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C Jones

Publications and source records attributed to C Jones.

At least 469 records · Page 26Linked to original sources

E1A-mediated activation of the adenovirus E4 promoter can occur independently of the cellular transcription factor E4F.

The cellular factors E4F and ATF-2 (a member of the activating transcription factor [ATF] family) bind to common sites in the adenovirus E4 promoter and have both been suggested to mediate transcriptional activation by the viral E1A protein. To assess the role of E4F, we have introduced mutations into the E4F/ATF binding sites of the E4 promoter and monitored promoter activity in HeLa cells. We find that the core motif (TGACG) of the E4F/ATF binding site is important for E4 promoter activity. However, a point mutation adjacent to the core motif that reduces E4F binding (but has no effect on ATF binding) has no effect on E4 promoter activity. Together with previous results, these findings indicate that there are at least two cellular factors (a member of the ATF family and E4F) that can function with E1A to induce transcription of the E4 promoter. We also find that certain mutations strongly reduce E4 transcription in vivo but have no effect on ATF-2 binding in vitro. These results are therefore incompatible with the possibility that (with respect to members of the ATF family) ATF-2 alone can function with E1A to transactivate the E4 promoter in HeLa cells.

Adenovirus Early Proteins↗

Platelet-derived growth factor and growth-related genes in rat lung. I. Developmental expression.

The autocrine, paracrine, or systemic growth factors responsible for fetal lung cell growth are not completely defined. The progression-type insulin-like growth factors and epidermal growth factor, or transforming growth factor-alpha acting through the epidermal growth factor receptor, appear to act on the developing lung epithelium. The competence factors that facilitate the actions of progression factors during lung growth are unknown. Fetal rat lung cells in vitro synthesize a platelet-derived growth factor (PDGF)-like polypeptide, which we have hypothesized may play a paracrine role in normal lung development. Slot blot and Northern blot analyses of fetal rat lung mRNA have been used to determine if there is a relationship between expression of message for PDGF-A or PDGF-B chains, or their cognate receptors, and periods of maximal growth during late fetal rat lung development. Whole lung mRNA was extracted on 18, 19, 20, 21, and 22 days of gestation (term = 22 days). The peak of DNA synthesis, as assessed by expression of message for DNA polymerase alpha, histone 3, and the proto-oncogenes c-fos and c-myc, which are stimulated by binding of growth factors including PDGF, occurred during the canalicular stage of lung development on days 19 and 20 of gestation. Expression of message for PDGF-A and PDGF-B chains was low during the pseudoglandular stage on day 18, peaked during the canalicular stage on days 19 and 20, then fell again during the saccular stage at days 21 and 22 of gestation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Isolation and mapping of 62 new RFLP markers on human chromosome 11.

To obtain new RFLP markers on human chromosome 11 for a high-resolution map, we constructed a cosmid library from a Chinese hamster x human somatic hybrid cell line that retains only human chromosome 11 in a Chinese hamster genomic background. A total of 3,500 cosmids were isolated by colony hybridization with labeled human genomic DNA. DNA was prepared from 130 of these cosmid clones and examined for RFLP. In 62 of them, polymorphism was detected with one or more enzymes; four RFLPs were VNTR systems. All polymorphic clones were assigned to one of 22 intervals obtained by mapping on a deletion panel of 15 somatic hybrid cell lines containing parts of chromosome 11; 11 clones were finely mapped by in situ hybridization. Although RFLP markers were scattered on the whole chromosome, they were found predominantly in the regions of R-banding. These DNA markers will contribute to fine mapping of genes causing inherited disorders and tumor-suppressor genes that reside on chromosome 11. Furthermore, as one-third of the cosmid clones revealed a band or bands in Chinese hamster DNA, indicating sequence conservation, this subset of clones may be useful for isolating biologically important genes on chromosome 11.

Animals↗

Treatment modality patterns and transplantation among the United States pediatric end-stage renal disease population: a longitudinal study.

