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  • 1
    Electronic Resource
    Electronic Resource
    EGF induces cell cycle arrest of A431 human epidermoid carcinoma cells (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 127 (1986), S. 175-182 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The human carcinoma cell line A431 is unusual in that physiologic concentrations of epidermal growth factor (EGF) inhibit proliferation. In the presence of 5-10 nM EGF proliferation of A431 cells is abruptly and markedly decreased compared to the untreated control cultures, with little loss of cell viability over a 4-day period. This study was initiated to examine how EGF affects the progression of A431 cells through the cell cycle. Flow cytometric analysis of DNA in EGF-treated cells reveals a marked change in the cell cycle distribution. The percentage of cells in late S/G2 increases and early S phase is nearly depleted. Since addition of the mitotic inhibitor vinblastine causes accumulation of cells in mitosis and prevents reentry of cells into G1, it is possible to distinguish between slow progression through G1 and G2 and blocks in those phases. When control cells, not treated with EGF, are exposed to vinblastine, the cells accumulate mitotic figures, as expected, and show progression into S, thus diminishing the number of cells in G1. In contrast, no mitotic figures are found among the EGF-treated cells in the presence or absence of vinblastine, and progression from G1 into S is not observed, as the number of cells in G1 remains constant. These results suggest that there are two EGF-induced blocks in cell cycle transversal; one is in late S and/or G2, blocking entry into mitosis, and the other is in G1, blocking entry into S phase. After 24 hours of EGF treatment, DNA synthesis is reduced to less than 10% compared to untreated controls as measured by the incorporation of [3H]thymidine or BrdU. In contrast, protein synthesis is inhibited by about twofold. Although inhibition of protein synthesis is less extensive, it occurs 6 hours prior to an equivalent inhibition of DNA synthesis. The rapid decrease in protein synthesis may result in the subsequent cell cycle arrest which occurs several hours later.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041270121
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  • 2
    Electronic Resource
    Electronic Resource
    Genetic recombination in avian retroviruses (1982)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 19 (1982), S. 293-304 
    Details
    ISSN: 0730-2312
    Keywords: reverse-transcription ; strand-displacement synthesis ; heteroduplex DNA ; DNA H-structures ; proviral integration ; homologous recombination ; transduction ; recombination models ; RNA tumor viruses ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The avian retroviruses - and probably other retroviruses as well - undergo a variety of recombinational events with relatively high efficiency. An understanding of the molecular basis of these events should provide insight into the important biological properties these agents exhibit when they become integrated into somatic or germ-line host cells, when they exchange genetic information among themselves, or when they transduce host cell genes. In this article we review molecular models for homologous recombination, against a background of the other types of recombination events that arc typical of these viruses. It seems probable that the retroviruses will provide useful models for analysis of a variety of DNA rearrangements known to occur in eukaryotic cells.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240190311
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  • 3
    Electronic Resource
    Electronic Resource
    Developmental regulation of 14-3-3 ε isoform in rat heart (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 195-199 
    Details
    ISSN: 0730-2312
    Keywords: 14-3-3 protein ; developmental regulation ; heart development ; Raf-1 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Human heart cDNA sequencing yielded a cDNA clone that is similar in DNA and amino acid sequences to that of mouse 14-3-3 ε isoform. The 6xHis-tagged H1433ε recombinant protein was expressed in Escherichia coli and its size was approximately 30 kDa. From Northern blot results with human multiple tissues, human skeletal muscle was found to have the highest level of h1433ε mRNA expression, whereas Northern blots of human cancer cell lines detected the highest mRNA level of h1433ε in colorectal adenocarcinoma SW480. The protein expression level of h1433ε and Raf-1 is found to be regulated coordinately during rat heart development, and their protein expression was highest from 14.5 to 16.5 days postcoitum. J. Cell. Biochem. 68:195-199, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
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  • 4
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    Pathological alpha-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-20
    Description: Parkinson's disease is characterized by abundant alpha-synuclein (alpha-Syn) neuronal inclusions, known as Lewy bodies and Lewy neurites, and the massive loss of midbrain dopamine neurons. However, a cause-and-effect relationship between Lewy inclusion formation and neurodegeneration remains unclear. Here, we found that in wild-type nontransgenic mice, a single intrastriatal inoculation of synthetic alpha-Syn fibrils led to the cell-to-cell transmission of pathologic alpha-Syn and Parkinson's-like Lewy pathology in anatomically interconnected regions. Lewy pathology accumulation resulted in progressive loss of dopamine neurons in the substantia nigra pars compacta, but not in the adjacent ventral tegmental area, and was accompanied by reduced dopamine levels culminating in motor deficits. This recapitulation of a neurodegenerative cascade thus establishes a mechanistic link between transmission of pathologic alpha-Syn and the cardinal features of Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552321/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552321/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luk, Kelvin C -- Kehm, Victoria -- Carroll, Jenna -- Zhang, Bin -- O'Brien, Patrick -- Trojanowski, John Q -- Lee, Virginia M-Y -- NS053488/NS/NINDS NIH HHS/ -- P50 NS053488/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):949-53. doi: 10.1126/science.1227157.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, Institute on Aging and Center for Neurodegenerative Disease Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-4283, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23161999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Corpus Striatum/drug effects/*metabolism/pathology ; Dopamine ; Dopaminergic Neurons/drug effects/metabolism/pathology ; Injections ; Lewy Bodies/drug effects/*metabolism/pathology ; Mice ; Parkinsonian Disorders/*metabolism/pathology ; Protein Folding ; Protein Transport ; Recombinant Proteins/administration & dosage/chemistry/metabolism ; Substantia Nigra/drug effects/metabolism/pathology ; alpha-Synuclein/administration & dosage/chemistry/*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)
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  • 5
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    Ornithine decarboxylase: essential in proliferation but not differentiation of human promyelocytic leukemia cells (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-04-02
    Description: The ornithine decarboxylase inhibitor DL-alpha-difluoromethyl ornithine inhibited a proliferation-associated increase in ornithine decarboxylase activity in cultured human promyelocytic leukemia cells, resulting in a marked suppression of cell proliferation and subsequent cell loss. It also inhibited increases in ornithine decarboxylase activity associated with the phorbol ester-induced conversion of promyelocytic HL-60 cells to monocyte-like cells and the retinoic acid-induced conversion to granulocyte-like cells. However, the inhibition of ornithine decarboxylase activity did not prevent cellular differentiation. These results suggest that polyamine biosynthesis has a specific role in cell proliferation rather than in inducing differentiation that is not accompanied by proliferation. The data also demonstrate that cessation of proliferation in HL-60 cells is not necessarily associated with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luk, G D -- Civin, C I -- Weissman, R M -- Baylin, S B -- AM-27447/AM/NIADDK NIH HHS/ -- CA-18404/CA/NCI NIH HHS/ -- HL-19157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1982 Apr 2;216(4541):75-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6950518" target="_blank"〉PubMed〈/a〉
    Keywords: Carboxy-Lyases/*physiology ; Cell Adhesion ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Female ; Granulocytes/pathology ; Humans ; Leukemia, Myeloid, Acute/*enzymology/pathology ; Macrophages/pathology ; Ornithine Decarboxylase/*physiology ; Polyamines/biosynthesis ; Tetradecanoylphorbol Acetate/pharmacology ; Tretinoin/pharmacology
    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)
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