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Relevant bibliographies by topics / Knockin mouse model

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Academic literature on the topic 'Knockin mouse model'

Author: Grafiati

Published: 18 May 2024

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Journal articles on the topic "Knockin mouse model"

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Savva, Isavella, Charalampos Stefanou, Myrtani Pieri, Dorin B. Borza, Kostas Stylianou, George Lapathitis, Christos Karaiskos, Gregoris Papagregoriou, and Constantinos Deltas. "MP036A NOVEL KNOCKIN MOUSE MODEL FOR ALPORT SYNDROME." Nephrology Dialysis Transplantation 31, suppl_1 (May 2016): i354. http://dx.doi.org/10.1093/ndt/gfw182.06.

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Luo, Yichen, Liang Du, Zhimeng Yao, Fan Liu, Kai Li, Feifei Li, Jianlin Zhu, et al. "Generation and Application of Inducible Chimeric RNA ASTN2-PAPPAas Knockin Mouse Model." Cells 11, no. 2 (January 14, 2022): 277. http://dx.doi.org/10.3390/cells11020277.

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Chimeric RNAs (chiRNAs) play many previously unrecognized roles in different diseases including cancer. They can not only be used as biomarkers for diagnosis and prognosis of various diseases but also serve as potential therapeutic targets. In order to better understand the roles of chiRNAs in pathogenesis, we inserted human sequences into mouse genome and established a knockin mouse model of the tamoxifen-inducible expression of ASTN2-PAPPA antisense chimeric RNA (A-PaschiRNA). Mice carrying the A-PaschiRNA knockin gene do not display any apparent abnormalities in growth, fertility, histological, hematopoietic, and biochemical indices. Using this model, we dissected the role of A-PaschiRNA in chemical carcinogen 4-nitroquinoline 1-oxide (4NQO)-induced carcinogenesis of esophageal squamous cell carcinoma (ESCC). To our knowledge, we are the first to generate a chiRNA knockin mouse model using the Cre-loxP system. The model could be used to explore the roles of chiRNA in pathogenesis and potential targeted therapies.

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de Winter, J., M. Yuen, R. Van der Pijl, F. Li, S. Shengyi, S. Conijn, M. Van de Locht, et al. "P.162Novel Kbtbd13R408C-knockin mouse model phenocopies NEM6 myopathy." Neuromuscular Disorders 29 (October 2019): S95. http://dx.doi.org/10.1016/j.nmd.2019.06.217.

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Wegener, Eike, Cornelia Brendel, Andre Fischer, Swen Hülsmann, Jutta Gärtner, and Peter Huppke. "Characterization of the MeCP2R168X Knockin Mouse Model for Rett Syndrome." PLoS ONE 9, no. 12 (December 26, 2014): e115444. http://dx.doi.org/10.1371/journal.pone.0115444.

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Rose, Samuel J., Lisa H. Kriener, Ann K. Heinzer, Xueliang Fan, Robert S. Raike, Arn M. J. M. van den Maagdenberg, and Ellen J. Hess. "The first knockin mouse model of episodic ataxia type 2." Experimental Neurology 261 (November 2014): 553–62. http://dx.doi.org/10.1016/j.expneurol.2014.08.001.

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Sundberg, J. P., C. H. Pratt, K. A. Silva, V. E. Kennedy, L. Goodwin, W. Qin, and A. Bowcock. "394 Card14 knockin mouse model of psoriasis and psoriatic arthritis." Journal of Investigative Dermatology 136, no. 5 (May 2016): S70. http://dx.doi.org/10.1016/j.jid.2016.02.428.

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Baelde, R., A. Fortes Monteiro, E. Nollet, R. Galli, J. Strom, J. van der Velden, C. Ottenheijm, and J. de Winter. "P400 Kbtbd13R408C-knockin mouse model elucidates mitochondrial pathomechanism in NEM6." Neuromuscular Disorders 33 (October 2023): S123. http://dx.doi.org/10.1016/j.nmd.2023.07.231.

