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Journal articles on the topic 'Mutantp53'

Author: Grafiati
Published: 1 April 2023

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1

Shi, Xu-Bao, Nancy J. Nesslinger, Arline D. Deitch, Paul H. Gumerlock, and Ralph W. deVere White. "Complex functions of mutantp53 alleles from human prostate cancer." Prostate 51, no. 1 (March 19, 2002): 59–72. http://dx.doi.org/10.1002/pros.10072.

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2

de Kant, Eric, Immo Heide, Christian Thiede, Richard Herrmann, and Christoph F. Rochlitz. "MDR1 expression correlates with mutantp53 expression in colorectal cancer metastases." Journal of Cancer Research and Clinical Oncology 122, no. 11 (November 1996): 671–75. http://dx.doi.org/10.1007/bf01209030.

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3

Wyllie, Fiona S., Nick R. Lemoine, Claire M. Barton, Tim Dawson, Jane Bond, and David Wynford-Thomas. "Direct growth stimulation of normal human epithelial cells by mutantp53." Molecular Carcinogenesis 7, no. 2 (1993): 83–88. http://dx.doi.org/10.1002/mc.2940070205.

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4

Karlsson, Lena, Gunilla Leser, Ulla Delle, and György Horvath. "Tumour Growth and Cell Kinetics in Variants of a Human Endometrial Adenocarcinoma Expressing Either Wild-Type or Mutantp53." Acta Oncologica 36, no. 7 (January 1997): 729–33. http://dx.doi.org/10.3109/02841869709001346.

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5

Di Agostino, Silvia, Giancarlo Cortese, Olimpia Monti, Stefania Dell'Orso, Ada Sacchi, Miriam Eisenstein, Gennaro Citro, Sabrina Strano, and Giovanni Blandino. "The disruption of the protein complex mutantp53/p73 increases selectively the response of tumor cells to anticancer drugs." Cell Cycle 7, no. 21 (November 2008): 3440–47. http://dx.doi.org/10.4161/cc.7.21.6995.

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6

Kawashima, Kunihiro, Koichiro Mihara, Hisashi Usuki, Nobuyoshi Shimizu, and Masayoshi Namba. "Transfected mutantp53 gene increases X-ray-induced cell killing and mutation in human fibroblasts immortalized with 4-nitroquinoline 1-oxide but does not induce neoplastic transformation of the cells." International Journal of Cancer 61, no. 1 (March 29, 1995): 76–79. http://dx.doi.org/10.1002/ijc.2910610113.

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7

CHEN, Hong-Lin, Yang-Hai XIANG, Ji-Ying ZHAO, De-Dong YIN, Guo-Hua LIANG, Wen-Xue ZHAI, and Guang-Huai JIANG. "Genetic Analysis and Gene Fine Mapping of Rice Lesion Mimic Mutantc5." Acta Agronomica Sinica 39, no. 7 (2013): 1148. http://dx.doi.org/10.3724/sp.j.1006.2013.01148.

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8

Kanai, Nobuko, Theresa M. Vreeke, and Charles J. Parker. "Paroxysmal nocturnal hemoglobinuria: Analysis of the effects of mutantPIG-A on gene expression." American Journal of Hematology 61, no. 4 (August 1999): 221–31. http://dx.doi.org/10.1002/(sici)1096-8652(199908)61:4<221::aid-ajh1>3.0.co;2-#.

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9

Pothin, H. S., K. V. C. L. da Silva, M. Brendel, and J. A. P. Henriques. "Genetic effects of photoactivated psoralens during meiosis in DNA repair mutantpso3-1 ofSaccharomyces cerevisiae." Current Genetics 25, no. 1 (January 1994): 19–23. http://dx.doi.org/10.1007/bf00712961.

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10

Neff, Anton W., F. Briggs, and H. M. Chung. "Craniofacial development mutantpi (pinhead) in the Axolotl (Ambystoma mexicanum) which exhibits reduced interocular distance." Journal of Experimental Zoology 241, no. 3 (March 1987): 309–16. http://dx.doi.org/10.1002/jez.1402410305.

