Three new HLA class I alleles with synonymous mutations: HLA-A*03:01:62 , -C*07:02:82 and -C*12:03:42

HLA ◽  
2017 ◽  
Vol 91 (1) ◽  
pp. 60-61 ◽  
Author(s):  
M. R. Moya-Quiles ◽  
A. Balas ◽  
M. Muro ◽  
A. M. García-Alonso ◽  
J. L. Vicario
Keyword(s):  
Hla Class I ◽  
Class I ◽  
Synonymous Mutations

scholarly journals Transcriptional and Posttranscriptional Regulations of theHLA-GGene

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Erick C. Castelli ◽  
Luciana C. Veiga-Castelli ◽  
Layale Yaghi ◽  
Philippe Moreau ◽  
Eduardo A. Donadi
Keyword(s):  
Promoter Region ◽  
Hla Class I ◽  
Regulatory Elements ◽  
Class I ◽  
Proximal Promoter ◽  
Null Alleles ◽  
Gene Control ◽  
Coding Region ◽  
Synonymous Mutations ◽  
Classical Class

HLA-Ghas a relevant role in immune response regulation. The overall structure of theHLA-Gcoding region has been maintained during the evolution process, in which most of its variable sites are synonymous mutations or coincide with introns, preserving major functionalHLA-Gproperties. TheHLA-Gpromoter region is different from the classical class I promoters, mainly because (i) it lacks regulatory responsive elements for IFN-γand NF-κB, (ii) the proximal promoter region (within 200 bases from the first translated ATG) does not mediate transactivation by the principal HLA class I transactivation mechanisms, and (iii) the presence of identified alternative regulatory elements (heat shock, progesterone and hypoxia-responsive elements) and unidentified responsive elements for IL-10, glucocorticoids, and other transcription factors is evident. At least three variable sites in the 3′ untranslated region have been studied that may influenceHLA-Gexpression by modifying mRNA stability or microRNA binding sites, including the 14-base pair insertion/deletion, +3142C/G and +3187A/G polymorphisms. Other polymorphic sites have been described, but there are no functional studies on them. TheHLA-Gcoding region polymorphisms might influence isoform production and at least two null alleles with premature stop codons have been described. We reviewed the structure of theHLA-Gpromoter region and its implication in transcriptional gene control, the structure of theHLA-G3′UTR and the major actors of the posttranscriptional gene control, and, finally, the presence of regulatory elements in the coding region.

62-W: Correlations of molecular modeling predictions with serologic reactivity of new HLA class I alleles with non-synonymous mutations

2007 ◽  
Vol 68 (1) ◽  
pp. S132
Author(s):  
Medhat Askar ◽  
Edward Ball ◽  
Dawn Thomas ◽  
Paul Kawczak ◽  
Ray Jurcago ◽  
...  
Keyword(s):  
Molecular Modeling ◽  
Hla Class I ◽  
Class I ◽  
Synonymous Mutations

scholarly journals Evidence for reduced selection pressure on the hepatitis B virus core gene in hepatitis B e antigen-negative chronic hepatitis B

2011 ◽  
Vol 92 (8) ◽  
pp. 1800-1808 ◽  
Author(s):  
Brook G. Warner ◽  
Peter Tsai ◽  
Allen G. Rodrigo ◽  
Malakai ‘Ofanoa ◽  
Edward J. Gane ◽  
...  
Keyword(s):  
Hepatitis B ◽  
Selection Pressure ◽  
Hla Class I ◽  
Core Gene ◽  
Class I ◽  
Positive Selection Pressure ◽  
Synonymous Mutations ◽  
B Virus ◽  
Chronic Hbv ◽  
Negative Chronic Hepatitis