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Yuan, Weiming, Xiangshu Wen, Ping Rao, Seil Kim, and Peter Cresswell. "Characterization of a human CD1d-knockin mouse (106.44)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 106.44. http://dx.doi.org/10.4049/jimmunol.188.supp.106.44.

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Abstract CD1d-restricted natural killer T (NKT) cells regulate the immune system in response to a broad range of diseases. The CD1d/NKT antigen presentation pathway is largely conserved between human and mouse, however, there is distinct difference between the two species. To better study human CD1d antigen presentation in an in vivo setting, we have generated a human CD1d knock-in (KI) mouse. We have expressed human CD1d (hCD1d) in place of mouse CD1d (mCD1d). The expression of hCD1d was verified on CD4+CD8+DP thymocytes and thymic dendritic cells, which are involved in NKT cell positive and negative selections, respectively, in thymus. CD1d-α-GalCer tetramer+ invariant NKT (iNKT) cells have been shown in thymus, spleen and liver. However, reduced numbers of iNKT cells were observed in these organs compared to that in wild-type mice. Among these iNKT cells, Vβ8 has been over-represented comparing with wild-type mouse, suggesting hCD1d preferentially selects for mouse Vβ8 chain, which is highly homologous to human Vβ11 chain. In vitro presentation of various glycolipids by BMDCs from hCD1d KI mice showed that hCD1d is functional in presenting different groups of lipids. Furthermore, lipid administration in the KI mice showed that in vivo hCD1d-restricted NKT cells are functional. In summary, our hCD1d KI mouse can be a novel model for in vivo studying hCD1d-specific antigen presentation in antitumor and antimicrobial immunity as well as autoimmune diseases.

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Guo, Qinxi, Hui Zheng, and Nicholas John Justice. "Central CRF system perturbation in an Alzheimer's disease knockin mouse model." Neurobiology of Aging 33, no. 11 (November 2012): 2678–91. http://dx.doi.org/10.1016/j.neurobiolaging.2012.01.002.

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Nomura, Naohiro, Masato Tajima, Noriko Sugawara, Tetsuji Morimoto, Yoshiaki Kondo, Mayuko Ohno, Keiko Uchida, et al. "Generation and analyses of R8L barttin knockin mouse." American Journal of Physiology-Renal Physiology 301, no. 2 (August 2011): F297—F307. http://dx.doi.org/10.1152/ajprenal.00604.2010.

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Barttin, a gene product of BSND, is one of four genes responsible for Bartter syndrome. Coexpression of barttin with ClC-K chloride channels dramatically induces the expression of ClC-K current via insertion of ClC-K-barttin complexes into plasma membranes. We previously showed that stably expressed R8L barttin, a disease-causing missense mutant, is retained in the endoplasmic reticulum (ER) of Madin-Darby canine kidney (MDCK) cells, with the barttin β-subunit remaining bound to ClC-K α-subunits (Hayama A, Rai T, Sasaki S, Uchida S. Histochem Cell Biol 119: 485–493, 2003). However, transient expression of R8L barttin in MDCK cells was reported to impair ClC-K channel function without affecting its subcellular localization. To investigate the pathogenesis in vivo, we generated a knockin mouse model of Bartter syndrome that carries the R8L mutation. These mice display disease-like phenotypes (hypokalemia, metabolic alkalosis, and decreased NaCl reabsorption in distal tubules) under a low-salt diet. Immunofluorescence and immunoelectron microscopy revealed that the plasma membrane localization of both R8L barttin and the ClC-K channel was impaired in these mice, and transepithelial chloride transport in the thin ascending limb of Henle's loop (tAL) as well as thiazide-sensitive chloride clearance were significantly reduced. This reduction in transepithelial chloride transport in tAL, which is totally dependent on ClC-K1/barttin, correlated well with the reduction in the amount of R8L barttin localized to plasma membranes. These results suggest that the major cause of Bartter syndrome type IV caused by R8L barttin mutation is its aberrant intracellular localization.

