Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P13232 (Interleukin-7)
 580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-7 (IL-7) is essential for both T cell and B cell development. Recent studies have suggested that IL-7 also functions as a survival-promoting factor for resting and activated T cells. In this study we examined the effects of IL-7 on survival and cytotoxicity of tumor-specific CD8(+) cytotoxic T lymphocyte (CTL) clones established and maintained either with IL-2 alone or with a combination of IL-2 and IL-7. While the CTL clones cultured in IL-2 alone died around day 10, the CTL clones cultured in the presence of IL-2 and IL-7 survived for more than 4 weeks after seeding. The long-term survival of the latter was correlated with the presence of IL-7 in the medium. In addition, IL-7 alone prolonged survival of other IL-2-dependent CTL clones after the removal of IL-2. IL-7 maintained the CTLs in G1 arrest after a slight proliferation during the initial phase during which low-level but sustained DNA synthesis was observed. However, there was no direct correlation between DNA synthesis and enhancement of long-term survival by IL-7 as demonstrated by the inhibiting proliferation of the CTL clones with the protein kinase inhibitor genistein. During long-term survival in the presence of IL-7, the cytotoxic activities of the CTL clones decreased gradually to background levels although they were restored soon after the next passage. These results suggested that IL-7 had the ability to set machinery in motion against apoptosis in the IL-2-dependent CTL clones. Such an effect of IL-7 might play a role in vivo in the process leading activated T cells to the resting, that is, memory state.
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PMID:Survival-promoting activity of IL-7 on IL-2-dependent cytotoxic T lymphocyte clones: resultant induction of G1 arrest. 1069 78

Transcription factors mediate their regulatory effects through interaction with DNA and numerous nuclear proteins. The fetal Alz-50 clone 1 (FAC1) protein, a novel DNA-binding protein with the capacity to repress transcription, is likely to function through a similar mechanism (1). Using the two-hybrid yeast screen, we have shown that FAC1 interacts with the myc-associated zinc finger protein (ZF87/MAZ). This association was confirmed in vitro with recombinant protein. The ZF87/MAZ interaction domain was mapped to the region containing a putative nuclear localization signal (NLS) and nuclear export sequence (NES) of FAC1, using deletion mutants of the FAC1 protein. FAC1, on the other hand, recognizes a conformational interface that includes the proline/alanine-rich domain of ZF87/MAZ and the first zinc finger. Cotransfection of NIH3T3 cells with ZF87/MAZ and a luciferase reporter containing the SV40 promoter and enhancer results in an increase in transcriptional activation, suggesting ZF87/MAZ is able to recognize its consensus binding site present in the SV40 promoter. Cotransfection with FAC1 reduces the level of ZF87/MAZ-induced activation of the SV40 promoter in a dose dependent manner. A mutant FAC1, lacking the ZF87/MAZ interaction domain, does not alter ZF87/MAZ activation of the SV40 promoter. These data demonstrate that interaction between FAC1 and ZF87/MAZ alters the transactivation capacity of ZF87/MAZ. By immunoblot analysis, FAC1 and ZF87/MAZ exhibit similar tissue distribution and co-localize to pathologic structures in Alzheimer's disease brain. Coexpression of FAC1 and ZF87/MAZ suggest that interaction of these two proteins will have biological implications for gene regulation in neurodegeneration.
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PMID:Fetal Alz-50 clone 1 (FAC1) protein interacts with the Myc-associated zinc finger protein (ZF87/MAZ) and alters its transcriptional activity. 1072 12

Two sets of Staphylococcus aureus isolates recovered from two patients exhibited similar susceptibility profiles except for oxacillin susceptibility (MSSA) or resistance (MRSA). SMA:I macrorestriction and inter-IS256 PCR analysis showed patterns closely related to the Belgian epidemic MRSA clone 1 in each pair of MSSA/MRSA strains. Loss of one large SMA:I DNA fragment and concurrent gain of a smaller fragment in the MSSA isolates was observed. The mecA sequence present in the MRSA was absent in the MSSA variant. Therefore, in vivo deletion of the mec region may occur in some lineages of S. aureus more frequently than previously thought.
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PMID:In vivo deletion of the methicillin resistance mec region from the chromosome of Staphylococcus aureus strains. 1102 Feb 61

