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Relevant bibliographies by topics / Cre Lox

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Academic literature on the topic 'Cre Lox'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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Journal articles on the topic "Cre Lox"

1

Lee, Linda, and Paul D. Sadowski. "Lox and Cre sandwich." Nature Chemical Biology 1, no. 5 (October 2005): 246–47. http://dx.doi.org/10.1038/nchembio1005-246.

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Becher, B., A. Waisman, and L. F. Lu. "Cre-lox: Target Sensitivity Matters." Immunity 51, no. 4 (October 2019): 595. http://dx.doi.org/10.1016/j.immuni.2019.09.012.

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Gewin, Leslie S. "The Cre/lox system: Cre-ating unintended damage." American Journal of Physiology-Renal Physiology 316, no. 5 (May 1, 2019): F873—F874. http://dx.doi.org/10.1152/ajprenal.00428.2018.

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Gilbertson, Larry. "Cre–lox recombination: Cre-ative tools for plant biotechnology." Trends in Biotechnology 21, no. 12 (December 2003): 550–55. http://dx.doi.org/10.1016/j.tibtech.2003.09.011.

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Testa, Giuseppe, and A. Francis Stewart. "Cre ating a trans lox ation." EMBO reports 1, no. 2 (August 2000): 120–21. http://dx.doi.org/10.1093/embo-reports/kvd035.

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Cui, Yunxia, Lu Huang, Florent Elefteriou, Guoqing Yang, John M. Shelton, Jerald E. Giles, Orhan K. Oz, et al. "Essential Role of STAT3 in Body Weight and Glucose Homeostasis." Molecular and Cellular Biology 24, no. 1 (January 1, 2004): 258–69. http://dx.doi.org/10.1128/mcb.24.1.258-269.2004.

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ABSTRACT STAT3 is a ubiquitous transcription factor that is indispensable during early embryogenesis. To study the functions of STAT3 postnatally, we generated conditional STAT3-deficient mice. To that end, STAT3lox/lox mice were crossed with mice expressing Cre under the control of rat insulin II gene promoter (RIP-Cre mice). Immunohistochemical and Western blot analyses showed that STAT3 is deleted from β cells in the islets of Langerhans. Genomic DNA PCR revealed that STAT3 deletion also occurred in the hypothalamus. Hypothalamic Cre expression was further confirmed by crossing RIP-Cre/STAT3lox/lox mice with the ROSA26 Cre reporter strain and staining for lacZ activity. Double immunohistochemical staining confirmed that deletion of STAT3 occurred in leptin receptor (OB-Rb isoform)-positive neurons. RIP-Cre/STAT3lox/lox mice are mildly hyperglycemic and hyperinsulinemic at the time of weaning, become hyperphagic immediately after weaning, and exhibit impaired glucose tolerance. Body weight, body fat, and mRNA and protein levels of leptin are all significantly increased in RIP-Cre/STAT3lox/lox mice. Administration of recombinant leptin by intracerebroventricular infusion failed to cause complete loss of body fat in RIP-Cre/STAT3lox/lox mice. Transplantation of wild-type islets into RIP-Cre/STAT3lox/lox mice also failed to decrease adiposity or to correct other abnormalities in these mice. These data thus suggest that loss of STAT3 in the hypothalamus caused by RIP-Cre action likely interferes with normal body weight homeostasis and glucose metabolism.

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Parrish, Diana C., Eric N. Alston, Hermann Rohrer, Sam M. Hermes, Sue A. Aicher, Paul Nkadi, William R. Woodward, Jutta Stubbusch, Ryan T. Gardner, and Beth A. Habecker. "Absence of gp130 in dopamine β-hydroxylase-expressing neurons leads to autonomic imbalance and increased reperfusion arrhythmias." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 3 (September 2009): H960—H967. http://dx.doi.org/10.1152/ajpheart.00409.2009.

