Relevant bibliographies by topics / Dbx1

Academic literature on the topic 'Dbx1'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Dbx1"

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Takahashi, Masanori, and Noriko Osumi. "Pax6 regulates specification of ventral neurone subtypes in the hindbrain by establishing progenitor domains." Development 129, no. 6 (March 15, 2002): 1327–38. http://dx.doi.org/10.1242/dev.129.6.1327.

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Recent studies have shown that generation of different kinds of neurones is controlled by combinatorial actions of homeodomain (HD) proteins expressed in the neuronal progenitors. Pax6 is a HD protein that has previously been shown to be involved in the differentiation of the hindbrain somatic (SM) motoneurones and V1 interneurones in the hindbrain and/or spinal cord. To investigate in greater depth the role of Pax6 in generation of the ventral neurones, we first examined the expression patterns of HD protein genes and subtype-specific neuronal markers in the hindbrain of the Pax6 homozygous mutant rat. We found that Islet2 (SM neurone marker) and En1 (V1 interneurone marker) were transiently expressed in a small number of cells, indicating that Pax6 is not directly required for specification of these neurones. We also observed that domains of all other HD protein genes (Nkx2.2, Nkx6.1, Irx3, Dbx2 and Dbx1) were shifted and their boundaries became blurred. Thus, Pax6 is required for establishment of the progenitor domains of the ventral neurones. Next, we performed Pax6 overexpression experiments by electroporating rat embryos in whole embryo culture. Pax6 overexpression in the wild type decreased expression of Nkx2.2, but ectopically increased expression of Irx3, Dbx1 and Dbx2. Moreover, electroporation of Pax6 into the Pax6 mutant hindbrain rescued the development of Islet2-positive and En1-positive neurones. To know reasons for perturbed progenitor domain formation in Pax6 mutant, we examined expression patterns of Shh signalling molecules and states of cell death and cell proliferation. Shh was similarly expressed in the floor plate of the mutant hindbrain, while the expressions of Ptc1, Gli1 and Gli2 were altered only in the progenitor domains for the motoneurones. The position and number of TUNEL-positive cells were unchanged in the Pax6 mutant. Although the proportion of cells that were BrdU-positive slightly increased in the mutant, there was no relationship with specific progenitor domains. Taken together, we conclude that Pax6 regulates specification of the ventral neurone subtypes by establishing the correct progenitor domains.
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Du, Ailing, Xiaojing Wu, Hanhan Chen, Qing-Ran Bai, Xiao Han, Bin Liu, Xiaohu Zhang, Zhaoying Ding, Qin Shen, and Chunjie Zhao. "Foxg1 Directly Represses Dbx1 to Confine the POA and Subsequently Regulate Ventral Telencephalic Patterning." Cerebral Cortex 29, no. 12 (March 4, 2019): 4968–81. http://dx.doi.org/10.1093/cercor/bhz037.

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Abstract During early development, signaling centers, such as the cortical hem and the preoptic area (POA), are critical for telencephalic patterning. However, the mechanisms underlying the maintenance of signal centers are poorly understood. Here, we report that the transcription factor Foxg1 is required to confine the POA, a resource of Sonic Hedgehog (Shh) that is pivotal for ventral telencephalic development. Cell-specific deletion of Foxg1 achieved by crossing Foxg1fl/fl with Dbx1-cre or Nestin-CreER combined with tamoxifen induction results in a dramatic expansion of the POA accompanied by the significantly increased activity of the Shh signaling pathway. Ventral pattern formation was severely impaired. Moreover, we demonstrated that Foxg1 directly represses Dbx1 to restrict the POA. Furthermore, we found that the ventral pallium was expanded, which might also contribute to the observed patterning defects. These findings will improve our understanding of the maintenance of signal centers and help to elucidate the mechanisms underlying ventral telencephalic patterning.
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Rogers, Nicholas, Dale McAninch, and Paul Thomas. "Dbx1 Is a Direct Target of SOX3 in the Spinal Cord." PLoS ONE 9, no. 4 (April 21, 2014): e95356. http://dx.doi.org/10.1371/journal.pone.0095356.

