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
Filter
  • Mutation
  • 2010-2014
  • 2000-2004
  • 1995-1999  (22)
  • 1955-1959
  • 1950-1954
  • 1997  (22)
  • 1
    facet.materialart.
    Unknown
    Positional cloning of the gene for multiple endocrine neoplasia-type 1 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-18
    Description: Multiple endocrine neoplasia-type 1 (MEN1) is an autosomal dominant familial cancer syndrome characterized by tumors in parathyroids, enteropancreatic endocrine tissues, and the anterior pituitary. DNA sequencing from a previously identified minimal interval on chromosome 11q13 identified several candidate genes, one of which contained 12 different frameshift, nonsense, missense, and in-frame deletion mutations in 14 probands from 15 families. The MEN1 gene contains 10 exons and encodes a ubiquitously expressed 2.8-kilobase transcript. The predicted 610-amino acid protein product, termed menin, exhibits no apparent similarities to any previously known proteins. The identification of MEN1 will enable improved understanding of the mechanism of endocrine tumorigenesis and should facilitate early diagnosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandrasekharappa, S C -- Guru, S C -- Manickam, P -- Olufemi, S E -- Collins, F S -- Emmert-Buck, M R -- Debelenko, L V -- Zhuang, Z -- Lubensky, I A -- Liotta, L A -- Crabtree, J S -- Wang, Y -- Roe, B A -- Weisemann, J -- Boguski, M S -- Agarwal, S K -- Kester, M B -- Kim, Y S -- Heppner, C -- Dong, Q -- Spiegel, A M -- Burns, A L -- Marx, S J -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):404-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Transfer, National Human Genome Research Institute (NHGRI), National Institutes of Health (NIH), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103196" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; *Cloning, Molecular ; DNA, Complementary/genetics ; Exons ; Frameshift Mutation ; *Genes, Tumor Suppressor ; Humans ; Molecular Sequence Data ; Multiple Endocrine Neoplasia Type 1/*genetics ; Mutation ; Neoplasm Proteins/chemistry/*genetics ; *Proto-Oncogene Proteins
    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
    Altered neural cell fates and medulloblastoma in mouse patched mutants (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: The PATCHED (PTC) gene encodes a Sonic hedgehog (Shh) receptor and a tumor suppressor protein that is defective in basal cell nevus syndrome (BCNS). Functions of PTC were investigated by inactivating the mouse gene. Mice homozygous for the ptc mutation died during embryogenesis and were found to have open and overgrown neural tubes. Two Shh target genes, ptc itself and Gli, were derepressed in the ectoderm and mesoderm but not in the endoderm. Shh targets that are, under normal conditions, transcribed ventrally were aberrantly expressed in dorsal and lateral neural tube cells. Thus Ptc appears to be essential for repression of genes that are locally activated by Shh. Mice heterozygous for the ptc mutation were larger than normal, and a subset of them developed hindlimb defects or cerebellar medulloblastomas, abnormalities also seen in BCNS patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodrich, L V -- Milenkovic, L -- Higgins, K M -- Scott, M P -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1109-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305-5427, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262482" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/genetics ; Animals ; Body Patterning ; Cell Lineage ; Central Nervous System/cytology/*embryology ; Cerebellar Neoplasms/*genetics/pathology ; Ectoderm/metabolism ; Endoderm/metabolism ; *Gene Expression Regulation, Developmental ; Genes, Tumor Suppressor ; Heterozygote ; Homozygote ; Intracellular Signaling Peptides and Proteins ; Medulloblastoma/*genetics/pathology ; Membrane Proteins/*genetics/physiology ; Mesoderm/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Oncogene Proteins/genetics ; Receptors, Cell Surface ; Trans-Activators ; Transcription Factors/genetics
    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 a gene that causes primary open angle glaucoma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: Glaucoma is a major cause of blindness and is characterized by progressive degeneration of the optic nerve and is usually associated with elevated intraocular pressure. Analyses of sequence tagged site (STS) content and haplotype sharing between families affected with chromosome 1q-linked open angle glaucoma (GLC1A) were used to prioritize candidate genes for mutation screening. A gene encoding a trabecular meshwork protein (TIGR) mapped to the narrowest disease interval by STS content and radiation hybrid mapping. Thirteen glaucoma patients were found to have one of three mutations in this gene (3.9 percent of the population studied). One of these mutations was also found in a control individual (0.2 percent). Identification of these mutations will aid in early diagnosis, which is essential for optimal application of existing therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, E M -- Fingert, J H -- Alward, W L -- Nguyen, T D -- Polansky, J R -- Sunden, S L -- Nishimura, D -- Clark, A F -- Nystuen, A -- Nichols, B E -- Mackey, D A -- Ritch, R -- Kalenak, J W -- Craven, E R -- Sheffield, V C -- EY02477/EY/NEI NIH HHS/ -- EY08905/EY/NEI NIH HHS/ -- EY10564/EY/NEI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):668-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005853" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Chromosome Mapping ; Chromosomes, Artificial, Yeast ; *Chromosomes, Human, Pair 1 ; Cytoskeletal Proteins ; Eye Proteins/*genetics ; Female ; Genetic Linkage ; Glaucoma, Open-Angle/*genetics ; *Glycoproteins ; Haplotypes ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Pedigree ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Sequence Tagged Sites ; Trabecular Meshwork/*metabolism
    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
  • 4
    facet.materialart.
