ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-04-14
    Description: Previous studies have demonstrated that allelic deletions of the short arm of chromosome 17 occur in over 75% of colorectal carcinomas. Twenty chromosome 17p markers were used to localize the common region of deletion in these tumors to a region contained within bands 17p12 to 17p13.3. This region contains the gene for the transformation-associated protein p53. Southern and Northern blot hybridization experiments provided no evidence for gross alterations of the p53 gene or surrounding sequences. As a more rigorous test of the possibility that p53 was a target of the deletions, the p53 coding regions from two tumors were analyzed; these two tumors, like most colorectal carcinomas, had allelic deletions of chromosome 17p and expressed considerable amounts of p53 messenger RNA from the remaining allele. The remaining p53 allele was mutated in both tumors, with an alanine substituted for valine at codon 143 of one tumor and a histidine substituted for arginine at codon 175 of the second tumor. Both mutations occurred in a highly conserved region of the p53 gene that was previously found to be mutated in murine p53 oncogenes. The data suggest that p53 gene mutations may be involved in colorectal neoplasia, perhaps through inactivation of a tumor suppressor function of the wild-type p53 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, S J -- Fearon, E R -- Nigro, J M -- Hamilton, S R -- Preisinger, A C -- Jessup, J M -- vanTuinen, P -- Ledbetter, D H -- Barker, D F -- Nakamura, Y -- White, R -- Vogelstein, B -- GM07184/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- HD20619/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 14;244(4901):217-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2649981" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Chromosome Deletion ; *Chromosomes, Human, Pair 17/ultrastructure ; Colorectal Neoplasms/*genetics ; Humans ; Mice ; Mice, Nude ; *Mutation ; Neoplasm Proteins/*genetics ; Nucleic Acid Hybridization ; Oncogenes ; Phosphoproteins/*genetics ; Suppression, Genetic ; Tumor Suppressor Protein p53
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Identification of a chromosome 18q gene that is altered in colorectal cancers (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-05
    Description: Allelic deletions involving chromosome 18q occur in more than 70 percent of colorectal cancers. Such deletions are thought to signal the existence of a tumor suppressor gene in the affected region, but until now a candidate suppressor gene on this chromosomal arm had not been identified. A contiguous stretch of DNA comprising 370 kilobase pairs (kb) has now been cloned from a region of chromosome 18q suspected to reside near this gene. Potential exons in the 370-kb region were defined by human-rodent sequence identities, and the expression of potential exons was assessed by an "exon-connection" strategy based on the polymerase chain reaction. Expressed exons were used as probes for cDNA screening to obtain clones that encoded a portion of a gene termed DCC; this cDNA was encoded by at least eight exons within the 370-kb genomic region. The predicted amino acid sequence of the cDNA specified a protein with sequence similarity to neural cell adhesion molecules and other related cell surface glycoproteins. While the DCC gene was expressed in most normal tissues, including colonic mucosa, its expression was greatly reduced or absent in most colorectal carcinomas tested. Somatic mutations within the DCC gene observed in colorectal cancers included a homozygous deletion of the 5' end of the gene, a point mutation within one of the introns, and ten examples of DNA insertions within a 0.17-kb fragment immediately downstream of one of the exons. The DCC gene may play a role in the pathogenesis of human colorectal neoplasia, perhaps through alteration of the normal cell-cell interactions controlling growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fearon, E R -- Cho, K R -- Nigro, J M -- Kern, S E -- Simons, J W -- Ruppert, J M -- Hamilton, S R -- Preisinger, A C -- Thomas, G -- Kinzler, K W -- CA 09243/CA/NCI NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jan 5;247(4938):49-56.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2294591" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Blotting, Southern ; Cell Adhesion Molecules, Neuronal/genetics ; *Chromosome Deletion ; *Chromosomes, Human, Pair 18 ; Cloning, Molecular ; Colorectal Neoplasms/*genetics ; Cross Reactions ; DNA Probes ; DNA, Neoplasm/*genetics ; Exons ; Gene Expression Regulation, Neoplastic ; Humans ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA, Neoplasm/genetics ; Sequence Homology, Nucleic Acid ; *Suppression, Genetic ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Identification of IGF2 signaling through phosphoinositide-3-kinase regulatory subunit 3 as a growth-promoting axis in glioblastoma (2007)
    National Academy of Sciences
    Details
    Publication Date: 2007-02-20
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Addendum: The rise and fall of methanotrophy following a deepwater oil-well blowout (2015)
    Springer Nature
    Details
    Publication Date: 2015-05-29
    Description: Nature Geoscience 8, 490 (2015). doi:10.1038/ngeo2447 Authors: M. Crespo-Medina, C. D. Meile, K. S. Hunter, A-R. Diercks, V. L. Asper, V. J. Orphan, P. L. Tavormina, L. M. Nigro, J. J. Battles, J. P. Chanton, A. M. Shiller, D-J. Joung, R. M. W. Amon, A. Bracco, J. P. Montoya, T. A. Villareal, A. M. Wood & S. B. Joye
    Print ISSN: 1752-0894
    Electronic ISSN: 1752-0908
    Topics: Geosciences
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    The rise and fall of methanotrophy following a deepwater oil-well blowout (2014)
    Springer Nature
    Details
    Publication Date: 2014-05-30
    Description: Nature Geoscience 7, 423 (2014). doi:10.1038/ngeo2156 Authors: M. Crespo-Medina, C. D. Meile, K. S. Hunter, A-R. Diercks, V. L. Asper, V. J. Orphan, P. L. Tavormina, L. M. Nigro, J. J. Battles, J. P. Chanton, A. M. Shiller, D-J. Joung, R. M. W. Amon, A. Bracco, J. P. Montoya, T. A. Villareal, A. M. Wood & S. B. Joye The blowout of the Macondo oil well in the Gulf of Mexico in April 2010 injected up to 500,000 tonnes of natural gas, mainly methane, into the deep sea. Most of the methane released was thought to have been consumed by marine microbes between July and August 2010. Here, we report spatially extensive measurements of methane concentrations and oxidation rates in the nine months following the spill. We show that although gas-rich deepwater plumes were a short-lived feature, water column concentrations of methane remained above background levels throughout the rest of the year. Rates of microbial methane oxidation peaked in the deepwater plumes in May and early June, coincident with a rapid rise in the abundance of known and new methane-oxidizing microbes. At this time, rates of methane oxidation reached up to 5,900 nmol l−1 d−1—the highest rates documented in the global pelagic ocean before the blowout. Rates of methane oxidation fell to less than 50 nmol l−1 d−1 in late June, and continued to decline throughout the remainder of the year. We suggest the precipitous drop in methane consumption in late June, despite the persistence of methane in the water column, underscores the important role that physiological and environmental factors play in constraining the activity of methane-oxidizing bacteria in the Gulf of Mexico.
    Print ISSN: 1752-0894
    Electronic ISSN: 1752-0908
    Topics: Geosciences
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...