Isolation, expression, and the primary structure of HLA-Cw1 and HLA-Cw2 genes: Evolutionary aspects

Güssow, Detlef; Rein, Reet; Meijer, Inge A.; Hoog, W. De; Seemann, G.; Hochstenbach, Frans; Ploegh, Hidde L.

doi:10.1007/bf00404424

Cited by 147 publications

(37 citation statements)

References 41 publications

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“…These probes display some cross-reactivity at the stringency used (20 mM NaPi, i.e. -0.1 x SSC at 650C) (Gussow et al, 1987) but do allow identification of the bands corresponding to HLA-A, -B and -C genes. The MluI PFG blots give particularly clear results: the strongly hybridizing fragment with the general HLA probe, i.e.…”

Section: Resultsmentioning

confidence: 99%

The chromosome region containing the highly polymorphic HLA class I genes displays limited large scale variability in the human population.

et al. 1988

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The large-scale organization and polymorphism of the HLA class I region was investigated by pulsed field gel (PFG) fractionation of DNA from various HLA-typed cell lines cleaved by different 'rare cutter' restriction enzymes, followed by hybridization with 'general' and locus-specific HLA probes. Results indicate that (i) most HLA class I sequences are contained in a 340 kb MluI DNA fragment which also carries the HLA-A gene; (ii) HLA-A, -B and -C genes are present on different fragments bounded by 'HTF islands' (CpG-rich, unmethylated DNA regions containing multiple sites for 'rare cutter' enzymes) which generally coincide with the 5' regions of expressed genes; and (iii) very little fragment size polymorphism is seen, implying that expansion/contraction events in the HLA class I region due to unequal crossing over (as documented in the mouse class I system) are infrequently found in the human population.

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Section: Resultsmentioning

confidence: 99%

The chromosome region containing the highly polymorphic HLA class I genes displays limited large scale variability in the human population.

et al. 1988

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“…The possible contamination of the tumor samples with factors which could produce a bias towards truncated PCR products was further addressed by an analysis of additional transcripts in the same samples which contained abnormal TSG101 transcripts. RT ± PCR analyses were carried out to examine transcripts of FHIT Sozzi et al, 1996) and b2-microglobulin (Gussow et al, 1987). In contrast to the TSG101 results, only full length transcripts were detected (Figure 4a and b).…”

Section: Tsg101mentioning

confidence: 88%

“…Human b2 microglobulin transcripts were ampli®ed for 37 cycles of 30 s at 958C, 40 s at 568C, 30 s at 728C and ®nal extension of 7 min at 728C. The sequences of the primers were 5'-ATCCAGCGTACTCCAAAGATTCAG-3' and 5'-AAATTGAAAGTTAACTTATGCACGC-3' (Gussow et al, 1987).…”

Section: Rna Extraction and Rt ± Pcrmentioning

confidence: 99%

Frequent abnormalities of TSG101 transcripts in human prostate cancer

et al. 1997

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TSG101 has been identi®ed as a candidate tumor suppressor gene and abnormal transcripts have been identi®ed in a substantial fraction of breast cancers. To determine whether TSG101 expression is commonly altered in other tumors, a series of 15 primary and metastatic prostate cancers were analysed by reverse transcriptase-PCR ampli®cation. Abnormal transcripts with extensive deletions in the coding region were found in nine of these tumors, while only the normal transcript was found in control and benign prostatic hypertrophy tissues. More than one abnormal transcript was found in four of these nine cases and distinct abnormal TSG101 transcripts were found in separate biopsies taken from one tumor. Importantly, the normal TSG101 transcript was undetectable in two metastatic prostate cancers, indicating the absence of TSG101 protein. Sequence analysis demonstrated that there were at least six distinct deletions, with four of these deletions found in more than one tumor sample. The most commonly identi®ed deletion, from bp 153 to 1055, was identical to a deletion reported previously in breast cancer. These results demonstrate that TSG101 transcripts are frequently abnormal in prostate cancer and suggest that loss of TSG101 protein contributes to disease development or progression.

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“…The intactness of total RNA was con®rmed by tight bands of 28S and 18S rRNA separated on denaturing agarose gels and visualized by ethidium bromide staining. The b 2 m primers were designed according to the sequence published (Gussow et al, 1987). The primers of PCR were as follows: b 2 m forward 5'-GGCAGGATCCGAGATGTCTCGCTCCGTGGC (26 ± 55); b 2 m reverse 5'-AAACCTCGAGGATGCTGCTTA-CATGTCTCG (385 ± 416); b-actin forward 5'-CAGAGCAA-GAGAGGCATCCT (216 ± 235); b-actin reverse 5'-TTGAAGGTCTCAAACATGAT (405 ± 424).…”

Section: Rna Isolation and Rt ± Pcrmentioning

confidence: 99%

β2-microglobulin induces apoptosis in HL-60 human leukemia cell line and its multidrug resistant variants overexpressing MRP1 but lacking Bax or overexpressing P-glycoprotein

Rastegar

Gordon

et al. 2001

Oncogene

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In this study, we examined whether exogenous b 2 -microglobulin (b 2 m) can induce apoptosis in the drug sensitive HL-60 leukemia cell line and its drug resistant variants and investigated the molecular mechanism of b 2 m-induced apoptosis. Our data revealed that b 2 m is very signi®cantly down-regulated in two multidrug resistant variants of the HL-60 cells: (a) the MRP1-bearing, Bax-de®cient HL-60/ADR cell line, and (b) the P-glycoprotein (P-gp) overexpressing HL-60/VCR cell line. However, exogenous b 2 m induced similar levels of apoptosis in HL-60 cells and these drug resistant variants. b 2 m-induced apoptosis in HL-60 and HL-60/ VCR cells was associated with decreased mitochondrial membrane potential (Dcm) but did not a ect Dcm in HL-60/ADR cells. Surprisingly, cyclosporin A (CsA), a known inhibitor of the mitochondrial permeability transition (MPT) pore, inhibited b 2 m-induced apoptosis in HL-60/ADR cells but not in HL-60 and HL-60/VCR cells, suggesting that the pro-apoptotic e ect of b 2 m in these cells is not through MPT pore formation. Furthermore, b 2 m induced the release of cytochrome c and the apoptosis-inducing factor (AIF) from mitochondria in HL-60 and HL-60/VCR cells, but not in HL-60/ ADR cells. Additionally, Z-VAD-fmk, a general inhibitor of caspases which inhibited cytochrome c release in HL-60 and HL-60/VCR cells, had no e ect on AIF release in any of these cell lines, but inhibited b 2 m-induced apoptosis in all three cell lines. However, Western blot analysis revealed that caspases-1, -3, -6, -8, and -9 are not activated during b 2 m-induced apoptosis in these cells. Therefore, b 2 m-induces apoptosis through an unknown caspase-dependent mitochondrial pathway in HL-60 and HL-60/VCR cells and by a Bax-independent, nonmitochodrial, caspase-dependent pathway in HL-60/ ADR cells. Oncogene (2001) 20, 7006 ± 7020.

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Isolation, expression, and the primary structure of HLA-Cw1 and HLA-Cw2 genes: Evolutionary aspects

Cited by 147 publications

References 41 publications

The chromosome region containing the highly polymorphic HLA class I genes displays limited large scale variability in the human population.

The chromosome region containing the highly polymorphic HLA class I genes displays limited large scale variability in the human population.

Frequent abnormalities of TSG101 transcripts in human prostate cancer

β2-microglobulin induces apoptosis in HL-60 human leukemia cell line and its multidrug resistant variants overexpressing MRP1 but lacking Bax or overexpressing P-glycoprotein

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