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Inflammatory cytokines that act through glycoprotein (gp)130 are elevated in the heart after myocardial infarction and in heart failure. These cytokines are potent regulators of neurotransmitter and neuropeptide production in sympathetic neurons but are also important for the survival of cardiac myocytes after damage to the heart. To examine the effect of gp130 cytokines on cardiac nerves, we used gp130DBH-Cre/lox mice, which have a selective deletion of the gp130 cytokine receptor in neurons expressing dopamine β-hydroxylase (DBH). Basal sympathetic parameters, including norepinephrine (NE) content, tyrosine hydroxylase expression, NE transporter expression, and sympathetic innervation density, appeared normal in gp130DBH-Cre/lox compared with wild-type mice. Likewise, basal cardiovascular parameters measured under isoflurane anesthesia were similar in both genotypes, including mean arterial pressure, left ventricular peak systolic pressure, dP/d tmax, and dP/d tmin. However, pharmacological interventions revealed an autonomic imbalance in gp130DBH-Cre/lox mice that was correlated with an increased incidence of premature ventricular complexes after reperfusion. Stimulation of NE release with tyramine and infusion of the β-agonist dobutamine revealed blunted adrenergic transmission that correlated with decreased β-receptor expression in gp130DBH-Cre/lox hearts. Due to the developmental expression of the DBH-Cre transgene in parasympathetic ganglia, gp130 was eliminated. Cholinergic transmission was impaired in gp130DBH-Cre/lox hearts due to decreased parasympathetic drive, but tyrosine hydroxylase immunohistochemistry in the brain stem revealed that catecholaminergic nuclei appeared grossly normal. Thus, the apparently normal basal parameters in gp130DBH-Cre/lox mice mask an autonomic imbalance that includes alterations in sympathetic and parasympathetic transmission.

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Suzuki, Nobuaki, Hiroshi Nonaka, Yota Tsuge, Masayuki Inui, and Hideaki Yukawa. "New Multiple-Deletion Method for the Corynebacterium glutamicum Genome, Using a Mutant lox Sequence." Applied and Environmental Microbiology 71, no. 12 (December 2005): 8472–80. http://dx.doi.org/10.1128/aem.71.12.8472-8480.2005.

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ABSTRACT Due to the difficulty of multiple deletions using the Cre/loxP system, a simple, markerless multiple-deletion method based on a Cre/mutant lox system combining a right-element (RE) mutant lox site with a left-element (LE) mutant lox site was employed for large-scale genome rearrangements in Corynebacterium glutamicum. Eight distinct genomic regions that had been identified previously by comparative analysis of C. glutamicum R and C. glutamicum 13032 genomes were targeted for deletion. By homologous recombination, LE and RE mutant lox sites were integrated at each end of a target region. Highly efficient and accurate deletions between the two chromosomal mutant lox sites in the presence of Cre recombinase were realized. A deletion mutant lacking 190 kb of chromosomal regions, encoding a total of 188 open reading frames (ORFs), was obtained. These deletions represent the largest genomic excisions in C. glutamicum reported to date. Despite the loss of numerous predicted ORFs, the mutant exhibited normal growth under standard laboratory conditions. The Cre/loxP system using a pair of mutant lox sites provides a new, efficient genome rearrangement technique for C. glutamicum. It should facilitate the understanding of genome functions of microorganisms.

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Yan, Xin, Hao-Jie Yu, Qing Hong, and Shun-Peng Li. "Cre/lox System and PCR-Based Genome Engineering in Bacillus subtilis." Applied and Environmental Microbiology 74, no. 17 (July 18, 2008): 5556–62. http://dx.doi.org/10.1128/aem.01156-08.

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ABSTRACT We have developed a fast and accurate method to engineer the Bacillus subtilis genome that involves fusing by PCR two flanking homology regions with an antibiotic resistance gene cassette bordered by two mutant lox sites (lox71 and lox66). The resulting PCR products were used directly to transform B. subtilis, and then transient Cre recombinase expression in the transformants was used to recombine lox71 and lox66 into a double-mutant lox72 site, thereby excising the marker gene. The mutation process could also be accomplished in 2 days by using a strain containing a cre isopropyl-β-d-thiogalactopyranoside (IPTG)-inducible expression cassette in the chromosome as the recipient or using the lox site-flanked cassette containing both the cre IPTG-inducible expression cassette and resistance marker. The in vivo recombination efficiencies of different lox pairs were compared; the lox72 site that remains in the chromosome after Cre recombination had a low affinity for Cre and did not interfere with subsequent rounds of Cre/lox mutagenesis. We used this method to inactivate a specific gene, to delete a long fragment, to realize the in-frame deletion of a target gene, to introduce a gene of interest, and to carry out multiple manipulations in the same background. Furthermore, it should also be applicable to large genome rearrangement.

