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propose that HIV-1 infectivity might depend both on the amounts of HLA-C molecules and on their stability as trimeric complex. According to this model, individuals with low-expression HLA-C alleles and unstable binding to beta2m/peptide might have worse control of HIV-1 infection and an intrinsically higher capacity to support viral replication
KIR2DL2/HLA-C( *)12:02 and KIR2DL2/HLA-C( *)14:03 compound genotypes have protective effects on control of HIV-1.
Data establish the C2 allele as a novel genetic risk factor associated with congenital heart block. This observation supports a model in which fetuses with C2 ligand expression and maternal anti-SSA/Ro (显示 TROVE2 ELISA试剂盒) positivity may have impaired NK cell surveillance, resulting in unchecked cardiac inflammation and scarring.
results provide the structural basis for understanding peptide repertoire selection in HLA-C*06:02.
Single-nucleotide polymorphisms FOXF1 rs9936833 and MHC rs9257809 remained significantly associated with presence of gastroesophageal acid reflux. The association for risk allele C in FOXF1 rs9936833 and risk allele A in MHC rs9257809 with the presence of acid reflux suggests a potential pathophysiologic mechanism for the role of genetic influences in Barret Esophagus development.
The minor alleles of rs2395029, rs9264942, and rs3689068 in the HCP5 and HLA-C, and ZNRD1 (显示 ZNRD1 ELISA试剂盒) genes associate with lower viral loads (VL) among antiretroviral-naive individuals and with shorter time to first VL less 51 copies/ml during anti-HIV therapy.
HLA-C*04:01 predisposes to nevirapine-induced Stevens-Johnson syndrome/toxic epidermal necrolysis in , but not to other hypersensitivity phenotypes in a sub-Saharan African HIV-infected population
The HLA-B*42, HLA-C*17, HLA-DPA1*03, and HLA-DPB1*105 genotypes were associated with allergic asthma and the HLA-B*48 genotype with the nonallergic phenotype.
Genotyping analysis revealed that HLA-C2, which provides a ligand for killer-cell immunoglobulin-like receptors (KIR (显示 GEM ELISA试剂盒)) expressed by NK cells, was strongly associated with psoriasis susceptibility. However, no link between the KIR (显示 GEM ELISA试剂盒) genes themselves and disease was found
the signal overall signal that NK cells receive from paternal HLA-C on trophoblasts depends on the ratio of activating and inhibitory KIR (显示 GEM ELISA试剂盒) genes expressed by them
HLA-C belongs to the HLA class I heavy chain paralogues. This class I molecule is a heterodimer consisting of a heavy chain and a light chain (beta-2 microglobulin). The heavy chain is anchored in the membrane. Class I molecules play a central role in the immune system by presenting peptides derived from endoplasmic reticulum lumen. They are expressed in nearly all cells. The heavy chain is approximately 45 kDa and its gene contains 8 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the alpha1 and alpha2 domain, which both bind the peptide, exon 4 encodes the alpha3 domain, exon 5 encodes the transmembrane region, and exons 6 and 7 encode the cytoplasmic tail. Polymorphisms within exon 2 and exon 3 are responsible for the peptide binding specificity of each class one molecule. Typing for these polymorphisms is routinely done for bone marrow and kidney transplantation. Over one hundred HLA-C alleles have been described
HLA class I histocompatibility antigen, C alpha chain
, HLA class I histocompatibility antigen, Cw-1 alpha chain
, MHC class I antigen heavy chain HLA-C
, human leukocyte antigen-C alpha chain
, major histocompatibility antigen HLA-C