The mechanisms underlying the high levels of hepatitis B virus (HBV) replication that cause hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (e−CHB) are unknown. Impaired anti-HBV immunity, which may be measurable as a relaxation of selection pressure on the virus, is possible. A group of Tongans (n = 345) with a chronic HBV infection, including seven with e−CHB, were genotyped at HLA class I. The repertoire of HBV core-gene codons under positive selection pressure was defined by phylogenetic analysis (by using the paml program) of 708 cloned sequences extracted from the 67 of these 345 subjects with the same repertoire of HLA class I alleles as the seven e−CHB individuals and matched controls (see below). The frequency of non-synonymous mutations at these codons was measured in longitudinal data from 15 subjects. Finally, the number of non-synonymous mutations at these codons was compared in seven groups comprised of one subject with e−CHB and 1–3 HLA class I-matched controls with an inactive, HBeAg-negative chronic HBV infection (e−InD). Nineteen codons in the core gene were under positive selection pressure. There was a high frequency of new non-synonymous mutations at these codons (P<0.0001) in longitudinal data. The mean number of these 19 codons with non-synonymous mutations was lower (P = 0.02) in HBV from subjects with e−CHB (4.4±0.5 codons per subject) versus those with e−InD (6.4±0.4 codons per subject). There is a subtle relaxation in selection pressure on the HBV core gene in e−CHB. This may be due to impaired antiviral immunity, and could contribute to the high levels of viral replication that cause liver inflammation in this disease.

scholarly journals Mass spectrometry based immunopeptidomics leads to robust predictions of phosphorylated HLA class I ligands

2019 ◽  
Author(s):  
Marthe Solleder ◽  
Philippe Guillaume ◽  
Julien Racle ◽  
Justine Michaux ◽  
HuiSong Pak ◽  
...  
Keyword(s):  
Human Leukocyte ◽  
Hla Class I ◽  
Class I ◽  
Immune Recognition ◽  
Post Translational Modifications ◽  
Synonymous Mutations ◽  
Alternative Mrna Splicing ◽  
Phosphorylated Peptides ◽  
Specific Alternative

AbstractThe presentation of peptides on class I human leukocyte antigen (HLA-I) molecules plays a central role in immune recognition of infected or malignant cells. In cancer, non-self HLA-I ligands can arise from many different alterations, including non-synonymous mutations, gene fusion, cancer-specific alternative mRNA splicing or aberrant post-translational modifications. Identifying HLA-I ligands remains a challenging task that requires either heavy experimental work for in-vivo identification or optimized bioinformatics tools for accurate predictions. To date, no HLA-I ligand predictor includes post-translational modifications. To fill this gap, we curated phosphorylated HLA-I ligands from several immunopeptidomics studies (including six newly measured samples) covering 72 HLA-I alleles, and retrieved a total of 2,066 unique phosphorylated peptides. We then expanded our motif deconvolution tool to identify precise binding motifs of phosphorylated HLA-I ligands. Our results reveal a clear enrichment of phosphorylated peptides among HLA-C ligands and demonstrate a prevalent role of both HLA-I motifs and kinase motifs on the presentation of phosphorylated peptides. This data further enabled us to develop and validate the first predictor of interactions between HLA-I molecules and phosphorylated peptides.

scholarly journals Mass Spectrometry Based Immunopeptidomics Leads to Robust Predictions of Phosphorylated HLA Class I Ligands

2019 ◽  
Vol 19 (2) ◽  
pp. 390-404 ◽  
Author(s):  
Marthe Solleder ◽  
Philippe Guillaume ◽  
Julien Racle ◽  
Justine Michaux ◽  
Hui-Song Pak ◽  
...  
Keyword(s):  
Human Leukocyte ◽  
Hla Class I ◽  
Class I ◽  
Immune Recognition ◽  
Post Translational Modifications ◽  
Synonymous Mutations ◽  
Alternative Mrna Splicing ◽  
Phosphorylated Peptides ◽  
Specific Alternative

The presentation of peptides on class I human leukocyte antigen (HLA-I) molecules plays a central role in immune recognition of infected or malignant cells. In cancer, non-self HLA-I ligands can arise from many different alterations, including non-synonymous mutations, gene fusion, cancer-specific alternative mRNA splicing or aberrant post-translational modifications. Identifying HLA-I ligands remains a challenging task that requires either heavy experimental work for in vivo identification or optimized bioinformatics tools for accurate predictions. To date, no HLA-I ligand predictor includes post-translational modifications. To fill this gap, we curated phosphorylated HLA-I ligands from several immunopeptidomics studies (including six newly measured samples) covering 72 HLA-I alleles and retrieved a total of 2,066 unique phosphorylated peptides. We then expanded our motif deconvolution tool to identify precise binding motifs of phosphorylated HLA-I ligands. Our results reveal a clear enrichment of phosphorylated peptides among HLA-C ligands and demonstrate a prevalent role of both HLA-I motifs and kinase motifs on the presentation of phosphorylated peptides. These data further enabled us to develop and validate the first predictor of interactions between HLA-I molecules and phosphorylated peptides.

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