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Lambert, Jolanda M., Roger S. Bongers, and Michiel Kleerebezem. "Cre-lox-Based System for Multiple Gene Deletions and Selectable-Marker Removal in Lactobacillus plantarum." Applied and Environmental Microbiology 73, no. 4 (December 1, 2006): 1126–35. http://dx.doi.org/10.1128/aem.01473-06.

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ABSTRACT The classic strategy to achieve gene deletion variants is based on double-crossover integration of nonreplicating vectors into the genome. In addition, recombination systems such as Cre-lox have been used extensively, mainly for eukaryotic organisms. This study presents the construction of a Cre-lox-based system for multiple gene deletions in Lactobacillus plantarum that could be adapted for use on gram-positive bacteria. First, an effective mutagenesis vector (pNZ5319) was constructed that allows direct cloning of blunt-end PCR products representing homologous recombination target regions. Using this mutagenesis vector, double-crossover gene replacement mutants could be readily selected based on their antibiotic resistance phenotype. In the resulting mutants, the target gene is replaced by a lox66-P32-cat-lox71 cassette, where lox66 and lox71 are mutant variants of loxP and P32-cat is a chloramphenicol resistance cassette. The lox sites serve as recognition sites for the Cre enzyme, a protein that belongs to the integrase family of site-specific recombinases. Thus, transient Cre recombinase expression in double-crossover mutants leads to recombination of the lox66-P32-cat-lox71 cassette into a double-mutant loxP site, called lox72, which displays strongly reduced recognition by Cre. The effectiveness of the Cre-lox-based strategy for multiple gene deletions was demonstrated by construction of both single and double gene deletions at the melA and bsh1 loci on the chromosome of the gram-positive model organism Lactobacillus plantarum WCFS1. Furthermore, the efficiency of the Cre-lox-based system in multiple gene replacements was determined by successive mutagenesis of the genetically closely linked loci melA and lacS2 in L. plantarum WCFS1. The fact that 99.4% of the clones that were analyzed had undergone correct Cre-lox resolution emphasizes the suitability of the system described here for multiple gene replacement and deletion strategies in a single genetic background.

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Dissertations / Theses on the topic "Cre Lox"

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Paul, Sunirmal. "Topological constraint of lox-cre site-specific recombination." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621634.

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Mägdefrau, Marion. "Ortsgerichtete Rekombination in Chlamydomonas reinhardtii am Beispiel des Cre/lox-Systems." kostenfrei, 2007. http://www.opus-bayern.de/uni-regensburg/volltexte/2008/880/.

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Taveira-Marques, R. "Fate-mapping neural stem cells in the mouse ventral neural tube by Cre-lox transgenesis." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1333991/.