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Dissertations / Theses on the topic "Knockin mouse model"

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Liu, Huifang, and 刘慧芳. "Creation and characterization of a LRRK2 knockin mouse model to elucidate the pathogenesis of Parkinson's disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46090903.

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Manett, Taylor. "Investigating the pathogenicity of an autism-related CNTNAP2 missense variant in a novel mouse model." Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS721.pdf.

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Les troubles du spectre autistique (TSA) sont des troubles neurodéveloppementaux définis par des déficits d'interaction sociale et des comportements restreints ou répétitifs. Les TSA présentent une forte héritabilité, déterminée par de rares mutations monogéniques, ainsi que par des variations dans de nombreux gènes de susceptibilité. Le gène CNTNAP2, qui code pour la protéine Caspr2, est considéré comme l'un des principaux gènes de risque pour les TSA, un grand nombre de variants hétérozygotes faux-sens ayant été identifiés chez les patients. Les souris knock-out Cntnap2 présentent des déficits comportementaux de type TSA, ce qui supporte les données de génétique humaine. Cependant, la signification clinique des variants hétérozygotes n'a pas encore été démontrée et reste débattue. Le projet de thèse visait à élucider cette question en évaluant la pathogénicité in vivo d'un variant CNTNAP2 hétérozygote faux-sens identifié chez un patient français atteint de TSA, I236S, qui a été prédit comme pathogène et pourrait être représentatif d'une large classe de variants CNTNAP2. Nous avons généré un nouveau modèle de souris knockin, les souris KI-I236S, et mené une étude comparant les souris de type sauvage et les souris hétérozygotes (HET) KI-I236S. Caspr2 est une glycoprotéine transmembranaire d'adhésion cellulaire neuronale identifiée à l'origine dans les régions juxtaparanodales des nœuds de Ranvier dans les neurones myélinisés matures. Récemment, en étudiant des souris knock-out Cntnap2, le laboratoire a montré que Caspr2 agit également comme un régulateur majeur du développement de l'axone et de la myélinisation. Dans le cerveau, Caspr2 contrôle le diamètre des axones aux premiers stades du développement postnatal, l'excitabilité intrinsèque des neurones corticaux au début de la myélinisation, ainsi que le diamètre des axones et l'épaisseur de la myéline à l'âge adulte. Caspr2 module également le diamètre des axones, l'épaisseur de la myéline et la morphologie du nœud de Ranvier dans les nerfs périphériques. Nous avons donc évalué l'impact du variant I235S sur le développement des axones, la myélinisation et l'organisation des nœuds de Ranvier dans le système nerveux central et périphérique. Nous avons également caractérisé en détail le comportement des souris HET KI-I236S, en utilisant une batterie de tests qui peuvent indiquer des déficits cognitifs, moteurs et sensorimoteurs. De façon intéressante, les souris HET KI-I236S présentent des déficits cognitifs et somatosensoriels dépendants du sexe par rapport aux souris de type sauvage (interaction sociale légèrement réduite chez les femelles ; sensibilité à la chaleur et force musculaire légèrement réduites chez les mâles). Elles présentent également des altérations sexe-dépendantes des axones myélinisés et des fibres C sensorielles non myélinisées du système nerveux périphérique. Les analyses du cerveau ne montrent pas de défauts majeurs de myélinisation chez les souris mutantes