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Vann, Nikolas C., Francis D. Pham, John A. Hayes, Andrew Kottick, and Christopher A. Del Negro. "Transient Suppression of Dbx1 PreBötzinger Interneurons Disrupts Breathing in Adult Mice." PLOS ONE 11, no. 9 (September 9, 2016): e0162418. http://dx.doi.org/10.1371/journal.pone.0162418.

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Karlen-Amarante, Marlusa, Alyssa Huff, Nathan A. Baertsch, Debora S. A. Colombari, and Jan-Marino Ramirez. "Optogenetic stimulation of Dbx1 neurons promote increase in sympathetic activity in vivo." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.05862.

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Bluske, Krista K., and Yasushi Nakagawa. "Role of the homeodomain transcription factor Dbx1 in patterning the developing diencephalon." Developmental Biology 331, no. 2 (July 2009): 524. http://dx.doi.org/10.1016/j.ydbio.2009.05.511.

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Arai, Yoko, Andrzej W. Cwetsch, Eva Coppola, Sara Cipriani, Hidenori Nishihara, Hiroaki Kanki, Yoann Saillour, et al. "Evolutionary Gain of Dbx1 Expression Drives Subplate Identity in the Cerebral Cortex." Cell Reports 29, no. 3 (October 2019): 645–58. http://dx.doi.org/10.1016/j.celrep.2019.09.007.

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Puelles, Luis, Loreta Medina, Ugo Borello, Isabel Legaz, Anne Teissier, Alessandra Pierani, and John L. R. Rubenstein. "Radial derivatives of the mouse ventral pallium traced with Dbx1-LacZ reporters." Journal of Chemical Neuroanatomy 75 (September 2016): 2–19. http://dx.doi.org/10.1016/j.jchemneu.2015.10.011.

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Gard, Chris, Gloria Gonzalez Curto, Youcef El-Mokhtar Frarma, Elodie Chollet, Nathalie Duval, Valentine Auzié, Frédéric Auradé, et al. "Pax3- and Pax7-mediated Dbx1 regulation orchestrates the patterning of intermediate spinal interneurons." Developmental Biology 432, no. 1 (December 2017): 24–33. http://dx.doi.org/10.1016/j.ydbio.2017.06.014.

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Inamata, Y., and R. Shirasaki. "Dbx1 triggers crucial molecular programs required for midline crossing by midbrain commissural axons." Development 141, no. 6 (February 19, 2014): 1260–71. http://dx.doi.org/10.1242/dev.102327.

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Dissertations / Theses on the topic "Dbx1"

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Griveau, Amélie. "Characterization and function of Dbx1-derived Cajal-Retzius cells during cerebral cortex development." Paris 6, 2009. http://www.theses.fr/2009PA066265.

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Notre premier travail porte sur la théorie des classes de Chern pour les faisceaux cohérents. Sur les variétés projectives, elle est complètement achevée dans les anneaux de Chow grâce à l'existence de résolutions globales localement libres et se ramène formellement à la théorie pour les fibrés. Un résultat de Voisin montre que ce résolutions n'existent pas toujours sur des variétés complexes compactes générales. Nous construisons ici par récurrence sur la dimension de la variété de base des classes de Chern en cohomologie de Deligne rationnelle pour les faisceaux cohérents en imposant la formule de Grothendieck-Riemann-Roch pour les immersions et en utilisant des méthodes de dévissage. Ces classes sont les seules à vérifier la formule de fonctorialité par pull-back, la formule de Whitney et GRR pour les immersions; elles coïncident donc avec les classes topologiques et les classes d'Atiyah. Elles vérifient aussi GRR pour les morphismes projectifs. Notre second travail est l'étude des schémas de Hilbert ponctuels d'une variété symplectique ou presque-complexe de dimension 4. Ils ont été construits par Voisin et généralisent les schémas de Hilbert connus pour les surfaces projectives. En utilisant les structures complexes relatives intégrables introduites dans la construction de Voisin, nous pouvons étendre au cas presque-complexe ou symplectique la théorie classique. Nous calculons les nombres de Betti, nous construisons les opérateurs de Nakajima, nous étudions l'anneau de cohomologie de ces schémas de Hilbert et nous prouvons dans ce contexte un cas particulier de la conjecture de la résolution crêpante de Ruan.
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Weragalaarachchi, Krishanthi Tharanga Harshani. "Morphological Study of Dbx1+ Respiratory Rhythm-Generating Neurons in PreBoetzinger Complex in Neonatal Mice." W&M ScholarWorks, 2012. https://scholarworks.wm.edu/etd/1539626922.