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Neurons and glia (astrocytes and oligodendrocytes) are the two major cell types that make up the central nervous system (CNS). They are generated from precursor domains within the neuroepithelial germinal zone (ventricular zone, VZ) that surrounds the ventricles of the brain and the central canal of the spinal cord (the embryonic neural tube). In general, neurons are generated before glia. The intra-spinal circuits that control movement and locomotion are made up of different neuronal and glial elements that develop separately but come together to form interconnected functional units. To understand the logic of circuit development and ultimately circuit-driven behaviour, it is necessary to understand where and when each type of cell originates. To identify the products of the most ventral progenitor domain in the developing spinal cord, known as (Nkx2.2-expressing p3 domain), I made use of Cre-loxP technology. I generated a transgenic mouse line that expresses an inducible form of Cre recombinase (CreERT2) under Nkx2.2 transcriptional control and crossed this with a Cre-dependant reporter mouse to visualize p3-derived progeny. I confirmed that the p3 domain generates Sim1-expressing V3 interneurons, serotonergic interneurons as well as visceral motor neurons of the hindbrain. p3 progenitors also produce two spatially restricted subtypes of astrocytes, a few oligodendrocytes and ventrallypositioned ependymal cells. Unexpectedly, my studies also revealed that pre-ganglionic motor neurons of the sympathetic nervous system (SPNs, visceral motor neurons of the thoracic spinal cord), as well as a population of dorsally-located Sim1-expressing interneurons, are produced from Nkx2.2-expressing precursors. SPNs have been generally believed to originate from the same progenitor pool as HB9-positive somatic motor neurons (sMNs), defined by expression of Olig2 (pMN domain, immediately dorsal to p3). Supporting this idea, no spinal sMNs or SPNs are formed in Olig2-null mice. However, I found that Nkx2.2-expressing p3 precursors do not generate any HB9-positive sMNs, implying that sMNs and SPNs derive from distinct precursors - the latter from the most ventral part of the pMN domain that transiently co-expresses Nkx2.2 and Olig2. Thus, segregation of SPNs and sMNs occurs already in the neuroepithelium before their post-mitotic progenitors migrate away from the VZ into the ventral horns. This is how visceral and somatic MNs are known to develop in the brainstem, so my results provide a unifying theme to MN development at different levels of the neuraxis.

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Shaw, Daniel 1993. "Streamlining minimal bacterial genomes : Analysis of the pan bacterial essential genome, and a novel strategy for random genome deletions in Mycoplasma pneumoniae." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668244.

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Understanding what constitutes a true Minimal Cell is a key challenge in synthetic biology. In this work, we present two new tools to aid in this endeavour. i) A novel methodology for minimising the Mycoplasma pneumoniae genome via random deletions of genetic material. This protocol utilises the Cre Lox system coupled with random transposon mutagenesis to create a population with random lox sites dispersed around the genome. This allows for a population of cells containing a high variability of large and small-scale deletions ranging from 50bp to 25Kb within M. pneumoniae. ii) The first large scale analysis of the essentiality of genes from multiple bacterial species, and how the composition and function of the essential genome of a bacterium changes based on the genome’s complexity.
Discernir cuales son los componentes que podrían constituir una célula mínima es un desafío clave para la Biología Sintética. En esta tesis, se presentan dos nuevas herramientas para facilitar esta tarea. (i) Una nueva metodología para minimizar el genoma de Mycoplasma pneumoniae mediante la deleción aleatoria de material genético. Esta técnica combina el sistema Cre/lox con la mutagénesis aleatoria mediada por transposones para generar poblaciones bacterianas en las que los sitios lox están distribuidos de manera aleatoria a lo largo de su genoma. Esto permite la generación de poblaciones bacterianas en las que el tamaño de las deleciones efectuadas varia desde 50 pb hasta 25 kb. (ii) El primer análisis a gran escala de la esencialidad genética en múltiples especies bacterianas, y cómo la composición y función del grupo de genes esenciales de una bacteria cambia en función de la complejidad de su genoma.

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Kvist, A. P. (Ari-Pekka). "Type XIII collagen:organization and chromosomal localization of the mouse gene, distance between human COL13A1 and prolyl 4-hydroxylase α-subunit genes, and generation of mice expressing an N-terminally altered type XIII collagen." Doctoral thesis, Oulun yliopisto, 1999. http://urn.fi/urn:isbn:9514253949.

