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  • 1
    Electronic Resource
    Electronic Resource
    Characterization of the hamster DDT-1 cell aFGF/HGBF-I gene and cDNA and its modulation by steroids (1990)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 43 (1990), S. 17-26 
    Details
    ISSN: 0730-2312
    Keywords: DDT-1 cells ; acidic FGF ; HBGF-I ; gene and cDNA ; androgen ; in situ hybridization ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Syrian hamster DDT-1 cells are derived from smooth muscle of the ductus deferens. DDT-1 cell growth is increased by the addition of testosterone (T). Acidic fibroblast growth factor (aFGF) or basic fibroblast growth factor (bFGF) also known as heparin binding growth factor I and II (HBGF-I and HBGF-II) can replace T in the stimulation of growth in these cells. This phenomenon is correlated with testosterone's ability to elevate aFGF/HBGF-I mRNA. The increase steady-state levels of aFGF/HBGF-I mRNA were documented by northern blots and by in situ hybridization. Using a 520 bp human aFGF/HBGF-I cDNA probe, a genomic clone with a 38 kb DNA insert was isolated from a cosmid library. By restriction enzyme analysis and southern hybridization, it was determined that there are three coding exons. DNA sequence analysis showed all of the coding region and 3′ noncoding sequences were on this clone. A 5′ noncoding exon not in the 38 kb insert is indicated, based on the cDNA sequences and genomic sequences of aFGF/HBGF-I's from hamster DDT-1 cells and several other species. The cDNA for hamster aFGF/HBGF-I was isolated from a DDT-1 lambda gt11 library and sequenced. Comparison of the coding region of aFGF/HBGF-I from four species shows a 〉90% conservation of amino acid sequence.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240430103
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  • 2
    Electronic Resource
    Electronic Resource
    Acidic fibroblast growth factor gene 5′ non-coding exon and flanking region from hamster DDT1 cells: Identification of the promoter region and transcriptional regulation by testosterone and aFGF protein (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 51 (1993), S. 116-127 
    Details
    ISSN: 0730-2312
    Keywords: heparin binding growth factor 1 ; mRNA ; Syrian hamster ; acidic fibroblast growth factor gene ; testosterone ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Selected clones of Syrian hamster DDT1-MF2 cells are responsive to testosterone for growth. Heparin binding growth factor 1 (HBGF-1) or acidic fibroblast growth factor (aFGF) can replace testosterone (T) in the stimulation of growth in these cells. This phenomena is correlated with testosterone's ability to elevate aFGF mRNA two- to threefold in DDT1 cells. To better understand the possible mechanisms of regulation of aFGF mRNA by steroids and other growth factors, we isolated the aFGF 5′ non-coding exon and its flanking region from a EMBL3 DDT1 genomic library, using a 5′ non-coding exon 69 bp DDT1 aFGF cDNA probe. Clones spanning 30 kb of genomic DNA were isolated. After restriction mapping and DNA sequence analysis, the clones were shown to contain all of the 5′ non-coding exon included in the cDNA and approximately 10 kb of 5′ flanking region. RNase protection and primer extension assays confirmed that the 5′ non-coding exon is included in the DDT1 aFGF mRNA and that a major transcription start site is approximately 136 bp upstream of the 5′ non-coding splice junction of this exon. The 5′ flanking region DNA was inserted into pBLCAT3 reporter gene and transfected into DDT1 cells. Chloramphenicol acetyltransferase (CAT) assays demonstrated that there are promoter elements in the -1645/-392 and -392/+131 regions of the aFGF gene in the context of DDT1 cells. NIH 3T3 cells, on the other hand, show no CAT activity with these aFGF-CAT plasmids. CAT assays also demonstrated that addition of testosterone (T) or aFGF to DDT1 cells increased CAT activity threefold. This activity was mapped to -1645 to -4 bp region of this DDT1 aFGF gene promoter. © 1993 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240510118
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  • 3
    Electronic Resource
    Electronic Resource
    Platelet-derived growth factor-induced alterations in vinculin distribution in porcine vascular smooth muscle cells (1987)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 8 (1987), S. 91-105 
    Details
    ISSN: 0886-1544
    Keywords: vinculin ; PDGF ; cell growth ; vascular smooth muscle ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Exposure of porcine vascular smooth muscle cells to platelet-derived growth factor (PDGF; 18-180 ng/ml) but not epidermal growth factor (EGF; 30ng/ml), somatomedin C (SmC; 30 ng/ml), or insulin (10 μM), results in a rapid, reversible, time- and concentration-dependent disapperance of vinculin staining in adhesion plaques; actin-containing stress fibers also become disrupted following exposure of cells to PDGF. Disapperance of vinculin staining from adhesion plaques is also caused by 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 200-400 nM), though the time course of the disapperance of vinculin staining under these conditions takes longer than in cells exposed to PDGF. The PDGF-induced removal of vinculin from adhesion plaques was inhibited in a concentration-dependent fashion by 8-(N, N-diethylamin) octy1-3,4,5-trimethoxybenzoate (TMA-8; 0.25-4 μM) and leupepetin (2-300 μM), and by n-α-rosyl-L-lysine chloromethylketone (TLCK; 100 μM) and trifluoperazine (TFP; 2.5 μM). Addition of PDGF to vascular smooth muscle cells caused a rapid, tranient increase in cytosolic free calcium, from a basal resting level of 146 ± 6.9 nM (SEM, n=62) to 414 ± 34 nM (SEM, n=22) as determined using the calcium-sensitive indicator Fura-2 and Digitized Video Microscopy. This increase in cellular calcium preceded the disappearance of vinculin from adhesion plaques and was partially blocked by pretreatment of cells with TMB-8 but not leupeption. This rise in cytosolic free calcium was found to occur in ∼ 80% of the sample population and dispalyed both spatial and temporal subcellular heterogeneity. Exposure of cells to TPA (100 nM) did not result in a change in cytosolic free calcium. Both PDGF (20 ng/ml) and TPA (100 nM) caused cytosolic alkalinization which occurred after PDGF-induced disruption of vinculin from adhesion plaques, as determined using the pH-sensitive indicator BCECF and Digitized Video Microscopy. PDGF stimulated DNA synthesis and vinculin disruption in a similar dose-dependent fashion. Both could be inhibited by leupeptin or TMB-8. These results suggest that 1) exposure of vascular smooth muscle cells to PDGF is associated with the disruption of vinculin from adhesion plaques, 2) PDGF-induced vinculin disruption is regulated by an increase in cytosolic calcium (but not cytosolic alkalinization), and involves proteolysis; 3) activation of protein kinase C also causes vinculin removal from adhesion plaques but by a calcium-independent mechanism, and 4) the cellular response to PDGF-stimulated increases in cytosolic free calcium is heterogeneous. Our data also suggest that cytosolic vinculin distribution is a sensitive indicator of the response of vascular smooth muslce cells to PDGF.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970080202