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Vann, Nikolas C. "Role of Dbx1-Derived Pre-Bötzinger Complex Interneurons in Breathing Behaviors of Adult Mice." W&M ScholarWorks, 2017. https://scholarworks.wm.edu/etd/1530192336.

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Breathing is a rhythmic motor behavior essential to sustain homeostasis and life itself in humans and all terrestrial mammals. A specialized neuronal network is responsible for generating and controlling the rhythm and pattern for breathing. The core rhythm-generating microcircuit in particular is located within a site dubbed the preBötzinger complex (preBötC). The preBötC is a heterogeneous region containing neurons with both respiratory and non-respiratory activity that express excitatory and inhibitory transmitters, peptide transmitters and peptide receptors. More recently, preBötC neurons have been characterized by molecular genetics. The markers historically used to define the respiratory CPG within the preBötC intersect with an embryonic transcription factor, developing brain homeobox 1 (Dbx1). Our lab, and our French colleagues, hypothesized that neurons derived from the Dbx1-expressing precursor cells (hereafter referred to as Dbx1 neurons) form the core microcircuit for inspiration breathing rhythm, that is, the Dbx1 core hypothesis. Evidence from many labs supports the role of the Dbx1 core hypothesis at embryonic and neonatal stages of development. However, the role of Dbx1 neurons in adult animals remains incompletely understood. Furthermore, contemporary data suggests the portfolio of functions for brain stem Dbx1 neurons includes premotor and arousal-related functions, which casts doubt on the veracity of the Dbx1 core hypothesis. Here I investigate the role of Dbx1 neurons in adult animals with intact sensorimotor integration systems using intersectional mouse genetics to express light-responsive membrane proteins to excite or depress Dbx1 neurons while simultaneous measuring breathing. Using these light-sensitive proteins to manipulate Dbx1 neuron function, I offer evidence that affirms the Dbx1 core hypothesis by depressing or stopping breathing, enhancing breathing, and altering breathing timing. I conclude that .... Knowing the cellular point of origin for breathing behavior gives us a target to study the cellular and synaptic mechanisms this key physiological behavior and provides general insight into rhythmic networks and physiological brain function.
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Teissier, Anne. "L'évolution du néocortex des Mammifères : gène Dbx1 et les cellules transitoires de la plaque corticale." Paris 6, 2010. http://www.theses.fr/2010PA066336.

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L’évolution du cerveau chez les mammifères à permis l’augmentation du nombre de neurones et la formation d’un néocortex en six couches. Au cours du développement du télencéphale de la souris, le facteur de transcription Dbx1 est exprimé aux stades précoces de la neurogénèse par des progéniteurs palliaux présents à la frontière entre le pallium et le sous-pallium (PSB). Nous avons caractérisé par traçage génétique une nouvelle population de cellules glutamatergiques dérivant des progéniteurs exprimant Dbx1 à la PSB et migrant tangentiellement dès E11. 5 pour peupler l’ensemble du pallium à E14. 5. Cette population se distribue de façon homogène dans la plaque corticale (PC) de l’ensemble du neocortex à la naissance avant de mourir massivement par apoptose durant la première semaine postnatale. L’ablation génétique de ces cellules induit la différenciation précoce des progéniteurs corticaux conduisant à une diminution du nombre total de neurones générés. La cinétique de ces défauts nous permet de suggérer que ces cellules transitoires envoient des signaux pendant leur migration pour maintenir les progéniteurs dans un état de prolifération. L’expression du gène Dbx1 à la PSB étant spécifique des mammifères, l’acquisition de cette nouvelle population pourrait donc être à l’origine de l’augmentation du nombre de neurones dans le cortex cérébral
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Song, Hanbing. "Rhythmogenic and Premotor Functions of Dbx1 Interneurons in the Pre-Bötzinger Complex and Reticular Formation: Modeling and Simulation Studies." W&M ScholarWorks, 2016. https://scholarworks.wm.edu/etd/1499449835.