adultes, mais suggèrent que le variant pourrait perturber les fonctions de Caspr2 au début de la myélinisation, conduisant probablement à une accélération des processus de myélinisation à des stades précoces. Ainsi, nos résultats indiquent que les variants faux-sens hétérozygotes de CNTNAP2 tels que I236S peuvent affecter la fonction de Caspr2 de manière dépendante du sexe in vivo, et suggèrent que les variants de CNTNAP2 de la même classe pourraient être pathogènes et contribuer au développement des TSA chez les patients, et/ou contribuer à la variabilité interindividuelle dans les conditions physiologiques
Autism spectrum disorders (ASD) are neurodevelopmental disorders, defined by deficits in social interaction and restricted or repetitive behavior. ASD show high heritability, shaped by rare monogenic mutations, as well as variations in numerous susceptibility genes. Intriguingly, CNTNAP2, encoding the protein Caspr2, is considered to be one of the major ASD-risk genes, with a large number of heterozygous missense variants identified in patients. Cntnap2 knockout mice display ASD-related behavioral deficits supporting human genetic data. However, the clinical significance of the heterozygous variants has not yet been demonstrated and is still debated. The PhD project aimed to unravel this question by evaluating the pathogenicity of an inherited heterozygous missense CNTNAP2 variant identified in a French ASD patient, I236S, which was predicted to be disease-causing and may be representative of a large class of CNTNAP2 variants. We generated a novel knockin mouse model, the KI-I236S mice, and conducted a study comparing wild-type and KI-I236S heterozygous (HET) mice. Caspr2 is a neuronal cell-adhesion transmembrane glycoprotein originally identified in the juxtaparanodal regions of the nodes of Ranvier in mature myelinated neurons. Recently, studying Cntnap2 knockout mice the lab showed that Caspr2 also acts as a major regulator of axon development and myelination. In the brain, Caspr2 controls axon diameter at early postnatal developmental stages, cortical neuron intrinsic excitability at the onset of myelination, and axon diameter and myelin thickness at adulthood. Caspr2 also modulates axon diameter, myelin thickness and node of Ranvier morphology in peripheral nerves. We thus assessed the impact of the variant I235S on axon development, myelination, and node of Ranvier organization in both the central and peripheral nervous system, as well as thoroughly characterizing the behavior of HET KI-I236S mice, using a battery of tests that may indicate cognitive, motor, and sensorimotor deficits. Interestingly, KI-I236S HET mice display sex-dependent cognitive and somatosensory behavioral deficits as compared to wild-type mice (social interaction slightly decreased in females; heat sensitivity and muscular strength slightly decreased in males). They also show sex-dependent alterations in myelinated axons and unmyelinated sensory C-fibers of the peripheral nervous system. Brain analyses do not show major myelination defects in adult mutant mice, but suggest that the variant could perturb the functions of Caspr2 at the onset of myelination, leading likely to an acceleration of the myelination processes at early stages. Thus, our results indicate that CNTNAP2 heterozygous missense variants such as I236S can affect Caspr2 function in a sex-dependent manner in vivo and suggest that the CNTNAP2 variants of the same class could indeed be pathogenic and contribute to the development of ASD patients, and/or contribute to inter-individual variability in physiological conditions