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11

Duan, Jingbo, Hong Yu, Kun Yuan, Zhigang Liao, Xiangbing Meng, Yanhui Jing, Guifu Liu, Jinfang Chu, and Jiayang Li. "Strigolactone promotes cytokinin degradation through transcriptional activation ofCYTOKININ OXIDASE/DEHYDROGENASE 9in rice." Proceedings of the National Academy of Sciences 116, no. 28 (June 24, 2019): 14319–24. http://dx.doi.org/10.1073/pnas.1810980116.

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Strigolactones (SLs), a group of terpenoid lactones derived from carotenoids, are plant hormones that control numerous aspects of plant development. Although the framework of SL signaling that the repressor DWARF 53 (D53) could be SL-dependently degraded via the SL receptor D14 and F-box protein D3 has been established, the downstream response genes to SLs remain to be elucidated. Here we show that the cytokinin (CK) content is dramatically increased in shoot bases of the rice SL signaling mutantd53. By examining transcript levels of all the CK metabolism-related genes after treatment with SL analog GR24, we identifiedCYTOKININ OXIDASE/DEHYDROGENASE 9(OsCKX9) as a primary response gene significantly up-regulated within 1 h of treatment in the wild type but not ind53. We also found that OsCKX9 functions as a cytosolic and nuclear dual-localized CK catabolic enzyme, and that the overexpression ofOsCKX9suppresses the browning ofd53calli. Both the CRISPR/Cas9-generatedOsCKX9mutants andOsCKX9-overexpressing transgenic plants showed significant increases in tiller number and decreases in plant height and panicle size, suggesting that the homeostasis ofOsCKX9plays a critical role in regulating rice shoot architecture. Moreover, we identified the CK-inducible rice type-A response regulatorOsRR5as the secondary SL-responsive gene, whose expression is significantly repressed after 4 h of GR24 treatment in the wild type but not inosckx9. These findings reveal a comprehensive plant hormone cross-talk in which SL can induce the expression ofOsCKX9to down-regulate CK content, which in turn triggers the response of downstream genes.
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12

O’Neil, Michael T., Michael L. J. Korsinczky, Karryn J. Gresty, Alyson Auliff, and Qin Cheng. "A NovelPlasmodium falciparumExpression System for Assessing Antifolate Resistance Caused by MutantP. vivaxDihydrofolate Reductase–Thymidylate Synthase." Journal of Infectious Diseases 196, no. 3 (August 2007): 467–74. http://dx.doi.org/10.1086/519286.

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13

Hall, Jeremy A., David Peirson, Sibdas Ghosh, and Bernard Glick R. "ROOT ELONGATION IN VARIOUS AGRONOMIC CROPS BY THE PLANT GROWTH PROMOTING RHIZOBACTERIUM PSEUDOMONAS PUTIDA GR12–2." Israel Journal of Plant Sciences 44, no. 1 (May 13, 1996): 37–42. http://dx.doi.org/10.1080/07929978.1996.10676631.

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Seeds of canola, lettuce, tomato, barley, wheat, and oats were inoculated with either the wild-type plant growth promoting rhizobacterium (PGPR),Pseudomonas putidaGR12–2, or the mutantP. putidaGR 12–2lacd68 (deficient in the activity of the enzyme 1-aminocyclopropane-1-carboxylate deaminase) alone and in conjunction with either an inhibitor of ethylene biosynthesis, L-α-(aminoethoxyvinyl)-glycine (AVG), or the chemical ethylene generator, (2-chloroethyl) phosphonic acid (ethophon). For the different treatments, variations in root length under gnotobiotic conditions were compared. Canola, lettuce, tomato, and wheat responded to all of the treatments in a similar manner: The root lengths increased when seeds were treated withP. putidaGR 12–2 and/or AVG but not with the mutant strain, in comparison with a MgSO4control treatment, while the ethophon treatment inhibited root elongation. With barley and oat, none of the treatments had any effect on root lengths; however, when the ethophon concentration was increased, root elongation of these two plants was also inhibited. These observations are consistent with a model in which promotion of root growth byP. putidaGR 12–2 is a consequence of inhibition of ethylene production within the developing seedling.
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14

Son, Myunghan, Yuseok Moon, Mi Jin Oh, Sang Bin Han, Ki Hyun Park, Jung-Gon Kim, and Jung Hoon Ahn. "Lipase and Protease Double-Deletion Mutant of Pseudomonas fluorescens Suitable for Extracellular Protein Production." Applied and Environmental Microbiology 78, no. 23 (October 5, 2012): 8454–62. http://dx.doi.org/10.1128/aem.02476-12.

