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  • Articles  (185)
  • Biochemistry and Biotechnology  (98)
  • Mutation  (87)
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  • Articles  (185)
  • 1
    Publication Date: 2009-12-17
    Description: The molecular mechanisms underlying major phenotypic changes that have evolved repeatedly in nature are generally unknown. Pelvic loss in different natural populations of threespine stickleback fish has occurred through regulatory mutations deleting a tissue-specific enhancer of the Pituitary homeobox transcription factor 1 (Pitx1) gene. The high prevalence of deletion mutations at Pitx1 may be influenced by inherent structural features of the locus. Although Pitx1 null mutations are lethal in laboratory animals, Pitx1 regulatory mutations show molecular signatures of positive selection in pelvic-reduced populations. These studies illustrate how major expression and morphological changes can arise from single mutational leaps in natural populations, producing new adaptive alleles via recurrent regulatory alterations in a key developmental control gene.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109066/" 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/PMC3109066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Yingguang Frank -- Marks, Melissa E -- Jones, Felicity C -- Villarreal, Guadalupe Jr -- Shapiro, Michael D -- Brady, Shannon D -- Southwick, Audrey M -- Absher, Devin M -- Grimwood, Jane -- Schmutz, Jeremy -- Myers, Richard M -- Petrov, Dmitri -- Jonsson, Bjarni -- Schluter, Dolph -- Bell, Michael A -- Kingsley, David M -- P50 HG002568/HG/NHGRI NIH HHS/ -- P50 HG002568-09/HG/NHGRI NIH HHS/ -- P50 HG02568/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):302-5. doi: 10.1126/science.1182213. Epub 2009 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007865" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Biological Evolution ; Chromosome Fragile Sites ; Chromosome Mapping ; Crosses, Genetic ; DNA, Intergenic ; *Enhancer Elements, Genetic ; Fish Proteins/*genetics ; Molecular Sequence Data ; Mutation ; Paired Box Transcription Factors/*genetics ; Pelvis/anatomy & histology ; Selection, Genetic ; *Sequence Deletion ; Smegmamorpha/*anatomy & histology/*genetics/growth & development
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 53 (1997), S. 397-405 
    ISSN: 0006-3592
    Keywords: airlift reactor ; biofilm ; biofilm detachment ; control biofilm formation ; heterotrophic layer ; hydraulic retention time ; nitrification ; oxygen diffusion limitation ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: A Biofilm Airlift Suspension (BAS) reactor was operated with nitrifying biofilm growth and heterotrophic suspended growth, simultaneously converting ammonium and acetate. Growth of heterotrophs in suspension decreases the diffusion limitation for the nitrifiers, and enlarges the nitrifying capacity of a biofilm reactor. Neither nitrifiers nor heterotrophs suffer from additional oxygen diffusion limitation when the heterotrophs grow in suspension. Control of the location of heterotrophic growth, either in suspension or in biofilms over the nitrifying biofilms, was possible by manipulation of the hydraulic retention time. A time delay for formation and disappearance of the heterotrophic biofilms of 10 to 15 days was observed. Surprisingly, it was found that in the presence of the heterotrophic layers the maximum specific activity on ammonia of the nitrifying biofilms increased. The reason for the increase in activity is unknown. The effect of heterotrophic biofilm formation on oxygen diffusion limitation for the nitrifiers is discussed. Some phenomena compensating the increased mass transfer resistance due to the growth of a heterotrophic layer are also presented. © 1997 John Wiley & Sons, Inc. Biotechnol Bioeng 53: 397-405, 1997.