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  • 4
    Electronic Resource
    Electronic Resource
    Localization of p35 (annexin I, lipocortin I) in normal adult rat kidney and during recovery from ischemia (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 153 (1992), S. 467-476 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The 35-kDa protein (p35, lipocortin I, annexin I), originally discovered as a Ca++-dependent substrate for the EGF receptor tyrosine kinase, binds Ca++ and phospholipids, is developmentally regulated in embryos and has restricted expression in adults. Immunohistochemistry of normal rat kidney shows that p35 is enriched in epithelia of Bowman's capsule, the macula densa, and medullary/papillary collecting ducts, suggesting that p35 is related to specialized renal functions. Light staining is observed in the thick ascending limb; elsewhere, immunoreactivity is nil. Since renal recovery from ischemia involves both hyperplasia and hypertrophy and reportedly is accelerated by EGF, we examined p35 distribution during this process. After 48 hours of recovery, both the distribution and amount of renal p35 are altered. Immunoblots show p35 levels increased at least threefold in whole-kidney homogenates. The expression of p35 is still highly restricted in recovering kidneys; however, the thick ascending limb now stains heavily. This is the first documentation of alterations in annexin levels during a pathophysiologic response. However, our attempts to discern effects of exogenous EGF on the recovery from ischemia were negative for both mitotic index and renal function assays. © 1992 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041530305
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  • 5
    Electronic Resource
    Electronic Resource
    Recipes for the molecular biologist. Current Protocols in Molecular Biology. Edited by F. M. Ausubel, R. Brent, R. E. Kingston, D. D. Moore, J. F. Seidman, J. A. Smith and K. Struhl John Wiley and Sons. Inc., N.Y. Pp. 650. $180.00 for core volume; $300 for the core book + supplements (1989)
    New York, NY : Wiley-Blackwell
    BioEssays 10 (1989), S. 132-132 
    Details
    ISSN: 0265-9247
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bies.950100413
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  • 6
    Electronic Resource
    Electronic Resource
    Roots: Cell fusion (1985)
    New York, NY : Wiley-Blackwell
    BioEssays 2 (1985), S. 176-179 
    Details
    ISSN: 0265-9247
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: There is a tendency for living things to join up, establish linkage, live inside each other, return to earlier arrangements, get along, whenever possible. This is the way of the world.The new phenomenon of cell fusion, a laboratory trick on which much of today's science of molecular genetics relies for its data, is the simplest and most spectacular symbol of the tendency. In a way, it is the most unbiologic of all phenomena, violating the most fundamental myths of the last century, for it denies the importance of specificity, integrity, and separateness in living things. Any cell - man, animal, fish, fowl, or insect - given the chance and under the right conditions, brought into contact with any other cell, however foreign, will fuse with it. Cytoplasm will flow easily from one to the other, the nuclei will combine, and it will become, for a time anyway, a single cell with two complete, alien genomes, ready to dance, ready to multiply. It is a Chimera, a Griffon, a Sphinx, a Ganesha, a Peruvian God, a Ch'i-lin, an omen of good fortune, a wish for the world.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bies.950020409
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  • 7
    Electronic Resource
    Electronic Resource
    Growth promoting agents in cell fractions of chick embryosSupported by grants from the Cancer Research Coordinating Committee, University of California, and from the Oak Ridge Institute of Nuclear Studies. (1954)
    Philadelphia : Wiley-Blackwell
    Journal of Cellular and Comparative Physiology 43 (1954), S. 193-204 
    Details
    ISSN: 0095-9898
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Additional Material: 2 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1030430205
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  • 8
    Electronic Resource
    Electronic Resource
    Occurrence of respiration deficient mutants in baker's yeast cultivated anaerobically (1956)
    Philadelphia : Wiley-Blackwell
    Journal of Cellular and Comparative Physiology 48 (1956), S. 95-112 
    Details
    ISSN: 0095-9898
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1030480107
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  • 9
    Electronic Resource
    Electronic Resource
    The use of dialyzed media for studies in cell nutrition (1952)
    Philadelphia : Wiley-Blackwell
    Journal of Cellular and Comparative Physiology 40 (1952), S. 279-301 
    Details
    ISSN: 0095-9898
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1030400209
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  • 10
    Electronic Resource
    Electronic Resource
    Utilization of added sugars by chick heart fibroblasts in dialyzed mediaSupported by grants from the Cancer Research Coordinating Committee, University of California. (1953)
    Philadelphia : Wiley-Blackwell
    Journal of Cellular and Comparative Physiology 42 (1953), S. 449-469 
    Details
    ISSN: 0095-9898
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1030420310
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