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Abstract The complete exon-intron organization of the gene coding for the mouse α1(XIII) collagen chain, Col13a1, was characterized from genomic clones and multiple transcription initiation points were determined. Detailed comparison of the human and mouse genes showed that the exon-intron structures are completely conserved between the species, and both genes have their 5' untranslated region preceded by a highly conserved putative promoter region. The chromosomal location of the mouse gene was determined to be at chromosome 10, band B4, between markers D10Mit5 – (2.3 ± 1.6 cM) – Col13a1 – (3.4 ± 1.9 cM) – D10Mit15. The location of the genes for both the catalytically important α-subunit of prolyl 4-hydroxylase (P4HA) and human type XIII collagen (COL13A1) were previously mapped to 10q21.3-23.1. Prolyl-4-hydroxylase catalyzes the formation of 4-hydroxyproline in collagens by the hydroxylation of peptide-bound proline and plays a crucial role in the synthesis of these proteins. The order and transcriptional orientation of the COL13A1 and P4HA was determined. These two genes were found to lie at tail to tail orientation on chromosome 10 and the distance between these genes was determined to be about 550 kbp. To study the function of type XIII collagen we used gene targeting in ES cells to generate a mouse line that carries a mutated type XIII collagen gene. Instead of normal protein, mutant mice express type XIII collagen with an altered amino-terminus in which the cytosolic and the transmembrane domains have been replaced with an unrelated sequence. The homozygous mice are fertile and viable but they show alterations in skeletal muscles, mainly wavy sarcolemma and increased variation in muscle fiber diameter. Ultrastructural studies revealed additional abnormalities such as streaming of z-disks, accumulation and enlargement of mitochondria, and disorganized myofilaments. The basement membranes of the muscle cells showed areas of detachment from the plasma membrane and the fibrillar matrix of the cells was less compact than in control animals. Fibroblasts cultured from mutant mice had normal levels of type XIII collagen but exhibited decreased adhesion to substratum which might be explained by a reduced anchoring strength of the altered protein.

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Machado, Caroline. "STUDIES OF ERGOT ALKALOID BIOSYNTHESIS GENES IN CLAVICIPITACEOUS FUNGI." UKnowledge, 2004. http://uknowledge.uky.edu/gradschool_diss/433.

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Neotyphodium species, endophytic fungi associated with cool-season grasses, enhance host fitness and stress tolerance, but also produce biologically active alkaloids including ergot alkaloids associated with fescue toxicosis in grazing animals. One approach to reduce fescue toxicosis is to manipulate genes in the ergot alkaloid pathway. The gene, dmaW, encoding the first pathway-specific step in ergot alkaloid biosynthesis, was cloned previously from Claviceps spp. and its function was demonstrated by expression in yeast. Putative homologs have been cloned from Neotyphodium coenophialum (from tall fescue) and Neotyphodium sp. Lp1 (from perennial ryegrass). In order to confirm the function of dmaW in ergot alkaloid production, dmaW in Neotyphodium sp. isolate Lp1 was knocked out by gene replacement. The dmaW knockout mutant produced no detectable ergovaline or simpler ergot alkaloids. Complementation with Claviceps fusiformis dmaW restored ergovaline production. These results confirmed that the cloned endophyte gene was dmaW, and represented the first genetic experiments to show the requirement of dmaW for ergot alkaloid biosynthesis. Neotyphodium coenophialum, endophyte of the grass tall fescue (Lolium arundinaceum) has two homologs of dmaW. Considering the possible field applications in future, the Cre/lox site-specific recombination system was chosen because of the potential to sequentially knock out both homologs and obtain marker-free dmaW mutants of N. coenophialum. One homolog, dmaW-2, was disrupted by marker exchange, and the marker was eliminated by Cre, thus demonstrating the application of Cre/lox system in N. coenophialum to eliminate a marker gene. The dmaW-2 knockout did not eliminate ergovaline production, indicating that the dmaW-1 was probably also active in N. coenophialum. A putative ergot alkaloid biosynthesis gene cluster was identified in Claviceps purpurea and C. fusiformis. C. purpurea and C. fusiformis produce different subsets of ergot alkaloids. Identification of nine common genes between them suggests the possible role of these genes in the early part of the ergot alkaloid biosynthetic pathway.

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Duran, Ortiz Silvana. "Characterization and Lifespan Assessment of Inducible Growth Hormone ReceptorDisrupted Mice at Six Months of Age." Ohio University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1602089078681852.

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Cattin, Anne-Laure. "Le récepteur nucléaire HNF-4α : un facteur au carrefour entre homéostasie, architecture et fonction de l'épithélium intestinal adulte." Paris 6, 2009. http://www.theses.fr/2009PA066379.