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-07-15
    Description: Mutation at the mouse progressive ankylosis (ank) locus causes a generalized, progressive form of arthritis accompanied by mineral deposition, formation of bony outgrowths, and joint destruction. Here, we show that the ank locus encodes a multipass transmembrane protein (ANK) that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. A highly conserved gene is present in humans and other vertebrates. These results identify ANK-mediated control of pyrophosphate levels as a possible mechanism regulating tissue calcification and susceptibility to arthritis in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, A M -- Johnson, M D -- Kingsley, D M -- 5T32GM07365/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):265-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Howard Hughes Medical Institute, Beckman Center B300, Stanford University School of Medicine, Stanford, CA 94305-5327, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*genetics/metabolism/pathology ; Base Sequence ; Biological Transport ; COS Cells ; Calcinosis/*genetics ; Chromosome Mapping ; Cloning, Molecular ; Dna ; Diphosphates/*metabolism ; Durapatite/metabolism ; Gene Expression ; Genetic Complementation Test ; Humans ; Membrane Proteins/*genetics/metabolism/*physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Phenotype ; Phosphate Transport Proteins ; Physical Chromosome Mapping ; Sequence Homology, Nucleic Acid ; Tissue Distribution
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2003-12-13
    Description: Even though human and chimpanzee gene sequences are nearly 99% identical, sequence comparisons can nevertheless be highly informative in identifying biologically important changes that have occurred since our ancestral lineages diverged. We analyzed alignments of 7645 chimpanzee gene sequences to their human and mouse orthologs. These three-species sequence alignments allowed us to identify genes undergoing natural selection along the human and chimp lineage by fitting models that include parameters specifying rates of synonymous and nonsynonymous nucleotide substitution. This evolutionary approach revealed an informative set of genes with significantly different patterns of substitution on the human lineage compared with the chimpanzee and mouse lineages. Partitions of genes into inferred biological classes identified accelerated evolution in several functional classes, including olfaction and nuclear transport. In addition to suggesting adaptive physiological differences between chimps and humans, human-accelerated genes are significantly more likely to underlie major known Mendelian disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Andrew G -- Glanowski, Stephen -- Nielsen, Rasmus -- Thomas, Paul D -- Kejariwal, Anish -- Todd, Melissa A -- Tanenbaum, David M -- Civello, Daniel -- Lu, Fu -- Murphy, Brian -- Ferriera, Steve -- Wang, Gary -- Zheng, Xianqgun -- White, Thomas J -- Sninsky, John J -- Adams, Mark D -- Cargill, Michele -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671302" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus/genetics ; Amino Acids/metabolism ; Animals ; Biological Evolution ; Computational Biology ; *Evolution, Molecular ; Female ; Genes ; Genetic Diseases, Inborn/genetics ; *Genome ; *Genome, Human ; Humans ; Likelihood Functions ; Male ; Mice/genetics ; Models, Genetic ; Models, Statistical ; Mutation ; Pan troglodytes/*genetics ; Phylogeny ; Proteins/chemistry/genetics ; Pseudogenes ; Receptors, Odorant/genetics ; *Selection, Genetic ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Signal Transduction/genetics ; Smell/genetics ; Species Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-10-30