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ABSTRACTPseudomonas fluorescens, a widespread Gram-negative bacterium, is an ideal protein manufacturing factory (PMF) because of its safety, robust growth, and high protein production.P. fluorescenspossesses a type I secretion system (T1SS), which mediates secretion of a thermostable lipase (TliA) and a protease (PrtA) through its ATP-binding cassette (ABC) transporter. Recombinant proteins inP. fluorescensare attached to the C-terminal signal region of TliA for transport as fusion proteins to the extracellular medium. However, intrinsic TliA from theP. fluorescensgenome interferes with detection of the recombinant protein and the secreted recombinant protein is hydrolyzed, due to intrinsic PrtA, resulting in decreased efficiency of the PMF. In this research, the lipase and protease genes ofP. fluorescensSIK W1 were deleted using the targeted gene knockout method. Deletion mutantP. fluorescensΔtliAΔprtAsecreted fusion proteins without TliA or protein degradation. Using wild-typeP. fluorescensas an expression host, degradation of the recombinant protein varied depending on the type of culture media and aeration; however, degradation did not occur with theP. fluorescensΔtliAΔprtAdouble mutant irrespective of growth conditions. By homologous expression oftliAand the ABC transporter in a plasmid, TliA secreted fromP. fluorescensΔprtAandP. fluorescensΔtliAΔprtAcells was found to be intact, whereas that secreted from the wild-typeP. fluorescensandP. fluorescensΔtliAcells was found to be hydrolyzed. Our results demonstrate that theP. fluorescensΔtliAΔprtAdeletion mutant is a promising T1SS-mediated PMF that enhances production and detection of recombinant proteins in extracellular media.
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15

Klinke, Stefan, Michael Dauner, George Scott, Birgit Kessler, and Bernard Witholt. "Inactivation of Isocitrate Lyase Leads to Increased Production of Medium-Chain-Length Poly(3-Hydroxyalkanoates) inPseudomonas putida." Applied and Environmental Microbiology 66, no. 3 (March 1, 2000): 909–13. http://dx.doi.org/10.1128/aem.66.3.909-913.2000.

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ABSTRACT Medium-chain-length (mcl) poly(3-hydroxyalkanoates) (PHAs) are storage polymers that are produced from various substrates and accumulate in Pseudomonas strains belonging to rRNA homology group I. In experiments aimed at increasing PHA production inPseudomonas strains, we generated an mcl PHA-overproducing mutant of Pseudomonas putida KT2442 by transposon mutagenesis, in which the aceA gene was knocked out. This mutation inactivated the glyoxylate shunt and reduced the in vitro activity of isocitrate dehydrogenase, a rate-limiting enzyme of the citric acid cycle. The genotype of the mutant was confirmed by DNA sequencing, and the phenotype was confirmed by biochemical experiments. The aceA mutant was not able to grow on acetate as a sole carbon source due to disruption of the glyoxylate bypass and exhibited two- to fivefold lower isocitrate dehydrogenase activity than the wild type. During growth on gluconate, the difference between the mean PHA accumulation in the mutant and the mean PHA accumulation in the wild-type strain was 52%, which resulted in a significant increase in the amount of mcl PHA at the end of the exponential phase in the mutantP. putida KT217. On the basis of a stoichiometric flux analysis we predicted that knockout of the glyoxylate pathway in addition to reduced flux through isocitrate dehydrogenase should lead to increased flux into the fatty acid synthesis pathway. Therefore, enhanced carbon flow towards the fatty acid synthesis pathway increased the amount of mcl PHA that could be accumulated by the mutant.
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16

Baumgarten, Thomas, Susan Schlegel, Samuel Wagner, Mirjam Löw, Jonas Eriksson, Ida Bonde, Markus J. Herrgård, et al. "Isolation and characterization of the E. coli membrane protein production strain Mutant56(DE3)." Scientific Reports 7, no. 1 (March 24, 2017). http://dx.doi.org/10.1038/srep45089.

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