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L’épithélium intestinal est un système en renouvellement constant. Son homéostasie repose sur la coordination précise des processus de prolifération, de différenciation et de survie cellulaire. L’objectif de mon travail de thèse a été d’étudier le rôle du facteur de transcription HNF-4α dans l’homéostasie, l’architecture et la fonction de l’épithélium intestinal. Dans un modèle de souris adultes, où l’invalidation du gène Hnf-4α est inductible et spécifique de l’intestin, j’ai montré qu’HNF-4α est un acteur clé du maintien de l’homéostasie de cet épithélium : HNF-4α module la prolifération dans les cryptes, en interférant avec la signalisation Wnt/β-caténine ; il régule négativement l’expression de Math-1 et limite l’engagement des progéniteurs en cellules mucosécrétrices ; il participe à la différenciation des entérocytes et des cellules entéroendocrines. HNF-4α joue aussi un rôle majeur dans la fonction intestinale de barrière, sa perte s’accompagnant de modifications d’expression et d’organisation des composants des jonctions serrées et d’une augmentation de la perméabilité paracellulaire. Enfin, HNF-4α est nécessaire au maintien d’un transfert intestinal efficace des lipides alimentaires dans la circulation, et intervient dès l’étape entérocytaire de captage des lipides alimentaires. En conclusion, dans l’intestin, HNF-4α est au carrefour entre homéostasie, architecture cellulaire et fonction de transfert des lipides alimentaires. Ses effets sur la voie Wnt/β-caténine nous conduisent à émettre l’hypothèse qu‘Hnf-4α est un gène suppresseur de tumeur, concernant entre autres le cancer colorectal.

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Kalamarides, Michel. "Modélisation de la tumorigenèse méningée chez la souris récapitulant les altérations génétiques des méningiomes humains." Paris 7, 2005. http://www.theses.fr/2005PA077146.

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Rehmani, Taha. "An In-vivo Analysis of SLMAP Function in the Postnatal Mouse Myocardium." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36666.

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SLMAP is a tail anchored membrane protein that alternatively splices to generate three isoforms, SLMAP1, SLMAP2 and SLMAP3. Previous studies in our lab have shown that the postnatal cardiac-specific overexpression of SLMAP1 results in intracellular vesicle expansion and enhanced endosomal recycling. I generated a postnatal cardiac-specific knockout model using the Cre-Lox system to nullify all three SLMAP isoforms and further evaluate its role in the mouse myocardium. SLMAP knockdown and knockout mouse hearts were analyzed with western blotting and qPCR. I found that only SLMAP3 was nullified and phenotypic evaluation through echocardiography indicated that young and old SLMAP3 knockout animals showed no remarkable changes in cardiac function. Furthermore, challenge with stressor isoproterenol had a similar response to wildtype and knockout mice in cardiac structure and function. Surprisingly the level of expression of SLMAP1 and SLMAP2 was maintained in the myocardium from SLMAP3 deficient mice. Interestingly the machinery involved in endosomal recycling was not impacted by the loss of SLMAP3. These data indicate that loss of SLMAP3 does not alter cardiac structure and function in the postnatal myocardium in the presence of SLMAP1 and SLMAP2.

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Books on the topic "Cre Lox"

1

Primary low vision care. Norwalk, CT: Appleton & Lange, 1994.

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Sánchez, Germán. Los enigmas del Che. El Silencio, Caracas, Venezuela: Ediciones Ko'eyu, 1997.

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Ku lou ma che. Nanning: Jie li chu ban she, 2004.

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Rushing, Felder. Tough plants for Florida gardens: Low care, no care, tried and true winners. Nashville, Tenn: Cool Springs Press, 2004.

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Melby, Jeffrey A. CORE-LOC concrete armor units. Vicksburg, MS: U.S. Army Corps of Engineers, Waterways Experiment Station, 1997.

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Melby, Jeffrey A. CORE-LOC concrete armor units. Vicksburg, Miss: U.S. Army Engineer Waterways Experiment Station, 1997.