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Breathing in mammals depends on rhythms that originate from the preBötzinger complex (preBötC) of the ventral medulla and a network of brainstem and spinal premotor neurons. The rhythm-generating core of the preBötC, as well as some premotor circuits, consists of interneurons derived from Dbx1-expressing precursors but the structure and function of these networks remain incompletely understood. We previously developed a cell-specific detection and laser ablation system to interrogate respiratory network structure and function in a slice model of breathing that retains the preBötC, premotor circuits, and the respiratory related hypoglossal (XII) motor nucleus such that in spontaneously rhythmic slices, cumulative ablation of Dbx1 preBötC neurons decreased XII motor output by half after only a few cell deletions, and then decelerated and terminated rhythmic function altogether as the tally increased. In contrast, cumulatively deleting Dbx1 premotor neurons decreased XII motor output monotonically, but did not affect frequency nor stop functionality regardless of the ablation tally. This dissertation presents several network modeling and cellular modeling studies that would further our understanding of how respiratory rhythm is generated and transmitted to the XII motor nucleus. First, we propose that cumulative deletions of Dbx1 preBötC neurons preclude rhythm by diminishing the amount of excitatory inward current or disturbing the process of recurrent excitation rather than structurally breaking down the topological network. Second, we establish a feasible configuration for neural circuits including an Erdős-Rényi preBötC network and a small-world reticular premotor network with interconnections following an anti-preferential attachment rule, which is the only configuration that produces consistent outcomes with previous experimental benchmarks. Furthermore, since the performance of neuronal network simulations is, to some extent, affected by the nature of the cellular model, we aim to develop a more realistic cellular model based on the one we adopted in previous network studies, which would account for some recent experimental findings on rhythmogenic preBötC neurons.
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BURGMAN, BRANDON MICHAEL. "DISCOVERING GENETIC INTERACTIONS OF THE DEAD-BOX PROTEIN, DBP1." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/618701.

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Medulloblastoma is the single most common form of malignant brain cancer in children. A molecular understanding of the cellular processes that leads to its formation is imperative in order to design treatments or a cure to this deadly cancer. A recent genomic screening of medulloblastoma patients showed high mutation rates of the gene DDX3X indicating a possible connection to the cancer. Thus, we investigated a yeast ortholog of DDX3X, Dbp1, to gain some insight of the function of the protein within the cell and its role in medulloblastoma formation. In order to gain deeper understanding of this mostly uncharacterized DEADbox RNA helicase, previous lab members perfor med a synthetic lethal screen in Saccharomyces cerevisiae with dbp1null cells. We found that a wild type copy of SHM2, was found to rescue sectoring in one of these synthetic let hal yeast strains. However, it has been documented that shm2 mutations show synthetic lethal interactions with ade3 mutations, so we are unable to conclude that SHM2 has genetic interaction with DBP1. However, this finding can be used to rule out SHM2 as the cause of loss of sectoring phenotype in other dbp1 synthetic lethal mutant strains.
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Hett, Anne. "Studies on the metabolism of retained and excised introns in human cells." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/10515.