    Description: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530898/" 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/PMC3530898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biankin, Andrew V -- Waddell, Nicola -- Kassahn, Karin S -- Gingras, Marie-Claude -- Muthuswamy, Lakshmi B -- Johns, Amber L -- Miller, David K -- Wilson, Peter J -- Patch, Ann-Marie -- Wu, Jianmin -- Chang, David K -- Cowley, Mark J -- Gardiner, Brooke B -- Song, Sarah -- Harliwong, Ivon -- Idrisoglu, Senel -- Nourse, Craig -- Nourbakhsh, Ehsan -- Manning, Suzanne -- Wani, Shivangi -- Gongora, Milena -- Pajic, Marina -- Scarlett, Christopher J -- Gill, Anthony J -- Pinho, Andreia V -- Rooman, Ilse -- Anderson, Matthew -- Holmes, Oliver -- Leonard, Conrad -- Taylor, Darrin -- Wood, Scott -- Xu, Qinying -- Nones, Katia -- Fink, J Lynn -- Christ, Angelika -- Bruxner, Tim -- Cloonan, Nicole -- Kolle, Gabriel -- Newell, Felicity -- Pinese, Mark -- Mead, R Scott -- Humphris, Jeremy L -- Kaplan, Warren -- Jones, Marc D -- Colvin, Emily K -- Nagrial, Adnan M -- Humphrey, Emily S -- Chou, Angela -- Chin, Venessa T -- Chantrill, Lorraine A -- Mawson, Amanda -- Samra, Jaswinder S -- Kench, James G -- Lovell, Jessica A -- Daly, Roger J -- Merrett, Neil D -- Toon, Christopher -- Epari, Krishna -- Nguyen, Nam Q -- Barbour, Andrew -- Zeps, Nikolajs -- Australian Pancreatic Cancer Genome Initiative -- Kakkar, Nipun -- Zhao, Fengmei -- Wu, Yuan Qing -- Wang, Min -- Muzny, Donna M -- Fisher, William E -- Brunicardi, F Charles -- Hodges, Sally E -- Reid, Jeffrey G -- Drummond, Jennifer -- Chang, Kyle -- Han, Yi -- Lewis, Lora R -- Dinh, Huyen -- Buhay, Christian J -- Beck, Timothy -- Timms, Lee -- Sam, Michelle -- Begley, Kimberly -- Brown, Andrew -- Pai, Deepa -- Panchal, Ami -- Buchner, Nicholas -- De Borja, Richard -- Denroche, Robert E -- Yung, Christina K -- Serra, Stefano -- Onetto, Nicole -- Mukhopadhyay, Debabrata -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Gallinger, Steven -- Hruban, Ralph H -- Maitra, Anirban -- Iacobuzio-Donahue, Christine A -- Schulick, Richard D -- Wolfgang, Christopher L -- Morgan, Richard A -- Lawlor, Rita T -- Capelli, Paola -- Corbo, Vincenzo -- Scardoni, Maria -- Tortora, Giampaolo -- Tempero, Margaret A -- Mann, Karen M -- Jenkins, Nancy A -- Perez-Mancera, Pedro A -- Adams, David J -- Largaespada, David A -- Wessels, Lodewyk F A -- Rust, Alistair G -- Stein, Lincoln D -- Tuveson, David A -- Copeland, Neal G -- Musgrove, Elizabeth A -- Scarpa, Aldo -- Eshleman, James R -- Hudson, Thomas J -- Sutherland, Robert L -- Wheeler, David A -- Pearson, John V -- McPherson, John D -- Gibbs, Richard A -- Grimmond, Sean M -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- P01CA134292/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50CA062924/CA/NCI NIH HHS/ -- R01 CA097075/CA/NCI NIH HHS/ -- R01 CA97075/CA/NCI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Nov 15;491(7424):399-405. doi: 10.1038/nature11547. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kinghorn Cancer Centre, 370 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Carcinoma, Pancreatic Ductal/*genetics/*pathology ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genome/*genetics ; Humans ; Kaplan-Meier Estimate ; Mice ; Mutation ; Pancreatic Neoplasms/*genetics/*pathology ; Proteins/genetics ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2003-04-12
    Description: DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. To generate a higher order description, additional structural features such as imprinted genes, fragile sites, and segmental duplications were integrated at the level of the DNA sequence with medical genetic data, including 440 chromosome rearrangement breakpoints associated with disease. This approach enabled the discovery of candidate genes for developmental diseases including autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882961/" 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/PMC2882961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scherer, Stephen W -- Cheung, Joseph -- MacDonald, Jeffrey R -- Osborne, Lucy R -- Nakabayashi, Kazuhiko -- Herbrick, Jo-Anne -- Carson, Andrew R -- Parker-Katiraee, Layla -- Skaug, Jennifer -- Khaja, Razi -- Zhang, Junjun -- Hudek, Alexander K -- Li, Martin -- Haddad, May -- Duggan, Gavin E -- Fernandez, Bridget A -- Kanematsu, Emiko -- Gentles, Simone -- Christopoulos, Constantine C -- Choufani, Sanaa -- Kwasnicka, Dorota -- Zheng, Xiangqun H -- Lai, Zhongwu -- Nusskern, Deborah -- Zhang, Qing -- Gu, Zhiping -- Lu, Fu -- Zeesman, Susan -- Nowaczyk, Malgorzata J -- Teshima, Ikuko -- Chitayat, David -- Shuman, Cheryl -- Weksberg, Rosanna -- Zackai, Elaine H -- Grebe, Theresa A -- Cox, Sarah R -- Kirkpatrick, Susan J -- Rahman, Nazneen -- Friedman, Jan M -- Heng, Henry H Q -- Pelicci, Pier Giuseppe -- Lo-Coco, Francesco -- Belloni, Elena -- Shaffer, Lisa G -- Pober, Barbara -- Morton, Cynthia C -- Gusella, James F -- Bruns, Gail A P -- Korf, Bruce R -- Quade, Bradley J -- Ligon, Azra H -- Ferguson, Heather -- Higgins, Anne W -- Leach, Natalia T -- Herrick, Steven R -- Lemyre, Emmanuelle -- Farra, Chantal G -- Kim, Hyung-Goo -- Summers, Anne M -- Gripp, Karen W -- Roberts, Wendy -- Szatmari, Peter -- Winsor, Elizabeth J T -- Grzeschik, Karl-Heinz -- Teebi, Ahmed -- Minassian, Berge A -- Kere, Juha -- Armengol, Lluis -- Pujana, Miguel Angel -- Estivill, Xavier -- Wilson, Michael D -- Koop, Ben F -- Tosi, Sabrina -- Moore, Gudrun E -- Boright, Andrew P -- Zlotorynski, Eitan -- Kerem, Batsheva -- Kroisel, Peter M -- Petek, Erwin -- Oscier, David G -- Mould, Sarah J -- Dohner, Hartmut -- Dohner, Konstanze -- Rommens, Johanna M -- Vincent, John B -- Venter, J Craig -- Li, Peter W -- Mural, Richard J -- Adams, Mark D -- Tsui, Lap-Chee -- 38103/Canadian Institutes of Health Research/Canada -- P01 GM061354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 2;300(5620):767-72. Epub 2003 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Genomic Biology, The Hospital for Sick Children, Toronto, Ontario, Canada, M5G 1X8. steve@genet.sickkids.on.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics ; Chromosome Aberrations ; Chromosome Fragile Sites ; Chromosome Fragility ; Chromosome Mapping ; Chromosomes, Human, Pair 7/*genetics ; Computational Biology ; Congenital Abnormalities/genetics ; CpG Islands ; DNA, Complementary ; Databases, Genetic ; Euchromatin/genetics ; Expressed Sequence Tags ; Gene Duplication ; Genes, Overlapping ; Genetic Diseases, Inborn/genetics ; Genomic Imprinting ; Humans ; In Situ Hybridization, Fluorescence ; Limb Deformities, Congenital/genetics ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasms/genetics ; Pseudogenes ; RNA/genetics ; Retroelements ; *Sequence Analysis, DNA ; Williams Syndrome/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 8 (1966), S. 581-593 
    ISSN: 0006-3592
    Keywords: Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Biological systems can be used in three types of fuel cell: depolarization (or concentration) cell, product cell, and redox cell. The possibilities and theoretical limitations of each type of cell have been considered in terms of the metabolic activities of microorganisms and the coupling of these to electrochemical systems. The use of cell extracts and enzymes, particularly in an insoluble form, has been discussed.
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  • 8
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 9 (1967), S. 623-625 
    ISSN: 0006-3592
    Keywords: Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Additional Material: 1 Ill.
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  • 9
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 9 (1967), S. 515-531 
    ISSN: 0006-3592
    Keywords: Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: A method for the control of dissolved oxygen tension in growing microbial cultures is described. The apparatus consists of a motor-driven air sparge pipe which may be lowered or raised to give a variable point of entry of the air stream into the culture liquid and hence a variable gas dispersion and gas-liquid contact time. Control of the sparge pipe position is by means of a feedback control loop consisting of a dissolved oxygen probe, an on/off controller, and a reversing electric motor which drives the sparge pipe. The difficulty presented by the relatively slow response of the oxygen probe has been overcome by incorporating an adjustable rate of control action.
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  • 10
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 10 (1968), S. 815-828 
    ISSN: 0006-3592
    Keywords: Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: The intracellular levels of seven enzymes in mouse LS cells growing in suspension culture at controlled dissolved oxygen partial pressures (pO2) have been measured. During the growth of each culture large fluctuations were observed in the levels of some enzymes, particularly aldolase and cytochrome oxidase. Mean values for the concentration of each enzyme during the growth phase have been calculated. These results are discussed in relation to previous observations made on the growth of mouse LS cells.
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