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Vaca, Gustavo Parada. Los compañeros del Che Guevara. [Bolivia: s.n., 1997.

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Korol, Claudia. El Che y los argentinos. Buenos Aires: Ediciones Dialéctica, 1988.

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Melby, Jeffrey A. CORE-LOC concrete armor units. Vicksburg, MS: U.S. Army Corps of Engineers, Waterways Experiment Station, 1997.

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Symposium, Interdisciplinary Health Care. Interdisciplinary Health Care Symposium (1992: Portland, Ore.) Proceedings. Portland, Or: National College of Naturopathic Medicine, 1992.

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Book chapters on the topic "Cre Lox"

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Hoess, R. H., and K. Abremski. "The Cre-lox Recombination System." In Nucleic Acids and Molecular Biology, 99–109. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-84150-7_6.

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Srivastava, Vibha, and David W. Ow. "Simplifying Transgene Locus Structure Through Cre-lox Recombination." In Methods in Molecular Biology, 95–103. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2453-0_6.

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Albert, Henrik, and David W. Ow. "Cre-lox Directed Integration of Transgenes into the Tobacco Genome." In Plant Molecular Biology Manual, 59–73. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4217-5_3.

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Gilbertson, Larry, Waly Dioh, Prince Addae, Joanne Ekena, Greg Keithly, Mark Neuman, Virginia Peschke, et al. "Cre/lox Mediated Marker Gene Excision in Transgenic Crop Plants." In Plant Biotechnology 2002 and Beyond, 225–28. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-2679-5_43.

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Smith, Lorna I. F., Thomas G. Hill, and James E. Bowe. "Generating Beta-Cell-Specific Transgenic Mice Using the Cre-Lox System." In Methods in Molecular Biology, 181–205. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0385-7_13.

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Mobley, Aaron K., and Joseph H. McCarty. "Use of Cre-Lox Technology to Analyze Integrin Functions in Astrocytes." In Methods in Molecular Biology, 555–70. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-452-0_37.

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Baker, Lorina G., and Jennifer K. Lodge. "Multiple Gene Deletion in Cryptococcus neoformans Using the Cre–lox System." In Host-Fungus Interactions, 85–98. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-539-8_6.

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Kratochwil, Claudius F., and Filippo M. Rijli. "The Cre/Lox System to Assess the Development of the Mouse Brain." In Methods in Molecular Biology, 295–313. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-655-9_20.

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Kratochwil, Claudius F., and Filippo M. Rijli. "The Cre/Lox System to Assess the Development of the Mouse Brain." In Methods in Molecular Biology, 491–512. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9732-9_28.

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Dessen, Pierre, Joerg Huelsken, and Paloma Ordóñez-Morán. "Specific Gene Expression in Lgr5+ Stem Cells by Using Cre-Lox Recombination." In Methods in Molecular Biology, 249–55. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0747-3_16.

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Conference papers on the topic "Cre Lox"

1

Subbotin, K. A., V. V. Slavkina, D. A. Lis, O. N. Lis, and E. V. Zharikov. "Evolution of Cr4+, Cr3+and Cr2+contents in Cr:Mg2SiO4 crystals during those oxidizing annealing." In 2016 International Conference Laser Optics (LO). IEEE, 2016. http://dx.doi.org/10.1109/lo.2016.7549671.

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Zhang, Sheng, Adrian Tang, Zhewei Jiang, Simha Sethumadhavan, and Mingoo Seok. "Blacklist Core." In ISLPED '18: International Symposium on Low Power Electronics and Design. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3218603.3218624.

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van der Heide, Sjoerd, Juan Carlos Alvarado-Zacarias, Nicolas K. Fontaine, Roland Ryf, Haoshuo Chen, Rodrigo Amezcua-Correa, Ton Koonen, and Chigo Okonkwo. "Low-loss Low-MDL Core Multiplexer for 3-Core Coupled-core Multi-core Fiber." In Optical Fiber Communication Conference. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/ofc.2020.t3a.3.

