“…Among these, there are several non-class I genes that structurally belong to a variety of families (10,11). One of these genes is the human HLA-F adjacent transcript 10 (FAT10) gene.…”
mentioning
confidence: 99%
“…One of these genes is the human HLA-F adjacent transcript 10 (FAT10) gene. This gene encodes a diubiquitin-like (UBD) protein containing two tandem head-to-tail ubiquitin-like domains that are substantially different from those of other members of the ubiquitin family (2,7,10). There are few reports on FAT10 in the literature, and we have a very limited understanding of its biological role.…”
The FAT10 gene encodes a diubiquitin-like protein containing two tandem head-to-tail ubiquitin-like domains. There is a high degree of similarity between murine and human FAT10 sequences at both the mRNA and protein levels. In various cell lines, FAT10 expression was shown to be induced by gamma interferon or by tumor necrosis factor alpha. In addition, FAT10 expression was found to be up-regulated in some Epstein-Barr virus-infected B-cell lines, in activated dendritic cells, and in several epithelial tumors. However, forced expression of FAT10 in cultured cells was also found to produce apoptotic cell death. Overall, these findings suggest that FAT10 may modulate cellular growth or cellular viability. Here we describe the steps to generate, by genetic targeting, a FAT10 gene knockout mouse model. The FAT10 knockout homozygous mice are viable and fertile. No gross lesions or obvious histological differences were found in these mutated mice. Examination of lymphocyte populations from spleen, thymus, and bone marrow did not reveal any abnormalities. However, flow cytometry analysis demonstrated that the lymphocytes of FAT10 knockout mice were, on average, more prone to spontaneous apoptotic death. Physiologically, these mice demonstrated a high level of sensitivity toward endotoxin challenge. These findings indicate that FAT10 may function as a survival factor.
“…Among these, there are several non-class I genes that structurally belong to a variety of families (10,11). One of these genes is the human HLA-F adjacent transcript 10 (FAT10) gene.…”
mentioning
confidence: 99%
“…One of these genes is the human HLA-F adjacent transcript 10 (FAT10) gene. This gene encodes a diubiquitin-like (UBD) protein containing two tandem head-to-tail ubiquitin-like domains that are substantially different from those of other members of the ubiquitin family (2,7,10). There are few reports on FAT10 in the literature, and we have a very limited understanding of its biological role.…”
The FAT10 gene encodes a diubiquitin-like protein containing two tandem head-to-tail ubiquitin-like domains. There is a high degree of similarity between murine and human FAT10 sequences at both the mRNA and protein levels. In various cell lines, FAT10 expression was shown to be induced by gamma interferon or by tumor necrosis factor alpha. In addition, FAT10 expression was found to be up-regulated in some Epstein-Barr virus-infected B-cell lines, in activated dendritic cells, and in several epithelial tumors. However, forced expression of FAT10 in cultured cells was also found to produce apoptotic cell death. Overall, these findings suggest that FAT10 may modulate cellular growth or cellular viability. Here we describe the steps to generate, by genetic targeting, a FAT10 gene knockout mouse model. The FAT10 knockout homozygous mice are viable and fertile. No gross lesions or obvious histological differences were found in these mutated mice. Examination of lymphocyte populations from spleen, thymus, and bone marrow did not reveal any abnormalities. However, flow cytometry analysis demonstrated that the lymphocytes of FAT10 knockout mice were, on average, more prone to spontaneous apoptotic death. Physiologically, these mice demonstrated a high level of sensitivity toward endotoxin challenge. These findings indicate that FAT10 may function as a survival factor.
“…In humans, M-OR genes are located on nearly all chromosomes (Rouquier et al 1998b), and a few M-OR loci in close linkage to the HLA-F locus were described several years ago (Fan et al 1995;Gruen et al 1996). We have recently demonstrated that at least 36 OR genes, two of them of the V1-OR type and the rest M-OR loci, are located in the immediate vicinity of the HLA-F locus in one major and one minor cluster (Younger et al 2000;Ziegler et al 2000a).…”
“…Analyses of cDNAs homologous to HLA class I region clones have yielded a substantial wealth of new sequences for investigation (14)(15). Genomic analysis of the HLA-B and -C region covering over 237 kb has been carried out, yielding a more precise description of the gene content of this region (16).…”
We report here the genomic sequence of the centromeric portion of HLA class I, extending 424,015 bp from tumor necrosis factor ␣ to a newly identified gene Ϸ20 kb telomeric of Otf-3. As a source of DNA, we used cosmids centromeric of HLA-B that had been mapped previously with conventional restriction digestion and fingerprinting and previously characterized yeast artificial chromosomes subcloned into cosmids and mapped with multiple complete digest methodologies. The data presented provide a description of the gene content of centromeric HLA class I including new data on intron, promoter and f lanking sequences of previously described genes, and a description of putative new genes that remain to be characterized beyond the structural information uncovered. A complete accounting of the repeat structure including abundant di-, tri-, and tetranucleotide microsatellite loci yielded access to precisely localized mapping tools for the major histocompatibility complex. Comparative analysis of a highly polymorphic region between HLA-B and -C was carried out by sequencing over 40 kb of overlapping sequence from two haplotypes. The levels of variation observed were much higher than those seen in other regions of the genome and indeed were higher than those observed between allelic HLA class I loci.
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