Human endogenous retroviruses (HERV) have emerged as a possible cause of systemic lupus erythematosus (SLE). We previously detected serum antibodies to the gag region of HERV clone 4-1 in patients with SLE, but not in normal volunteers. In the present study, we detected clone 4-1 messenger RNA (mRNA) in peripheral blood mononuclear cells (PBMC) from SLE patients and performed sequence analysis of the cDNA or genomic DNA from clone 4-1 in these patients. Clone 4-1 mRNA was detected in all of the SLE patients tested, although it was not found in normal controls. Sequence analysis of clone 4-1 in these SLE patients revealed inactivation of the stop codons in part of the gag region. In addition, a computer search of current sequence libraries revealed that the clone 4-1 gag genomic DNA from SLE patients was more highly homologous with the clone 4-1 sequence in chromosome 11 from normal individuals when compared with the sequence of clone 4-1 integrated in the other chromosomes. It is possible that transcription of clone 4-1 from chromosome 11 occurs in SLE, and that the stop codon inactivation contributes to the translation of clone 4-1 gag proteins in patients with this disease.
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PMID:Sequence analysis of human endogenous retrovirus clone 4-1 in systemic lupus erythematosus. 1120 49

Attaching and effacing Escherichia coli (AEEC) strains isolated from diarrhoeic lambs and goat kids were characterized for intimin (eae) and EspB (espB) gene subtypes by PCR and sequencing, and for genetic relatedness by PFGE. Fifty (23 ovine and 27 caprine) AEEC strains of 398 (246 ovine and 152 caprine) analysed were detected by colony blot hybridization. These strains were epidemiologically unrelated since they were isolated from different outbreaks of neonatal diarrhoea over a long period. Ovine AEEC strains belonged to serogroups O2, O4, O26, O80, O91 or were untypable, and caprine strains belonged to serogroups O3, O153 and O163. Two intimin subtypes were detected among the ovine and caprine strains studied. Most of the strains (43/50) had the beta type intimin gene, but seven ovine strains possessed a variant gamma type intimin gene (gamma(V)). Analysis of deduced amino acid sequences of the eae gene revealed that the sequences of beta intimin of ovine and caprine strains were virtually identical to those of beta intimin of rabbit EPEC, human EPEC clone 2 and swine AEEC, whereas the gamma(V) intimin present in seven ovine strains had 75-76% identity with gamma intimin of human EHEC clone 1 strains, and 96% of identity with intimin of the human EHEC strain 95NR1 of serotype O111:H-. A PCR test was developed to identify the three different espB gene subtypes, espB of human EPEC clone 1 (espBalpha), espB of human EHEC clone 1 (espBgamma) and espB of rabbit EPEC and human EPEC clone 2 (espBbeta). There was close correlation between the intimin beta type and the espBbeta gene subtype in the ovine and caprine AEEC strains. The seven ovine strains possessing the gamma(V) intimin gene possessed the espBalpha gene subtype. None of the strains studied possessed the espBgamma gene found in human O157:H7 EHEC strains. PFGE analysis of genomic DNA of selected strains showed a great diversity among strains. Cluster analysis of PFGE patterns showed greater divergence between strains with the gamma(V) intimin gene than between strains with the beta intimin gene. This study showed that most of the AEEC strains isolated from diarrhoeic lambs and goat kids possessed beta intimin and espB genes identical to those of rabbit EPEC, and they may be associated with enteric disease in small ruminants.
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PMID:Association between intimin (eae) and EspB gene subtypes in attaching and effacing Escherichia coli strains isolated from diarrhoeic lambs and goat kids. 1149 11

