Disease relevance of H13

• Hepatitis C virus core protein: carboxy-terminal boundaries of two processed species suggest cleavage by a signal peptide peptidase [1].
• Resistance to murine 402AX teratocarcinoma: regulation by H-2IA and H-3 to H-13 region genes [2].
• Evidence from laboratory studies indicates that 3-nitropropionic acid produced by the fungus Arthrinium Spp. is the etiological factor of this food poisoning [3].
• Severe magnesium deficiency protects mice against infections by Plasmodium Spp. and Babesia hylomysci which invade mature erythrocytes [4].

High impact information on H13

• Minors held by majors: the H13 minor histocompatibility locus defined as a peptide/MHC class I complex [5].
• By expression cloning, we identified the H13 locus, a classical minor H locus first detected 30 years ago by the trait of graft rejection [5].
• Psl3 maps near D1Mit511 on distal chromosome 1 [6].
• The structures show that the basis of TCRs to distinguish self from nonself H13 peptides is their ability to distinguish a single solvent-exposed methyl group [7].
• How H13 histocompatibility peptides differing by a single methyl group and lacking conventional MHC binding anchor motifs determine self-nonself discrimination [7].

Biological context of H13

• These results suggest that ERR and H13 genes play an important role in cellular proliferation [8].
• (iv) H13 gene expression decreases upon terminal differentiation of the human promyelocytic leukemia cell line HL-60 into granulocytes or macrophages by dimethyl sulfoxide or PMA, respectively [8].
• The R13 peptide sequence (EEEDDDMGFGLFD) that corresponds to the C-terminal region of Trypanosoma cruzi ribosomal P1 and P2 proteins differs from the eukariotic P consensus sequence EESDDDMGFGLFD (H13) only in a nonconservative amino acid substitution [9].

Anatomical context of H13

• H60 immunodominance was an inherent quality, overcoming a lower memory precursor frequency compared with that of H13 and evoking a T cell response with diverse TCRV beta usage [10].
• In strains of mice that normally do not exhibit audiogenic seizures, H13/04 retarded the accumulation of 5-HTP in the telencephalon, diencephalon and brainstem and enhanced the accumulation DOPA in the diencephalon and brainstem [11].
• The known SPP isoform, which we renamed SPPalpha, contains an endoplasmic reticulum retention signal at the carboxy terminus [12].
• Variation in intramembranous particle distribution in the cell membrane of the sperm head of the plains rat and western chestnut mouse (Pseudomys Spp.) [13].
• Test skin allografts enjoy prolonged survival when alloantigenic pretreatment (implants of small fragments of liver or kidney on the host's kidney cortex) is separated from test grafting by 9 days and donor and host strains differ only at the relatively weak H-3 + H-13 histocompatibility barrier (Baldwin and Cohen 1971, 1974) [14].

Associations of H13 with chemical compounds

• Free OP efficiently blocked binding of the antibodies to C3a, whereas binding of another anti-C3a mAb (H13) remained unaffected [15].
• The audiogenic seizure-inducing drug H13/04 was found to elicit opposing effects on the in vivo accumulation of 5-HTP (5-hydroxytryptophan) and DOPA (3,4-dihydroxyphenylalanine) in the brain following inhibition of L-amino acid decarboxylase [11].
• The present study examined the effect of H13/04 on intracellular storage, release, and metabolism of serotonin (5-HT) and noradrenaline (NA) in vitro in order to differentiate between the primary effects of the drug and possible secondary effects due to neurotransmitter interaction [16].

Regulatory relationships of H13

• H13/04 was subsequently shown to competitively inhibit tryptophan hydroxylase [16].

Other interactions of H13

• B6dom1 did not block responses to the subdominant mHAgs H3 and H13 [17].

Analytical, diagnostic and therapeutic context of H13

• The mouse H13 minor histocompatibility (H) Ag, originally detected as a barrier to allograft transplants, is remarkable in that rejection is a consequence of an extremely subtle interchange, P4(Val/Ile), in a nonamer H2-D(b)-bound peptide [7].
• Since the immunization with R13 peptide coupled to a carrier protein like OVA would break the tolerance to a self-sequence and generate autoantibodies, we characterized the antibodies induced in mice by R13 immunization, analyzing by ELISA their capacity to bind to R13 and the self-sequence H13 [9].
• Application of flow cytometry and microscopical methods to characterize the effect of herbal drugs on Leishmania Spp [18].

References