Between 1985 and 1988, there were 3,393 children (Medicare insured) under age 20 who began treatment for chronic ESRD. Patterns of modality use, modality switch, mortality rates, and various aspects of transplantation were analyzed for different age and incident groups of this pediatric cohort. The pediatric cohort as a whole exhibited a distinct pattern of modality use when compared to adults in general, a point evidenced most clearly by their substantially higher rates of transplantation. Furthermore, notable differences were found within the pediatric cohort when the younger than 5, 5-9, 10-14, and 15- to 19-year-old age groups were analyzed separately. Younger pediatric patients, particularly those younger than 5 years, received peritoneal dialysis as initial ESRD therapy more frequently than their older pediatric counterparts. This result would be expected given vascular access problems often associated with very young patients. In addition, those patients younger than 5 years who began RRT with some form of hemodialysis had the highest likelihood of switching to CAPD/CCPD within the first year of therapy. Conversely, older pediatric patients were most likely to begin RRT therapy with some form of hemodialysis. By day 91, slightly over half of the 15- to 19-year-old age group was utilizing center hemodialysis; the CAPD/CCPD, other peritoneal, and functioning transplant modalities each contained about 10% of the patients with the remainder falling into the death and unknown dialysis categories. The overall pattern of switching to transplantation during the first year of RRT was similar for pediatric patients initiating RRT with center hemodialysis versus peritoneal dialysis (CAPD/CCPD), but differed by age group within each dialysis type. Pediatric patients on peritoneal dialysis were somewhat more likely to receive a transplant during the first year of ESRD compared to hemodialysis, although the difference was small. Mortality rates during the first year for patients who began treatment with center hemodialysis versus CAPD/CCPD were similar. The well-documented dominance of transplantation as a method of RRT for pediatric patients was further verified by this study. Results show that transplantation was implemented rapidly during the initial months of ESRD. Nearly 50% of surviving pediatric patients had a functioning transplant at 1 year following onset and 64% at 3 years. These percentages were exceeded for the 5- to 9-year-old age group, of which 74% had a functioning graft 3 years following onset.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

T7 endonuclease I resolves Holliday junctions formed in vitro by RecA protein.

T7 endonuclease I is known to bind and cleave four-way junctions in DNA. Since these junctions serve as analogues of Holliday junctions that arise during genetic recombination, we have investigated the action of T7 endonuclease I on recombination intermediates containing Holliday junctions. We find that addition of T7 endonuclease I to strand exchange reactions catalysed by RecA protein of Escherichia coli leads to the formation of duplex products that correspond to 'patch' and 'splice' type recombinants. Resolution of the recombination intermediates occurs by the introduction of nicks at the site of the Holliday junction. The recombinant molecules contain 5'-phosphate and 3'-hydroxyl termini which may be ligated to restore the integrity of the DNA.

DNA, Bacterial↗

Complete physical map of the WAGR region of 11p13 localizes a candidate Wilms' tumor gene.

A complete physical map of the 11p13 region containing the Wilms' tumor locus has been developed and used to localize a candidate Wilms' tumor gene. Our strategy to construct the map combined the use of pulsed-field gel electrophoresis and irradiation-reduced somatic cell hybrids. These hybrids, which contain limited segments of human chromosome 11 segregated from the remainder of the human genome, permit direct visualization of restriction fragments located in 11p13 using human interspersed repeated DNA sequences as hybridization probes. The physical map has provided a framework to identify the sites of genes responsible for the complex of disorders associated with hemizygous 11p13 deletion: Wilms' tumor, aniridia, genitourinary abnormalities, and mental retardation. The Wilms' tumor locus has been limited to a region of less than 345 kb, and a transcript with many of the characteristics expected for the Wilms' tumor gene has been localized to this region.

Cell Line↗

Expression and reconstitution of a biologically active human interferon-gamma receptor in hamster cells.

We report the expression of the human interferon-gamma (Hu-IFN-gamma) receptor from a cDNA clone in an animal cell where both stable expression of the cloned receptor as well as its biological activity is demonstrated for the first time. Biological activity of the receptor (i.e. expression of surface histocompatibility antigens in response to human interferon-gamma) requires the presence of human chromosome 21 demonstrating the requirement for at least one other species-specific factor in the modulation of receptor action. This system should now facilitate delineation of regions involved in the binding of human interferon-gamma and receptor signal transduction.

Animals↗

Enzymatic formation and resolution of Holliday junctions in vitro.

E. coli RecA protein promotes homologous pairing and reciprocal strand exchange reactions between duplex DNA molecules in vitro. Reaction intermediates contain Holliday junctions that are driven along the DNA at a maximal rate approaching 1000 bases per minute. T4 endonuclease VII cleaves Holliday junctions in vitro, and its inclusion in RecA-mediated reactions leads to the rapid formation of heteroduplex products. Product analysis indicates patch and splice recombinant molecules similar to those expected from in vivo recombination events. The combined formation and resolution of Holliday junctions has led us to propose a model for resolution based on the structure of RecA-DNA helices. One feature of this model is that resolution, which gives rise to the two types of recombinant product, may occur without need for isomerization of the junction.

Bacteriophage phi X 174↗

Metastatic ciliary body carcinoid tumor.

A 50-year-old man with a history of systemic carcinoid had decreased right eye vision and a darkly pigmented cilio-choroidal mass. Results of ultrasonographic and fluorescein angiographic examinations were consistent with a malignant melanoma. Fine-needle aspiration biopsy of the lesion identified it as a carcinoid metastasis. The patient refused both radiation and enucleation; complete excision with a cyclochoroidectomy was performed. Histopathologic examination showed a carcinoid neoplasm covered by marked hyperplasia of the retinal pigment epithelium that produced the pigmented appearance of the lesion.