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In eukaryotes the coding regions of most genes are interrupted by introns that must be removed by splicing to form a coding mRNA. However, while the splicing mechanism has received a lot of attention, much less is known about the metabolism of introns. This is partly due to the difficulties in studying introns as both aberrantly spliced transcripts and spliced introns are rapidly degraded. In this study, I have analysed intron metabolism in two respects: first I have investigated how introns are degraded following the completion of splicing. Second, I investigate the fate of transcripts, in which introns are retained due to splicing failure. In order to study the degradation of introns following splicing, I performed siRNA mediated knock down of the debrancing enzyme (Dbr1). Following splicing, introns are present in a circular lariat structure and Dbr1 is the enzyme thought to be responsible for opening this. Indeed, I found that knockdown of Dbr1 increased the amount of stabilised introns. Interestingly, introns were found to be stabilised in the cytoplasm and not in the nucleus as expected, even though immunofluoresence showed that Dbr1 is clearly nuclear. However, western blot analysis localised Dbr1 in the cytoplasm. Further investigation showed widely used methods to separate nuclear and cytoplasmic fractions are prone to generating artefacts which result in nucleoplasmic proteins delocalised to the cytoplasm. This finding may prevent future misinterpretation of data obtained by these methods. To investigate splicing failure, it was necessary to generated a sufficiently large pool of unspliced transcripts. To do this I used antisense morpholinos (AMOs) that bind to specific snRNAs (small nuclear RNAs). They are designed to block interaction surfaces that are important for splicing. Using this approach, I investigated the localisation of RNA transcripts and selected RNA processing and degradation factors in normal conditions and where splicing was inhibited. When splicing is inhibited I found splicing factors and unspliced, polyadenylated RNA localising to nuclear, splicing speckle marker SC35 positive speckles. I further discovered that for RNA to localise to nuclear speckles, polyadenylation and RNA cleavage are essential, indicating that SC-35 speckles might sequester unspliced transcripts preventing translation of potentially harmful transcripts. These transcripts remain functional however, and can be spliced where functional spliceosomes can be assembled.
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Cairns, Mari. "Identity and its relationship with borderline symptoms : the development of an identity questionnaire." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:b9a4f78e-dbf1-4586-af90-4a5e57d82e55.

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Clinical and theoretical literature suggests that some people who present with psychological problems have a poorly developed sense of their own identity. It has also been suggested that cognitive theory and therapy does not always adequately identify, conceptualise, and address these identity problems. The current study aims to develop a self-report questionnaire measure to assess these identity problems. It also tests some specific hypotheses about the relationship between identity problems and other psychological constructs, including borderline personality disorder symptomatology. anxiety and depression.
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Kent, Louisa. "The molecular pathogenesis of FUS mutations in amyotrophic lateral sclerosis using in vivo and in vitro models." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:f0968f9d-db01-4ace-bbd7-fc43319e19ea.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterised by degeneration of both upper and lower motor neurons. Most ALS occurs in a sporadic manner, though 5-10% is familial. Fused in sarcoma (FUS) is an RNA binding protein, and mutations in the FUS gene are responsible for approximately 4% of familial and < 1% of sporadic ALS cases. This work uses in vitro and in vivo models to examine the cellular effects of FUS mutations and the potential mechanisms of motor neuron toxicity. The first section describes a family with a severe clinical form of ALS due to a FUS truncation mutation p.G504Wfs*12. This mutation demonstrates a severe phenotype in vitro, with mislocalisation of mutant FUS from the nucleus to the cytoplasm, and co-localisation with stress granules. Comparing these results with other mutations highlights the correlation between FUS mislocalisation and clinical phenotype, suggesting that the distribution of FUS plays a role in the pathogenesis of ALS. The next section explores the phenotype of primary motor neurons from a FUS BAC transgenic mouse model expressing low levels of wild-type or P525L human FUS. P525L-FUS shows marked mislocalisation to the cytoplasm and co-localisation with stress granules, with evidence of reduced survival and alterations in stress granule dynamics. This suggests that motor neurons expressing mutant FUS show inherent vulnerability. The final section explores transcript levels and alternative splicing in both FUS and TDP-43 BAC transgenic mouse models. Key proteins such as TDP-43, FUS and SMN show alterations in mRNA levels in CNS tissue, and some subtle splicing alterations are described. This work suggests that mutations in FUS are likely to affect motor neurons even when expressed at very low levels. Alterations in FUS distribution, stress granule dynamics, and regulation of transcription may all play a part in conferring a susceptibility to developing ALS.
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Magni, Martina. "Functional characterization of the human protein deleted in breast cancer 1 (DBC1) involvement in the DNA damage response." Thesis, Open University, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701431.