Interleukin-7 (IL-7) and IL-15 have been recently identified as growth factors for cutaneous T-cell lymphoma (CTCL) cells, and they protect these cells from cell death. Using the CTCL cell line SeAx as a test system now shows that IL-7 and IL-15 are indeed necessary to maintain high levels of bcl-2. The up-regulation of bcl-2 was paralleled by increased DNA-binding activities of the transcription factors STAT2, STAT5, STAT6, and c-Myb to bcl-2 gene promoter-enhancer elements. Because STAT5 and c-Myb positively regulate bcl-2, IL-7 and IL-15 may mediate some of their effects on cell death survival gene expression through these 2 factors. Constitutive activities of the 3 STAT factors and c-Myb were found in the IL-7- and IL-15-independent CTCL cell lines HUT78 and MyLa 2059. The c-Myb protein was also present in CTCL cells of the skin lesions of all investigated patients. These results indicate that IL-7 and IL-15 may increase bcl-2 expression in CTCL cells by the activation of c-myb and STAT factors.
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PMID:Interleukin-7 and interleukin-15 regulate the expression of the bcl-2 and c-myb genes in cutaneous T-cell lymphoma cells. 1200 11

Clones with 24 or 25 chromosomes were obtained by pollinating an Andean cultivated tetraploid potato (Solanum tuberosum subsp. andigena clone 94H94, 2n = 4x = 48) with the Solanum phureja haploid-inducer clone 1.22. Their genetic composition was analyzed in an RAPD assay using 135 decamer primers and in an RFLP assay using 45 single-copy DNA probes. In total, 22 RAPD and 20 RFLP markers were found to be specific to S. phureja. None of these markers were found in the 24- and 25-chromosome clones. RFLP genotypes for the 45 RFLP loci were further determined for each clone. Genotypes of the 24-chromosome clones were characterized using two alleles randomly selected from four alleles of the parental tetraploid clone for almost all RFLP loci. Five 25-chromosome clones had extra alleles for all of the RFLP loci of chromosomes 4, 8, 10, 11, and 12, respectively, suggesting primary trisomy for one of these chromosomes. Clones with genotypes showing double reduction were also identified. Therefore, the obtained clones likely originated from random samples of female gametes, and hence are euhaploids or aneuhaploids of S. tuberosum subsp. andigena, strongly supporting parthenogenesis to be a primary mechanism for haploid induction in potato.
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PMID:Molecular marker analysis of 24- and 25-chromosome plants obtained from Solanum tuberosum L. subsp. andigena (2n = 4x = 48) pollinated with a Solanum phureja haploid inducer. 1203 27

To examine the p53-mediated biological activities and signalling pathways, we generated stable transfectants of the p53-null IW32 murine erythroleukemia cells expressing the temperature-sensitive p53 mutant DNA, tsp53(val135). Two clones with different levels of p53 protein expression were selected for further characterization. At permissive temperature, clone 1-5 cells differentiated along the erythroid pathway, and clone 3-2 cells that produced greater levels (3.5-fold) of p53 underwent apoptosis. Apoptosis of 3-2 cells was accompanied by mitochondrial cytochrome c release and caspase activation as well as by cleavage of caspase substrates. Bax protein was induced to a similar extent in these clones by wild-type p53; expression of p21(Cip1/Waf1) and p27(Kip1) proteins was also increased. However, significantly lesser extent of induction for both CDK inhibitors was detected in the apoptotic 3-2 clone. The general caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD.fmk) blocked the p53-induced apoptosis in 3-2 cells, with a concomitant elevation of p27(Kip1), suggesting that p27(Kip1) protein underwent caspase-dependent proteolysis in the apoptotic 3-2 cells. Together these results linked a pathway involving cytochrome c release, caspase activation and p27(Kip1) degradation to the p53-induced apoptosis in IW32 erythroleukemia cells.
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PMID:Modulation of caspase activation and p27(Kip1) degradation in the p53-induced apoptosis in IW32 erythroleukemia cells. 1222 Jun 22

