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Relevant bibliographies by topics / Conditional inducible rat knockdown

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Journal articles

Academic literature on the topic 'Conditional inducible rat knockdown'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Conditional inducible rat knockdown"

1

Sidorova, Maria, Golo Kronenberg, Susann Matthes, et al. "Enduring Effects of Conditional Brain Serotonin Knockdown, Followed by Recovery, on Adult Rat Neurogenesis and Behavior." Cells 10, no. 11 (2021): 3240. http://dx.doi.org/10.3390/cells10113240.

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Serotonin (5-hydroxytryptamine, 5-HT) is a crucial signal in the neurogenic niche of the hippocampus, where it is involved in antidepressant action. Here, we utilized a new transgenic rat model (TetO-shTPH2), where brain 5-HT levels can be acutely altered based on doxycycline (Dox)-inducible shRNA-expression. On/off stimulations of 5-HT concentrations might uniquely mirror the clinical course of major depression (e.g., relapse after discontinuation of antidepressants) in humans. Specifically, we measured 5-HT levels, and 5-HT metabolite 5-HIAA, in various brain areas following acute tryptophan

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Berger, Stefan M., Iván Fernández-Lamo, Kai Schönig, et al. "Forebrain-specific, conditional silencing of Staufen2 alters synaptic plasticity, learning, and memory in rats." Genome Biology 18, no. 1 (2017): 222. https://doi.org/10.1186/s13059-017-1350-8.

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<strong>Background: </strong>Dendritic messenger RNA (mRNA) localization and subsequent local translation in dendrites critically contributes to synaptic plasticity and learning and memory. Little is known, however, about the contribution of RNA-binding proteins (RBPs) to these processes in vivo.<strong>Results: </strong>To delineate the role of the double-stranded RBP Staufen2 (Stau2), we generate a transgenic rat model, in which Stau2 expression is conditionally silenced by Cre-inducible expression of a microRNA (miRNA) targeting Stau2 mRNA in adult forebrain neurons. Known physiological mRN

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Zhang, Hui, Neil B. Sweezey, and Feige Kaplan. "LGL1 modulates proliferation, apoptosis, and migration of human fetal lung fibroblasts." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 4 (2015): L391—L402. http://dx.doi.org/10.1152/ajplung.00119.2014.

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Rapid growth and formation of new gas exchange units (alveogenesis) are hallmarks of the perinatal lung. Bronchopulmonary dysplasia (BPD), common in very premature infants, is characterized by premature arrest of alveogenesis. Mesenchymal cells (fibroblasts) regulate both lung branching and alveogenesis through mesenchymal-epithelial interactions. Temporal or spatial deficiency of late-gestation lung 1/cysteine-rich secretory protein LD2 (LGL1/CRISPLD2), expressed in and secreted by lung fibroblasts, can impair both lung branching and alveogenesis (LGL1 denotes late gestation lung 1 protein; L

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Flemming, Sven, Anny-Claude Luissint, Dennis H. M. Kusters, et al. "Desmocollin-2 promotes intestinal mucosal repair by controlling integrin-dependent cell adhesion and migration." Molecular Biology of the Cell 31, no. 6 (2020): 407–18. http://dx.doi.org/10.1091/mbc.e19-12-0692.

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We report a key role for Dsc2 in simple epithelial cell migration and mucosal wound healing in vivo using newly generated mice with inducible conditional knockdown of Dsc2 in intestinal epithelial cells ( Villin-CreERT2; Dsc2fl/fl).

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5

Ogawa, Yoshitaka, Kohei Nishimura, Keisuke Obara, and Takumi Kamura. "Development of AlissAID system targeting GFP or mCherry fusion protein." PLOS Genetics 19, no. 6 (2023): e1010731. http://dx.doi.org/10.1371/journal.pgen.1010731.

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Conditional control of target proteins using the auxin-inducible degron (AID) system provides a powerful tool for investigating protein function in eukaryotes. Here, we established an Affinity-linker based super-sensitive auxin-inducible degron (AlissAID) system in budding yeast by using a single domain antibody (a nanobody). In this system, target proteins fused with GFP or mCherry were degraded depending on a synthetic auxin, 5-Adamantyl-IAA (5-Ad-IAA). In AlissAID system, nanomolar concentration of 5-Ad-IAA induces target degradation, thus minimizing the side effects from chemical compounds

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kun, Zhang, Yang yuling, Wang dongchun, Xie bingbing, Li xiaoli та Xu bin. "HIF-1α Inhibition Sensitized Pituitary Adenoma Cells to Temozolomide by Regulating Presenilin 1 Expression and Autophagy". Technology in Cancer Research & Treatment 15, № 6 (2016): NP95—NP104. http://dx.doi.org/10.1177/1533034615618834.