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4

Zhong, Guo-Qiang, Pei-Li Sun, and Hung-Shing Chen. "SPARKLE ESTIMATION OF METALLIC SAMPLES USING A LOW-COST SYSTEM." In CIE 2018. International Commission on Illumination, CIE, 2018. http://dx.doi.org/10.25039/x45.2018.po22.

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Sa-Ngadsup, Pracharat, Eric Dinet, Pichayada Katemake, and Alain Trémeau. "USING LIGHT TO FACILITATE THE MOBILITY OF LOW VISION PEOPLE." In CIE 2018. International Commission on Illumination, CIE, 2018. http://dx.doi.org/10.25039/x45.2018.op29.

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Karimi, Somayeh, Milad Saidian, and Hossein Kazemi. "Experimental Study of the Effect of Core Aging on Fluid Distribution in Middle Bakken Cores." In SPE Low Perm Symposium. Society of Petroleum Engineers, 2016. http://dx.doi.org/10.2118/180269-ms.

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Dugan, Edward T., William E. Lear, and Gerard E. Welch. "Pulsed Gas Core Reactor For Burst Power." In 1988 Los Angeles Symposium--O-E/LASE '88, edited by Raymond F. Askew. SPIE, 1988. http://dx.doi.org/10.1117/12.943627.

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Bussard, Robert W. "Fundamental Considerations Of Gas Core Reactor Systems." In 1988 Los Angeles Symposium--O-E/LASE '88, edited by Raymond F. Askew. SPIE, 1988. http://dx.doi.org/10.1117/12.943628.

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Qu, Yuan. "Electron mobility in GaN-based core-shell nanowires (Conference Presentation)." In Low-Dimensional Materials and Devices 2018, edited by Nobuhiko P. Kobayashi, A. Alec Talin, Albert V. Davydov, and M. Saif Islam. SPIE, 2018. http://dx.doi.org/10.1117/12.2320150.

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Bornstein, A., and L. Boehm. "Hollow And Glass Core Chalcogenide Fibers." In O-E/LASE'86 Symp (January 1986, Los Angeles), edited by Paul Klocek. SPIE, 1986. http://dx.doi.org/10.1117/12.961108.

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Reports on the topic "Cre Lox"

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Conti, Claudio J. Studies of Prostate Tumor Development via Cre/LoxP Technology. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416737.

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COnti, Claudio J. Studies of Prostate Tumor Development via Cre/LoxP Technology. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada407387.

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Conti, Claudio J. Studies of Prostate Tumor Development via Cre/LoxP Technology. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada435229.

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Smith, Kristin, and Reagan Baughman. Low wages prevalent In direct care and child care workforce. University of New Hampshire Libraries, 2007. http://dx.doi.org/10.34051/p/2020.26.

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Smith, Kristin, and Nicholas Adams. Child care subsidies critical for low-income families amid rising child care expenses. University of New Hampshire Libraries, 2013. http://dx.doi.org/10.34051/p/2020.195.

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Starguist, V. L. Core log: Valles caldera No. 2A, New Mexico. Office of Scientific and Technical Information (OSTI), January 1988. http://dx.doi.org/10.2172/5165076.

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Turk, George F., and Jeffrey A. Melby. CORE-LOC (trade name) Concrete Armor Units: Technical Guidelines. Fort Belvoir, VA: Defense Technical Information Center, June 1997. http://dx.doi.org/10.21236/ada328538.

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D.A. Gates, C. Jun, I. Zatz, A. Zolfaghari. All Metal Iron Core For A Low Aspect Ratio Tokamak. Office of Scientific and Technical Information (OSTI), June 2010. http://dx.doi.org/10.2172/981710.

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Ellis, Hoi, Michelle Dick, and Chris Kivett. Child Care and Transportation Options for Iowa City's Low-Income Residents. University of Iowa, May 1995. http://dx.doi.org/10.17077/sz2w-7vo5.

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Smith, Kristin, and Kristi Gozjolko. Low income and impoverished families pay disproportionately more for child care. University of New Hampshire Libraries, 2010. http://dx.doi.org/10.34051/p/2020.93.

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