ArticleProceedings of the National Academy of Sciences of the United States of America2005
A point mutation in the groove of HLA-DO allows egress from the endoplasmic reticulum independent of HLA-DM.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Human Hepatitis B Viral Infection Outcomes Are Linked to Naturally Occurring Variants ofJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Class II MHC antigen processing in immune tolerance and inflammation.Immunogenetics · 2019Review
- Human leukocyte Antigen-DM polymorphisms in autoimmune diseases.Open biology · 2016Review
- pH-susceptibility of HLA-DO tunes DO/DM ratios to regulate HLA-DM catalytic activity.Scientific reports · 2015Article
- HLA-DM and HLA-DO, key regulators of MHC-II processing and presentation.Current opinion in immunology · 2014Review
- The Membrane Associated RING-CH Proteins: A Family of E3 Ligases with Diverse Roles through the Cell.International scholarly research notices · 2014Review
- Major histocompatibility complex class-II molecules promote targeting of human immunodeficiency virus type 1 virions in late endosomes by enhancing internalization of nascent particles from the plasma membrane.Cellular microbiology · 2013Article
- Ubiquitination of HLA-DO by MARCH family E3 ligases.European journal of immunology · 2013Article
- HLA-DO and Its Role in MHC Class II Antigen Presentation.Frontiers in immunology · 2013Review
- Article
- Sibling rivalry: competition between MHC class II family members inhibits immunity.Nature structural & molecular biology · 2013Article
- HLA-DO acts as a substrate mimic to inhibit HLA-DM by a competitive mechanism.Nature structural & molecular biology · 2013Article
- Mapping the HLA-DO/HLA-DM complex by FRET and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Evidence for a human leucocyte antigen-DM-induced structural change in human leucocyte antigen-DObeta.Immunology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B lymphocytes express the nonclassical class II molecule HLA-DO, which modulates the peptide loading activity of HLA-DM in the endocytic pathway. Binding to HLA-DM is required for HLA-DO to egress from the endoplasmic reticulum (ER). To gain insights into the mode of action of DO and on the role of DM in ER release, we sought to identify DM-binding residues on DO. Our results show that DOalpha encompasses the binding site for HLA-DM. More specifically, mutation of residue DOalpha41 on an exposed lateral loop of the alpha1 domain affects the binding to DM, ER egress, and activity of DO. Using a series of chimeric DR/DO molecules, we confirmed the role of the alpha chain and established that a second DM-binding region is located C-terminal to the DOalpha80 residue, most probably in the alpha2 domain. Interestingly, after mutation of a buried proline (alpha11) on the floor of the putative peptide-binding groove, HLA-DO remained functional but became independent of HLA-DM for ER egress and intracellular trafficking. Collectively, these results suggest that the binding of HLA-DM to DOalpha allows the complex to egress from the ER by stabilizing intramolecular contacts between the N-terminal antiparallel beta-strands of the DOalphabeta heterodimer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.