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Pituitary adenomas usually develop temozolomide resistance, which could compromise the anticancer effects of temozolomide. Suppression of hypoxia-inducible factor 1α has been shown to sensitize glioblastoma cells to temozolomide treatment according to previous reports. However, whether and how the suppression of hypoxia-inducible factor 1α could sensitize pituitary adenomas to temozolomide treatment are still poorly understood. In the present study, using hypoxia-inducible factor 1α knockdown strategy, we demonstrated for the first time that hypoxia-inducible factor 1α knockdown could inhibit

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Makino‐Itou, Hatsune, Noriko Yamatani, Akemi Okubo, et al. "Establishment and characterization of mouse lines useful for endogenous protein degradation via an improved auxin‐inducible degron system (AID2)." Development, Growth & Differentiation 66, no. 7 (2024): 384–93. http://dx.doi.org/10.1111/dgd.12942.

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AbstractThe development of new technologies opens new avenues in the research field. Gene knockout is a key method for analyzing gene function in mice. Currently, conditional gene knockout strategies are employed to examine temporal and spatial gene function. However, phenotypes are sometimes not observed because of the time required for depletion due to the long half‐life of the target proteins. Protein knockdown using an improved auxin‐inducible degron system, AID2, overcomes such difficulties owing to rapid and efficient target depletion. We observed depletion of AID‐tagged proteins within

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8

Wiznerowicz, Maciej, and Didier Trono. "Conditional Suppression of Cellular Genes: Lentivirus Vector-Mediated Drug-Inducible RNA Interference." Journal of Virology 77, no. 16 (2003): 8957–51. http://dx.doi.org/10.1128/jvi.77.16.8957-8951.2003.

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ABSTRACT RNA interference has emerged as a powerful technique to downregulate the expression of specific genes in cells and in animals, thus opening new perspectives in fields ranging from developmental genetics to molecular therapeutics. Here, we describe a method that significantly expands the potential of RNA interference by permitting the conditional suppression of genes in mammalian cells. Within a lentivirus vector background, we subjected the polymerase III promoter-dependent production of small interfering RNAs to doxycycline-controllable transcriptional repression. The resulting syste

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Tsai, Steven C., David F. Chang, Chang-Mu Hong, et al. "Induced overexpression of OCT4A in human embryonic stem cells increases cloning efficiency." American Journal of Physiology-Cell Physiology 306, no. 12 (2014): C1108—C1118. http://dx.doi.org/10.1152/ajpcell.00205.2013.

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Our knowledge of the molecular mechanisms underlying human embryonic stem cell (hESC) self-renewal and differentiation is incomplete. The level of octamer-binding transcription factor 4 (Oct4), a critical regulator of pluripotency, is precisely controlled in mouse embryonic stem cells. However, studies of human OCT4 are often confounded by the presence of three isoforms and six expressed pseudogenes, which has complicated the interpretation of results. Using an inducible lentiviral overexpression and knockdown system to manipulate OCT4A above or below physiological levels, we specifically exam

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Weis, Sara M., Ssang-Taek Lim, Kimberly M. Lutu-Fuga, et al. "Compensatory role for Pyk2 during angiogenesis in adult mice lacking endothelial cell FAK." Journal of Cell Biology 181, no. 1 (2008): 43–50. http://dx.doi.org/10.1083/jcb.200710038.

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Focal adhesion kinase (FAK) plays a critical role during vascular development because knockout of FAK in endothelial cells (ECs) is embryonic lethal. Surprisingly, tamoxifen-inducible conditional knockout of FAK in adult blood vessels (inducible EC–specific FAK knockout [i-EC-FAK-KO]) produces no vascular phenotype, and these animals are capable of developing a robust growth factor–induced angiogenic response. Although angiogenesis in wild-type mice is suppressed by pharmacological inhibition of FAK, i-EC-FAK-KO mice are refractory to this treatment, which suggests that adult i-EC-FAK-KO mice

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