Biopsy, Needle↗

Sublocalization on chromosome 21 of human interferon-alpha receptor gene and the gene for an interferon-gamma response protein.

The cellular responses to alpha and beta interferons (IFN-alpha and -beta) are mediated through the IFN-alpha/beta (type I) receptor, while the response to IFN-gamma is mediated through the IFN-gamma (type II) receptor. The receptors for IFN-alpha/beta and IFN-gamma are encoded by genes on human chromosomes 21 and 6q, respectively. The presence of chromosome 21q confers both ligand binding and responsiveness to human IFN-alpha/beta, whereas chromosome 6q confers binding of Hu-IFN-gamma, but not cellular responsiveness on somatic cell hybrids. Chromosome 6q (i.e., the Hu-IFN-gamma receptor gene) and chromosome 21q are both necessary for the cellular response of somatic cell hybrids (from fibroblasts) to Hu-IFN-gamma. It is conceivable that the factor mediating activity through the IFN-gamma receptor is, in fact, the IFN-alpha receptor, or that the two genes are distinct but part of an "interferon response" region. Here we more precisely localize on human chromosome 21 the genes for the IFN-alpha receptor and for the factor(s) mediating the action of IFN-gamma through the chromosome 6-encoded receptor. Hamster-human somatic cell hybrids containing various fragments of human chromosome 21 were used. The presence of the human IFN-alpha/beta receptor was determined by binding 32P-labeled human IFN-alpha to cells, covalently cross-linking the [32P]IFN-alpha-receptor complex, and analyzing it by SDS-polyacrylamide gel electrophoresis. The presence of the IFN-gamma receptor-related factor mediating cellular responsiveness was determined by HLA induction in hybrid cells containing the IFN-gamma receptor (chromosome 6q), a transfected copy of the human HLA-B7 gene, and various portions of chromosome 21. In all hybrids examined, the two genes cosegregate. Specifically, both genes are localized to the region of chromosome 21 containing the markers D21S58, D21S65, and GART and appear to be proximal to D21S58. The implications for IFN action are discussed.

Animals↗

Development of a somatic cell hybrid mapping panel and molecular probes for human chromosome 3.

A somatic cell hybrid mapping panel and molecular probes have been developed for human chromosome 3. This panel defines 11 regions for the short and long arms of the chromosome. Four hundred thirty-two probes have been mapped using these hybrids. One hundred thirty-one of these probes were derived from EcoRI and HindIII flow-sorted libraries. The remaining 301 probes were isolated from NotI boundary and random (partial MboI) libraries constructed from a hybrid that provided a relative enrichment in 3p DNA sequences. For some regions of the chromosome, significant differences in the distribution of probes were noted. This was observed for both the unique sequence flow-sorted and NotI probes. These differences are in agreement with previous suggestions that Giemsa light bands are GC-rich, and therefore gene-rich (especially housekeeping genes), and that the Giemsa dark bands may contain DNA that is more highly condensed. The isolation of probes from different types of libraries, or by different screening strategies, appears to reduce deficiencies that might arise from the use of probes derived with a more limited approach. These hybrids and probes should facilitate the construction of physical and genetic linkage maps to identify various disease loci involving chromosome 3.

Animals↗

Human aminoacylase-1: cloning, regional assignment to distal chromosome 3p21.1, and identification of a cross-hybridizing sequence on chromosome 18.

Aminoacylase-1 (ACY1, EC 3.5.1.14) is a cytosolic enzyme with a wide range of tissue expression and has been postulated to function in the catabolism and salvage of acylated amino acids. ACY1 has been assigned to chromosome 3p21, a region reduced to homozygosity in small-cell lung cancer and renal cell carcinoma, and has been reported to exhibit reduced or absent expression in small-cell lung cancer cell lines and tumors. Using monoclonal antibodies to human ACY1, we have isolated cDNA clones from a liver lambda gt11 cDNA library. As proof of identity, the fusion protein encoded by a putative ACY1 cDNA displayed ACY1 enzymatic activity. Additionally, it was determined that the putative ACY1 cDNA clones hybridize to an EcoR1 restriction fragment that has been mapped to chromosome 3p. Both ACY1 activity and this restriction fragment have been further demonstrated to be syntenic to distal 3p21.1 through the use of a panel of human-rodent somatic cell hybrids containing fragments of chromosome 3. An additional EcoR1 restriction fragment to which the probe hybridizes has been assigned to chromosome 18. The major mRNA species to which the ACY1 cDNA hybridizes is 0.9 kb; faint hybridization to a 4.2-kb mRNA species is also detected. These studies further refine a region of interest in the investigation of gene inactivation in small-cell lung cancer and provide a new marker on chromosome 18.

Amidohydrolases↗