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Sarowar, Tasnuva [Verfasser]. "Characterization of RICH2 knock-out mouse model / Tasnuva Sarowar." Ulm : Universität Ulm, 2017. http://d-nb.info/1136370226/34.

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Naidu, Shan Krishnan. "PATHOLOGY OF THREE TRANSGENIC MOUSE LINES WITH UNIQUE PTEN MUTANT ALLELES." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1282941122.

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ALBINI, MARTINA. "Functional interaction between BDNF and Kidins220: a study in primary mouse astrocytes and in an adult conditional knock-out mouse model." Doctoral thesis, Università degli studi di Genova, 2022. http://hdl.handle.net/11567/1077504.

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Neurotrophins are a family of growth factors known for their pleiotropic effects on neuronal survival, maturation and plasticity. Brain-derived neurotrophic factor (BDNF) is the most expressed in the brain. The activation of specific BDNF downstream pathways hinges on BDNF binding to its receptor TrkB. Kidins220 is a scaffold protein that interacts with neurotrophin receptors and is directly involved in the activation of neurotrophin signaling. It is also required for neuron differentiation, survival and plasticity. This protein has been linked to several diseases including psychiatric and neurodegenerative pathologies and for this reason, several KO animal models have been generated. So far none of them was viable after birth, making it impossible to investigate the role of this protein in postnatal/adult brain development. Astrocytes are fundamental in maintaining nervous system homeostasis. They are capable of perceiving a wide variety of extracellular cues and transducing them via the activation of specific intracellular signaling pathways into responses that may be protective or disruptive toward neighboring neurons. Moreover, astrocytes are key regulators of neuronal circuit formation and synaptic transmission. Several aspects of astrocyte physiology are controlled by neurotrophins. However, the role of Kidins220 in astrocytes, as well as in the adult brain remains largely unknown. Thus, in this thesis we aimed to deeply understand the role of Kidins220 using both in vivo and in vitro models. First we compared the signaling competence of embryonic and postnatal primary cortical astrocytes exposed to BDNF, and observed a shift from a kinase-based response in embryonic cells to a predominantly Ca2+-based response in postnatal cultures. We demonstrated that Kidins220 ablation is accompanied by a decreased expression of both BDNF receptor TrkB isoforms. We also described the role of Kidins220 in BDNF-induced signaling in astrocytes, showing that it contributes to both kinase and Ca2+-activated pathways. To evaluate the effect of Kidins220 ablation in the adult brain we used a floxed line that expresses only the full-length isoform, which we crossed with mice expressing Cre under the CamKII promoter, leading to a conditional knockout (cKO) line where Kidins220 is absent only in the excitatory neurons of the forebrain, starting at the second postnatal week. In this animal model, we have observed altered dendritic arborization and spine number in the cortico-hippocampal regions. The deletion of Kidins220 also leads to behavioral changes, such as reduced anxiety-like traits due to to alterations in TrkB-BDNF signaling. Our data increase the knowledge of the complex role played by Kidins220 both in astrocytes and in adult brains, reveal a previously unidentified role of this protein in astrocytes, controlling the response to BDNF and to Ca2+ dynamics during development. Finally, our data confirm the fundamental role of Kidins220 in adult mice, where its ablation leads to both behavioral and biochemical impairments.

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Saka, Asantha. "Investigating the toxic fragment hypothesis of Huntingdon disease pathogenesis using knock-in mouse models." Thesis, University of Glasgow, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.443414.

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Ngai, Ying Fai Tiffany. "The low-density lipoprotein receptor knock-out mouse : a model for the study of energy balance." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/23477.

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The discovery of leptin and other humoral signals which regulate food intake and energy expenditure has greatly contributed to our understanding of molecular pathways controlling energy homeostasis. Leptin produced by adipocytes, insulin produced by the pancreas, and ghrelin produced by the stomach all contribute to the body’s energy balance. One question remaining is whether the lipid transport system also plays a role. Our hypothesis is that lipid clearance is important in the maintenance of energy homeostasis. The low-density lipoprotein receptor (Ldlr) is a key molecule involved with lipid clearance. The experiments presented in this thesis used the Ldlr-/- mouse to study the Ldlr’s role in energy balance. One aim of this thesis was to provide a detailed analysis of the energy balance phenotype of the Ldlr-/- mouse. Another aim of this thesis was to use the Ldlr-/- mouse to study the potential interaction between Ldlr and the leptin signaling pathway. Adult Ldlr-/- mice and Ldlr+/+ controls on a C57BL/6J background were fed either a chow or a high-fat, high-sucrose Western-type diet (WTD) for eight weeks. Physiological studies of food intake, energy expenditure, activity, heat production, insulin sensitivity, and leptin responsiveness were performed. As well, the effect of these diet interventions on circulating leptin and on leptin gene expression was examined. On the chow diet, Ldlr-/- mice had lower energy expenditure and higher activity levels relative to controls. On the WTD, Ldlr-/- mice gained less weight relative to Ldlr+/+ mice, specifically gaining less fat mass. Increased thermogenesis in Ldlr-/- mice fed the WTD was detected. Additionally, leptin responsiveness was blunted in chow-fed Ldlr-/- mice, suggesting a novel role for the Ldlr pathway that extends to leptin’s regulation of energy balance. In addition to its known role in lipid transport, these results from the Ldlr-/- mouse demonstrate the importance of the Ldlr in regulating energy homeostasis and suggest a direct physiological link between dyslipidemia and energy balance.