    Unknown
    Niemann-Pick C1 disease gene: homology to mediators of cholesterol homeostasis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: Niemann-Pick type C (NP-C) disease, a fatal neurovisceral disorder, is characterized by lysosomal accumulation of low density lipoprotein (LDL)-derived cholesterol. By positional cloning methods, a gene (NPC1) with insertion, deletion, and missense mutations has been identified in NP-C patients. Transfection of NP-C fibroblasts with wild-type NPC1 cDNA resulted in correction of their excessive lysosomal storage of LDL cholesterol, thereby defining the critical role of NPC1 in regulation of intracellular cholesterol trafficking. The 1278-amino acid NPC1 protein has sequence similarity to the morphogen receptor PATCHED and the putative sterol-sensing regions of SREBP cleavage-activating protein (SCAP) and 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carstea, E D -- Morris, J A -- Coleman, K G -- Loftus, S K -- Zhang, D -- Cummings, C -- Gu, J -- Rosenfeld, M A -- Pavan, W J -- Krizman, D B -- Nagle, J -- Polymeropoulos, M H -- Sturley, S L -- Ioannou, Y A -- Higgins, M E -- Comly, M -- Cooney, A -- Brown, A -- Kaneski, C R -- Blanchette-Mackie, E J -- Dwyer, N K -- Neufeld, E B -- Chang, T Y -- Liscum, L -- Strauss, J F 3rd -- Ohno, K -- Zeigler, M -- Carmi, R -- Sokol, J -- Markie, D -- O'Neill, R R -- van Diggelen, O P -- Elleder, M -- Patterson, M C -- Brady, R O -- Vanier, M T -- Pentchev, P G -- Tagle, D A -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):228-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211849" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Carrier Proteins ; Cholesterol/*metabolism ; Cholesterol, LDL/metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 18 ; Cloning, Molecular ; *Drosophila Proteins ; Homeostasis ; Humans ; Hydroxymethylglutaryl CoA Reductases/chemistry ; Insect Proteins/chemistry ; Intracellular Signaling Peptides and Proteins ; Lysosomes/metabolism ; *Membrane Glycoproteins ; Membrane Proteins/chemistry ; Molecular Sequence Data ; Mutation ; Niemann-Pick Diseases/*genetics/metabolism ; Polymorphism, Single-Stranded Conformational ; Proteins/chemistry/*genetics/physiology ; Receptors, Cell Surface/chemistry ; Sequence Homology, Amino Acid ; Transfection
    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
  • 5
    facet.materialart.
