Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Major histocompatibility complex-encoded antigen processing gene polymorphism in IDDM

P M van Endert1, R S Liblau, S D Patel

  • 1Department of Microbiology, Stanford University School of Medicine, CA 94305-5402.

Diabetes
|January 1, 1994
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Elevated levels of interleukin-12/23p40 may serve as a potential indicator of dysfunctional heart rate variability in type 2 diabetes.

Cardiovascular diabetology·2022
Same author

miRNA-27a-3p and miRNA-222-3p as Novel Modulators of Phosphodiesterase 3a (PDE3A) in Cerebral Microvascular Endothelial Cells.

Molecular neurobiology·2019
Same author

'25-Hydroxyvitamin D, Autoantigenic and Total Antibody Concentrations: Results from a Danish Case-control Study of Newly Diagnosed Patients with Childhood Type 1 Diabetes and their Healthy Siblings'.

Scandinavian journal of immunology·2017
Same author

Genetic markers for glutamic acid decarboxylase do not predict insulin-dependent diabetes mellitus in pairs of affected siblings.

Human genetics·2016
Same author

Increased mortality in a Danish cohort of young people with Type 1 diabetes mellitus followed for 24 years.

Diabetic medicine : a journal of the British Diabetic Association·2016
Same author

The genetic control of immune responses.

Immunology today·2014
Same journal

Females Are Completely Resistant to Semaglutide-Induced Muscle Loss in ob/ob Mice.

Diabetes·2026
Same journal

Ketone Bodies Derived From Medium-Chain Triglycerides Support Brain Metabolism and Function Under Hypoglycemia in Type 1 Diabetes Mellitus.

Diabetes·2026
Same journal

Targeting the ADA/ADO Axis Rescues β-Cell Failure in Type 2 Diabetes.

Diabetes·2026
Same journal

TXNIP Is Positioned as a Key Mediator of Hyperglycemia-Induced Vascular Senescence.

Diabetes·2026
Same journal

Sex Differences in ER Stress Pathways Are a Key Determinant of β-Cell Proliferation and Resilience.

Diabetes·2026
Same journal

The Mechanism of TNF-α Combined With High Glucose in Regulating Calnexin Aggravates Endoplasmic Reticulum Stress in Endothelial Cell Injury of Diabetic Retinopathy.

Diabetes·2026
See all related articles

Genetic variations in Transporter Associated with Antigen Processing (TAP) and Large Multifunctional Protease (LMP) genes are not linked to insulin-dependent diabetes mellitus (IDDM) susceptibility. Studies found no association between TAP and LMP gene polymorphisms and IDDM risk in Danish populations.

Area of Science:

  • Immunogenetics
  • Molecular Biology
  • Endocrinology

Background:

  • Insulin-dependent diabetes mellitus (IDDM) susceptibility is strongly linked to human leukocyte antigen (HLA) class II gene polymorphisms.
  • The potential involvement of nearby genes in IDDM pathogenesis remains under investigation.
  • Transporter Associated with Antigen Processing (TAP) and Large Multifunctional Protease (LMP) genes, located in the HLA class II region, are candidates due to their role in antigen presentation.

Purpose of the Study:

  • To investigate the association between polymorphisms in the LMP2, TAP1, and TAP2 genes and susceptibility to IDDM.
  • To determine if TAP and LMP gene variations contribute to IDDM pathogenesis.

Main Methods:

  • Genomic and coding sequence polymorphisms of LMP2, TAP1, and TAP2 genes were analyzed.

Related Experiment Videos

  • A cohort of 77 Danish IDDM patients and 102 healthy control subjects were studied.
  • Allelic frequencies were compared between patients and controls, and analyzed in relation to HLA DR types.
  • Main Results:

    • No significant differences were observed in TAP1 and LMP2 allele frequencies between IDDM patients and controls.
    • A notable absence of the TAP2 allele B (long form) was found in IDDM patients.
    • Further analysis indicated this absence was likely due to linkage disequilibrium with HLA DR types, not a direct association.

    Conclusions:

    • Polymorphisms in TAP and LMP genes are unlikely to be directly associated with IDDM susceptibility.
    • The observed TAP2 allele pattern is attributed to genetic linkage with HLA loci.
    • This study suggests that TAP and LMP genes do not play a significant role in IDDM pathogenesis through direct genetic association.