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The DNA damage response (DDR) is an intricate signalling network established by eukaryotic cells in order to manage the insults to their DNA, arising both from exogenous and from endogenous sources. Thanks to the activation of DDR, cells can block cell cycle progression, to have time to repair the DNA lesions; alternatively, in presence of irreparable damages, cells are committed to apoptosis or senescence, to prevent the replication of damaged genomes, because mutations could be maintained, leading to genomic instability and predisposition to cancer development. One of the proteins recently found to play an important role in the DDR is DBC1 (deleted in breast cancer 1, CCAR2). In particular, DBC1 is a substrate of ATMjATR and a biological inhibitor of the deacetylase SIRT1, the main protein involved in p53 deacetylation. DBC1, through its physical interaction with SIRT1, blocks its deacetylase activity, preserving p53 acetylation and activation and promoting p53-dependent apoptosis. The data presented in this thesis further characterize the mechanism through which DBC1 regulates SIRT1, as I found that it co-operates with Chk2 and the proteasome activator REGy to exert this function. Moreover, these studies unravel a novel role for DBC1 in the repair of heterochromatic DNA lesions through the promotion of Chk2 activity towards KAP1, a Chk2 substrate involved in the modulation of chromatin remodelling. In addition, the data obtained with a genome wide expression analysis of cells lacking DBC1 revealed a crosstalk between DBC1 and TSPYL2, a protein that we found to playa crucial role in the modulation of p53 activation and induction of apoptosis, by regulating the activity of SIRTl and p300. Overall, these studies extend the knowledge of DBCl functions in DDR and DNA repair, and report for the first time a novel role for TSPYL2 in the regulation of p53 activation upon DNA lesions.
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Books on the topic "Dbx1"

1

Self, Robert W. Learning dBXL. [California?: R.W. Self, 1990.

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Barbara, Clifford, ed. dBXL and Quicksilver programming: Beyond dBase. Carmel, Ind: Que Corp., 1988.

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Kalman, David M. The dBASE language handbook: Quicksilver, Clipper, dBXL, dBASE III, dBASE III plus, dBASE IV, and FoxBASE. London: Pitman, 1989.

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The dBase language handbook: Quicksilver, Clipper, dBXL, dBase III, dBase III Plus, dBase IV, and FoxBase+. San Marcos, CA: Microtrend Books, 1989.

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Cutting, E. J. ’Ted’. CUTTING EDGE CONVERSATIONS: The Aston Martin Race Car Chief Design/Engineer from 1949 - 1964. England: Self Published, 2012.

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Kalman, David M. Manual de referencia completo del lenguaje dBase: Clipper, FoxBase, dBXL, Quicksilver, dBase III plus y dBase IV. Madrid: Anaya Multimedia, 1991.

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Stultz, Russell Allen. Learn dBase programming in a day: For users of dBase-compatible database programs that use the xBase language including dBase III Plus, dBase IV, FoxBase, FoxPro, Clipper, Data₊Pro, DBXL, and Quicksilver. Plano, Tex: Wordware Pub., 1993.

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The dBASE language reference. Berkeley, Calif: Osborne McGraw-Hill, 1990.

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Greaney, Andrew. Aston Martin DB11's Aeroblade. Independently Published, 2018.

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Shieh. DBX Debugger for Unix. Pearson Education, Limited, 1999.

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Book chapters on the topic "Dbx1"

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Weik, Martin H. "dBx." In Computer Science and Communications Dictionary, 366. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_4452.

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Neophytou, Panayiotis, Neophytos Neophytou, and Paraskevas Evripidou. "Debugging MPI Grid Applications Using Net-dbx." In Grid Computing, 139–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-28642-4_17.

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Neophytou, Neophytos, and Paraskevas Evripidou. "Net-dbx: A Java powered tool for interactive debugging of MPI programs across the internet." In Euro-Par’98 Parallel Processing, 181–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0057851.

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Shestov, A. A., A. Mancuso, D. B. Leeper, and J. D. Glickson. "Metabolic Network Analysis of DB1 Melanoma Cells: How Much Energy Is Derived from Aerobic Glycolysis?" In Advances in Experimental Medicine and Biology, 265–71. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4989-8_37.

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"Doublecortin (DBX)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 553. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_4819.

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"Deckblatt Db1." In Paracelsus, 28–29. De Gruyter, 2021. http://dx.doi.org/10.1515/9783110712247-004.

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"Diagnosis and Classification." In Introductory Textbook of Psychiatry. American Psychiatric Association Publishing, 2020. http://dx.doi.org/10.1176/appi.books.9781615373758.db01.