    Unknown
    Interneuron migration from basal forebrain to neocortex: dependence on Dlx genes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: Although previous analyses indicate that neocortical neurons originate from the cortical proliferative zone, evidence suggests that a subpopulation of neocortical interneurons originates within the subcortical telencephalon. For example, gamma-aminobutyric acid (GABA)-expressing cells migrate in vitro from the subcortical telencephalon into the neocortex. The number of GABA-expressing cells in neocortical slices is reduced by separating the neocortex from the subcortical telencephalon. Finally, mice lacking the homeodomain proteins DLX-1 and DLX-2 show no detectable cell migration from the subcortical telencephalon to the neocortex and also have few GABA-expressing cells in the neocortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, S A -- Eisenstat, D D -- Shi, L -- Rubenstein, J L -- K02 MH01046/MH/NIMH NIH HHS/ -- R01 MH51561/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):474-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nina Ireland Laboratory of Developmental Neurobiology, Center for Neurobiology and Psychiatry, Department of Psychiatry, University of California at San Francisco, CA 94143-0984, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334308" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calbindins ; Cell Movement ; Corpus Striatum/*cytology/embryology/metabolism ; Culture Techniques ; DNA-Binding Proteins/*genetics/physiology ; *Genes, Homeobox ; Glutamate Decarboxylase/metabolism ; Homeodomain Proteins/*genetics/physiology ; Interneurons/chemistry/*physiology ; Mice ; Mutation ; Neocortex/*cytology/embryology/metabolism ; S100 Calcium Binding Protein G/analysis ; Telencephalon/*cytology/embryology/metabolism ; Transcription Factors ; gamma-Aminobutyric Acid/analysis
    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
  • 6
    facet.materialart.
    Unknown
    An information-intensive approach to the molecular pharmacology of cancer (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-17
    Description: Since 1990, the National Cancer Institute (NCI) has screened more than 60,000 compounds against a panel of 60 human cancer cell lines. The 50-percent growth-inhibitory concentration (GI50) for any single cell line is simply an index of cytotoxicity or cytostasis, but the patterns of 60 such GI50 values encode unexpectedly rich, detailed information on mechanisms of drug action and drug resistance. Each compound's pattern is like a fingerprint, essentially unique among the many billions of distinguishable possibilities. These activity patterns are being used in conjunction with molecular structural features of the tested agents to explore the NCI's database of more than 460,000 compounds, and they are providing insight into potential target molecules and modulators of activity in the 60 cell lines. For example, the information is being used to search for candidate anticancer drugs that are not dependent on intact p53 suppressor gene function for their activity. It remains to be seen how effective this information-intensive strategy will be at generating new clinically active agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinstein, J N -- Myers, T G -- O'Connor, P M -- Friend, S H -- Fornace, A J Jr -- Kohn, K W -- Fojo, T -- Bates, S E -- Rubinstein, L V -- Anderson, N L -- Buolamwini, J K -- van Osdol, W W -- Monks, A P -- Scudiero, D A -- Sausville, E A -- Zaharevitz, D W -- Bunow, B -- Viswanadhan, V N -- Johnson, G S -- Wittes, R E -- Paull, K D -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):343-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Pharmacology (LMP), Division of Basic Science, National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD 20892, USA. weinstein@dtpax2.ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994024" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Antineoplastic Agents/chemistry/*pharmacology ; Cluster Analysis ; *Computational Biology ; Computer Communication Networks ; *Databases, Factual ; *Drug Screening Assays, Antitumor ; Genes, p53 ; Humans ; Molecular Structure ; Mutation ; Software ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/physiology
    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
  • 7
    Electronic Resource
    Electronic Resource
    Spontaneous and induced minisatellite instability (1997)
    Weinheim : Wiley-Blackwell
    Electrophoresis 18 (1997), S. 1501-1511 
    Details
    ISSN: 0173-0835
    Keywords: Conversion ; Minisatellite ; Mutation ; Radiation ; Recombination ; Tandem repeat ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Minisatellites provide not only the basis for DNA fingerprinting and DNA profiling but also extremely informative systems for analysing processes of tandem repeat turnover in the human genome. Minisatellite instability appears to involve distinct mutation processes in somatic and germline cells; in the germline, mutation is frequently dominated by inter-allelic conversion-like events most likely occurring at meiosis and apparently regulated by cis-acting mutation initiator elements. Attempts to define these initiators in transgenic mice have so far been thwarted by what appears to be a major human/mouse barrier to the inter-species transfer of repeat instability. Minisatellites not only show high frequency spontaneous mutation in the germline, but also appear to be very sensitive to mutation induction by ionizing radiation, both in experimentally irradiated mice and in human populations exposed following the Chernobyl disaster; the mechanisms of mutation induction by radiation remain enigmatic.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/elps.1150180903
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    facet.materialart.
