD/SCID mice are a strain of genetically engineered mice that lack a functional immune system. They are commonly used in biomedical research as a model for studying human diseases and evaluating the efficacy of therapeutic interventions.

Matrigel by BD

Sourced in United States, United Kingdom, Germany, China, Canada, Japan, Italy, France, Belgium, Australia, Uruguay, Switzerland, Israel, India, Spain, Denmark, Morocco, Austria, Brazil, Ireland, Netherlands, Montenegro, Poland

Matrigel is a solubilized basement membrane preparation extracted from the Engelbreth-Holm-Swarm (EHS) mouse sarcoma, a tumor rich in extracellular matrix proteins. It is widely used as a substrate for the in vitro cultivation of cells, particularly those that require a more physiologically relevant microenvironment for growth and differentiation.

Nod scid mice by Jackson ImmunoResearch

Sourced in United States, Montenegro

NOD/SCID mice are a strain of immunodeficient mice commonly used in biomedical research. They have a severe combined immunodeficiency (SCID) mutation and lack functional T and B cells, as well as a mutation in the NOD background that impairs innate immune cells. This combination of genetic defects results in a highly immunocompromised phenotype, which makes NOD/SCID mice a valuable tool for the study of human cells and diseases.

Nod scid gamma mice by Jackson ImmunoResearch

Sourced in United States, Montenegro

NOD scid gamma (NSG) mice are an immunodeficient mouse model developed by Jackson ImmunoResearch. These mice lack mature T cells, B cells, and natural killer cells, making them a valuable tool for research involving human cell and tissue transplantation.

Matrigel by Corning

Sourced in United States, China, Germany, United Kingdom, Canada, Japan, France, Netherlands, Montenegro, Switzerland, Austria, Australia, Colombia, Spain, Morocco, India, Azerbaijan

Matrigel is a complex mixture of extracellular matrix proteins derived from Engelbreth-Holm-Swarm (EHS) mouse sarcoma cells. It is widely used as a basement membrane matrix to support the growth, differentiation, and morphogenesis of various cell types in cell culture applications.

Nod mice by Jackson ImmunoResearch

Sourced in United States, Montenegro, France

NOD mice, also known as non-obese diabetic mice, are a strain of laboratory mice that are used in research related to type 1 diabetes. These mice develop spontaneous autoimmune diabetes, similar to the human condition, making them a valuable model for studying the underlying mechanisms and potential treatments for the disease.

Female nod scid mice by Charles River Laboratories

Sourced in China, Japan, Italy, United States

Female NOD/SCID mice are a strain of immunodeficient rodents developed for use in biomedical research. These mice lack functional T cells, B cells, and natural killer cells, making them useful for the study of human cell and tissue engraftment.

Nod cg prkdcscid il2rgtm1wjl szj mice by Jackson ImmunoResearch

Sourced in Montenegro, United States

The NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mouse is a laboratory animal model. It is a severely immunodeficient strain that lacks mature T cells, B cells, and natural killer cells.

Nod shiltj mice by Jackson ImmunoResearch

Sourced in United States, Montenegro

The NOD/ShiLtJ mouse is a strain of laboratory mice that is commonly used in research. These mice have a genetic background that makes them susceptible to developing type 1 diabetes. They can be used as a model to study the underlying mechanisms of this autoimmune disease.

Nod shiltj by Jackson ImmunoResearch

Sourced in United States, Montenegro

The NOD/ShiLtJ is a mouse strain developed for research purposes. It serves as an animal model for type 1 diabetes and other autoimmune disorders. The strain is maintained by Jackson ImmunoResearch for scientific investigations.

More about "Mice, Inbred NOD"

Inbred NOD (non-obese diabetic) mice are a widely used animal model in biomedical research, particularly for studying type 1 diabetes.
These mice spontaneously develop autoimmune diabetes, making them a valuable tool for investigating the immunological and genetic factors involved in disease pathogenesis.
The NOD mouse strain is characterized by progressive insulitis, leading to the destruction of pancreatic beta cells and the onset of hyperglycemia.
Researchers leverage these mice to explore novel therapeutic interventions and the underlying mechanisms of autoimmune processes.
The NOD/SCID mouse is another important model, which lacks functional T and B cells, making it useful for studying the role of the immune system in disease development.
Similarly, the NOD scid gamma (NSG) mouse, a derivative of the NOD/SCID strain, is commonly used in immunology research due to its severely compromised immune system.
In addition to the standard NOD mice, researchers may also use female NOD/SCID mice or the NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ strain, which have unique characteristics that make them suitable for certain applications.
The NOD/ShiLtJ mouse, a substrain of the NOD mouse, is another variant that is often used in diabetes research.
These inbred mouse models, along with related strains like the NOD/SCID and NSG mice, have become indispensable tools in the field of type 1 diabetes research.
Researchers can utilize these mice to investigate the pathogenesis of the disease, test novel therapies, and gain valuable insights into the underlying mechanisms of autoimmunity.
Matrigel, a basement membrane extract, is also commonly used in studies involving these mouse models to provide a more physiologically relevant environment for cell growth and tissue formation.
By leveraging the insights and capabilities of these inbred mouse models, researchers can accelerate the development of new treatments and deepen our understanding of the complex processes involved in type 1 diabetes and other autoimmune disorders.