Disease relevance of FIM3

• The human homologues of Fim1, Fim2/c-Fms, and Fim3, three retroviral integration regions involved in mouse myeloblastic leukemias, are respectively located on chromosomes 6p23, 5q33, and 3q27 [1].
• Three mouse genomic domains, Fim1, Fim2, and Fim3, were previously described as proviral integration regions frequently involved in the early stages of myeloblastic leukemogenesis induced in vivo or in vitro by the Friend murine leukemia virus [1].
• Activation of the expression of the Evi-1 gene is frequently found in murine myeloid leukemias and leukemia cell lines and is due to retroviral insertions in the 5' region of the gene in either the Evi-1 or the CB-1/FIM3 common sites of viral integrations [2].
• Since B. pertussis fimbriae show weak serological cross-reactivity, the differences in primary structure in the heparin binding regions of Fim2, Fim3, and FimX may affect antibody binding but not heparin binding, allowing the bacteria to evade antibody-mediated immunity by switching the fimbrial gene expressed [3].

High impact information on FIM3

• A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved [3].
• FIM1 and FIM3 were localized on human chromosomes 6p22.3-p23 and 3q27 respectively [1].
• The chromosomal breakpoint at 3q26 of HNT-34 cell line was located to approximately 200 kb 5' of FIM3 locus and more upstream of the MDS1. which is the same region as that of somatic cell hybrid line H10C [4].

Chemical compound and disease context of FIM3

• Fimbriae (Fim2 and Fim3) purified from B. pertussis were dissociated in 6 M guanidine hydrochloride, pH 10.5, to produce proteins of defined size and to facilitate the production and characterisation of the conjugates [5].

Analytical, diagnostic and therapeutic context of FIM3

• Southern blotting investigations showed that the structure of other single-copy genes, including FIM3, localized near the breakpoints, were not affected by the translocation [6].
• Serotype Fim3 was most frequent during the periods with general vaccination schedules, whereas serotype Fim2 was predominant during the 17-year vaccine-free period [7].
• Epitope mapping the Fim2 and Fim3 proteins of Bordetella pertussis with sera from patients infected with or vaccinated against whooping cough [8].

References