    Unknown
    Requirement of the DEAD-Box protein ded1p for messenger RNA translation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-07
    Description: The DED1 gene, which encodes a putative RNA helicase, has been implicated in nuclear pre-messenger RNA splicing in the yeast Saccharomyces cerevisiae. It is shown here by genetic and biochemical analysis that translation, rather than splicing, is severely impaired in two newly isolated ded1 conditional mutants. Preliminary evidence suggests that the protein Ded1p may be required for the initiation step of translation, as is the distinct DEAD-box protein, eukaryotic initiation factor 4A (eIF4A). The DED1 gene could be functionally replaced by a mouse homolog, PL10, which suggests that the function of Ded1p in translation is evolutionarily conserved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chuang, R Y -- Weaver, P L -- Liu, Z -- Chang, T H -- GM48752/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular, Cellular, and Developmental Biology Program, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9045610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoplasm/metabolism ; DEAD-box RNA Helicases ; Eukaryotic Initiation Factor-4A ; Genes, Fungal ; Mice ; Mutation ; Peptide Initiation Factors/genetics/metabolism ; Phenotype ; *Protein Biosynthesis ; RNA Helicases ; RNA Nucleotidyltransferases/genetics/*metabolism ; RNA Splicing ; RNA, Fungal/*genetics ; RNA, Messenger/*genetics ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; *Saccharomyces cerevisiae Proteins
    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
  • 9
    facet.materialart.
    Unknown
    Integrating genetic approaches into the discovery of anticancer drugs (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-14
    Description: The discovery of anticancer drugs is now driven by the numerous molecular alterations identified in tumor cells over the past decade. To exploit these alterations, it is necessary to understand how they define a molecular context that allows increased sensitivity to particular compounds. Traditional genetic approaches together with the new wealth of genomic information for both human and model organisms open up strategies by which drugs can be profiled for their ability to selectively kill cells in a molecular context that matches those found in tumors. Similarly, it may be possible to identify and validate new targets for drugs that would selectively kill tumor cells with a particular molecular context. This article outlines some of the ways that yeast genetics can be used to streamline anticancer drug discovery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hartwell, L H -- Szankasi, P -- Roberts, C J -- Murray, A W -- Friend, S H -- N01-BC65017/BC/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1064-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Project, Molecular Pharmacology Department, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353181" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antineoplastic Agents/pharmacology/therapeutic use ; *Drug Design ; *Drug Screening Assays, Antitumor ; Humans ; Mutation ; Neoplasms/*drug therapy/genetics ; Signal Transduction ; Yeasts/genetics
    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
  • 10
    facet.materialart.
    Unknown
    Requirement of guanosine triphosphate-bound ran for signal-mediated nuclear protein export (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: A leucine-rich nuclear export signal (NES) allows rapid export of proteins from cell nuclei. Microinjection studies revealed a role for the guanosine triphosphatase (GTPase) Ran in NES-mediated export. Nuclear injection of a Ran mutant (Thr24 --〉 Asn) blocked protein export but not import, whereas depletion of the Ran nucleotide exchange factor RCC1 blocked protein import but not export. However, injection of Ran GTPase-activating protein (RanGAP) into RCC1-depleted cell nuclei inhibited export. Coinjection with Ran mutants insensitive to RanGAP prevented this inhibition. Therefore, NES-mediated protein export appears to require a Ran-GTP complex but does not require Ran-dependent GTP hydrolysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Richards, S A -- Carey, K L -- Macara, I G -- EST3207122/ES/NIEHS NIH HHS/ -- GM 50526/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1842-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Vermont, Burlington, VT 05405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Carrier Proteins/metabolism ; *Cell Cycle Proteins ; Cell Line ; Cell Nucleus/*metabolism ; Cricetinae ; Cytoplasm ; DNA-Binding Proteins/metabolism ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/metabolism ; *GTPase-Activating Proteins ; Glutathione Transferase/metabolism ; Green Fluorescent Proteins ; *Guanine Nucleotide Exchange Factors ; Guanosine Triphosphate/*metabolism ; Luminescent Proteins/metabolism ; Mutation ; Nuclear Envelope/metabolism ; Nuclear Localization Signals ; Nuclear Proteins/genetics/*metabolism ; Receptors, Glucocorticoid/metabolism ; Recombinant Fusion Proteins/metabolism ; Temperature ; ran GTP-Binding Protein
    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
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...