Solanum phureja clone 1-3 and S. chacoense clone 80-1 have a zero and high leptine content in their foliage, respectively. An F(1) hybrid (CP2) was intermediate for the trait, but self-incompatible. Two reciprocal backcross families, PBCp ( phu 1-3 x CP2) and PBCc (CP2 x phu 1-3), and a family of monoploids derived by anther culture of CP2, were characterized for leptine as the aglycon, acetylleptinidine (ALD), content in leaves by gas chromatography. ALD was present in 43 of 87 genotypes in the PBCp backcross, implying simple genetic control by a dominant gene. However, the ALD levels were low compared to CP2. In the PBCc backcross, only 7 of 42 genotypes expressed ALD at a level generally higher than in PBCp. This ratio was significantly different from the 1:1 segregation observed in the reciprocal backcross and suggests a cytoplasmic influence. ALD levels in the CP2 monoploids ranged from 0 to 8,968 &mgr;g.g(-1) of dry weight (dw) with 18 individuals expressing ALD and five with 0 ALD content. Ten high (mean ALD = 546 &mgr;g.g(-1) of dw) and ten low (mean ALD = 0) individual plants within PBCp and seven high (mean ALD = 3,037 &mgr;g.g(-1) of dw) and eight low (mean ALD = 0) individual plants within PBCc were used for bulk segregant analysis (BSA) using 214 RAPD (randomly amplified polymorphic DNA) primers. Three RAPD primers (OPQ-2, OPT-16 and OPT-20) amplified bands exclusively in bulks containing DNA mixes of high ALD producers in both PBCp and PBCc populations. These results suggest that these markers were associated in coupling to ALD content. ANOVAs for ALD content verified association between the markers and the trait. A CAPS (cleaved amplified polymorphic sequence) marker, GP82A, was also significantly associated with ALD production in both the monoploid and the PBCp populations. None of the RAPD markers was associated to ALD in the monoploids but one was associated in repulsion. The monoploid data indicate the likelihood of a recessive gene(s) that controls leptine production, but the backcross data indicate the action of modifying loci.
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PMID:Identification of molecular markers associated with leptine in reciprocal backcross families of diploid potato. 1258 28

We have presented previously evidence that the cytopathogenic 18f strain of hepatitis A virus (HAV) induced degradation of ribosomal RNA (rRNA) in infected cells [Arch. Virol. 148 (2003) 1275-1300]. In contrast, the non-cytopathogenic parent virus HM175 clone 1 had no effect on rRNA integrity. We present here data showing that rRNA degradation is followed by apoptosis accompanied by characteristic DNA laddering in the cytoplasm of 18f infected cells. The DNA laddering coincided with the detection of caspase 3 and PARP-1 cleavage and was dependent upon activation of the caspase pathway, since treatment with Z-VAD-FMK, a pan-caspase inhibitor, inhibited both events. RNase L mRNA was present in both virus-infected and uninfected cells. Messenger RNA for the interferon inducible enzyme 2'-5' oligoadenylate synthetase (2'-5' OAS), which polymerizes ATP into 2'-5' oligo adenylate (2-5A, the activator of RNase L) in the presence of double-stranded RNA, was not detected following virus infection. 2'-5' OAS mRNA was induced by treatment of the cells with interferon-beta (IFN-beta). IFN-beta mRNA was marginally induced following infection. However, phosphorylated STAT 1, a key regulator of interferon-stimulated gene transcription was not detected in virus infected cells. STAT 1 phosphorylation in response to IFN treatment was lower in virus-infected cells, compared to uninfected cells treated with interferon, suggesting that 18f virus infection interferes with interferon signaling. The results suggest that 18f infection causes the induction of a 2-5A independent RNase L like activity.
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PMID:Apoptosis induced by a cytopathic hepatitis A virus is dependent on caspase activation following ribosomal RNA degradation but occurs in the absence of 2'-5' oligoadenylate synthetase. 1545 Nov 83


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