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"Feeding and Eating Disorders." In Introductory Textbook of Psychiatry. American Psychiatric Association Publishing, 2020. http://dx.doi.org/10.1176/appi.books.9781615373758.db11.

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"Somatic Treatments." In Introductory Textbook of Psychiatry. American Psychiatric Association Publishing, 2020. http://dx.doi.org/10.1176/appi.books.9781615373758.db21.

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Fitzsimons, B., B. Husband, S. Leathers, J. McLean, and I. Minards. "Der neue Aston Martin DB11 V12 Motor/The New Aston Martin DB11 V12 Engine." In 37. Internationales Wiener Motorensymposium 28. – 29. April 2016, I—137—I—158. VDI Verlag, 2016. http://dx.doi.org/10.51202/9783186799128-i-137.

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Conference papers on the topic "Dbx1"

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Xu, Wei, Danny Wong, Simon Fleming, and Paul Blazkiewicz. "Evolution of Charge Layers during Thermal Poling of Silica Fibres." In Bragg Gratings, Photosensitivity, and Poling in Glass Waveguides. Washington, D.C.: OSA, 1999. http://dx.doi.org/10.1364/bgpp.1999.db11.

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Park, Sun, Philip A. Riley, Benjamin Cieply, and Steven M. Frisch. "Abstract 4956: Regulation of anoikis by DBC1 (Deleted-In-Breast Cancer 1) through NF-kB." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4956.

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Yu, Zhen, Jialong He, Qinquan Gao, and Jiajia Liu. "System Design of OE Mail File Parsing Based on DBX File Analysis." In 2009 International Conference on Information Engineering and Computer Science. IEEE, 2009. http://dx.doi.org/10.1109/iciecs.2009.5364493.

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Paradowska-Gorycka, A., B. Stypinska, E. Haladyj, K. Romanowska-Prochnicka, A. Pawlik, and M. Olesinska. "THU0012 HLA-DBR1 alleles profile in patients with rheumatoid arthritis: relation to disease susceptibility and severity." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5794.

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Sanborn, William, John Fronabarger, and Michael Williams. "Critical Temperature Determinations for the Lead-Free Primary Explosives DBX-1 and KDNP." In 46th AIAA/ASME/SAE/ASEE Joint Propulsion Conference & Exhibit. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2010. http://dx.doi.org/10.2514/6.2010-6514.

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Akande, Oluwatoyin E., Priyadarshan K. Damle, Nicholas E. Sherman, and Steven R. Grossman. "Abstract 2571: DBC1, a novel CBP-interacting protein, promotes p53 stability by regulating CBP-dependent p53 polyubiquitination." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2571.

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Alley, Thomas G., S. R. J. Brueck, and Michael Wiedenbeck. "Space Charge in Thermally Poled Fused Silica." In Bragg Gratings, Photosensitivity, and Poling in Glass Waveguides. Washington, D.C.: OSA, 1999. http://dx.doi.org/10.1364/bgpp.1999.db1.

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Cui*, Yongfu, Guochen Wu, Zhengwen Liu, Ruirui Zhao, and Haijun Sun. "Full-azimuth seismic study for complex structural imaging and fracture detection: A case study in Well DB1 area, Tarim Basin." In Beijing 2014 International Geophysical Conference & Exposition, Beijing, China, 21-24 April 2014. Society of Exploration Geophysicists and Chinese Petroleum Society, 2014. http://dx.doi.org/10.1190/igcbeijing2014-093.

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Xu, Zengkui, Yousheng Yan, Mingli Yi, and Xin Wei. "3‐C offset VSP PP, PSV and SS imagings for sub‐salt structure: a case study in DB1 well‐site, Tarim Basin, P.R.China." In SEG Technical Program Expanded Abstracts 2005. Society of Exploration Geophysicists, 2005. http://dx.doi.org/10.1190/1.2148272.

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Reports on the topic "Dbx1"

1

Baskerville, David B. Graphic Presentation of Data Structures in the DBX Debugger. Fort Belvoir, VA: Defense Technical Information Center, July 1985. http://dx.doi.org/10.21236/ada611773.

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