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Pietra, Gianluca. "Spontaneous and stimulus-evoked spiking activities in olfactory sensory neurons from Kir2.1 knock-in and TMEM16B knock-out mouse models." Doctoral thesis, SISSA, 2016. http://hdl.handle.net/20.500.11767/4895.

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The sense of smell enables animals to detect myriads of different odors carrying information about the quality of food, the presence of pathogens, prey, predators, or potential mates. Olfactory sensory neurons (OSNs) in the nasal cavity are the interface of the main olfactory system with the external environment. The binding of an odorant molecule to specific olfactory receptors (OR) located in the cilia of these neurons triggers a transduction cascade that transduces the chemical signal into action potentials which travel along the axon of the OSNs to the olfactory bulb. Here, the odor information is processed and conveyed to higher brain centers, ultimately leading to the perception of smell. In this Thesis I studied the effect of two genetic manipulations on the firing activity of the OSNs: the ectopic overexpression of the inward rectifier potassium channel Kir2.1 and the deletion of the TMEM16b/Ano2 gene, that codes for the Ca2+- activated chloride channel TMEM16B. The overexpression of Kir2.1 reduces the excitability of the neurons, and when expressed in OSNs, mice show a general disorganization of the glomerular map in the olfactory bulb. Since spontaneous and sensory-evoked electrical activity play important roles in the formation of several sensory circuits, including the olfactory system, in the first part of this Thesis, I investigated how the spiking activity of mouse OSNs is influenced by the Kir2.1 overexpression, using loose-patch recordings from the OSNs knobs. I found that the overexpression of Kir2.1 caused a decrease in the spontaneous firing activity of OSNs but did not influence the evoked firing properties induced by odorant stimulation, indicating that the olfactory bulb disorganization was caused by a reduced spontaneous firing activity. Ca2+-activated Cl¯ current (CaCC) is an important component of the transduction current evoked by odor stimulation in OSNs. Binding of odorants to their specific receptor on the cilia of OSNs causes the activation of adenylyl cyclase with a relative increase of intracellular cAMP, activating cyclic nucleotide-gated (CNG) channels. Ca2+ entry through CNG channels increases the open probability of Ca2+-activated Cl- channels. The molecular identity of these channels has been elusive for a long time, but recently it has been shown that the olfactory CaCC are mediated by the membrane protein TMEM16B/Anoctamin2. However, the physiological role of olfactory CaCC is still unclear, and the first description of TMEM16B knockout (KO) mice reported no clear olfactory deficits. In the second part of this Thesis, I studied basal firing properties and stimulus-evoked responses with loose-patch recordings in OSNs from TMEM16B KO or WT mice. OSNs responded to a stimulus with a transient burst of action potentials. Responses of OSNs from TMEM16B KO mice showed an increased number of action potentials compared to responses from WT mice, both in OSNs expressing a random or I7 OR. The basal spiking activity of individual OSNs is correlated with the expressed OR that drives basal transduction activity. I measured a reduced basal activity in TMEM16B KO OSNs expressing the I7 OR compared to WT OSNs. Moreover, axonal targeting was altered and TMEM16B KO had supernumerary I7 glomeruli compared to WT. These results show that the expression of TMEM16B affects OSNs firing properties and contributes to the glomerular formation and refinement of I7-expressing OSNs in the olfactory bulb, suggesting a crucial role for TMEM16B in normal olfaction.

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Silva, Lopes Katharina da [Verfasser]. "Novel insights into Titin’s mobility and function derived from a knock-in mouse model / Katharina da Silva Lopes." Berlin : Freie Universität Berlin, 2011. http://d-nb.info/1026356598/34.

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Sierig, Ralph [Verfasser], Christoph [Gutachter] Englert, and Falk [Gutachter] Weih. "Analysis of Wt1 function using a conditional knock-out mouse model / Ralph Sierig ; Gutachter: Christoph Englert, Falk Weih." Jena : Friedrich-Schiller-Universität Jena, 2010. http://d-nb.info/1177668505/34.

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Book chapters on the topic "Knockin mouse model"

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Huang, Weihua, Wenhao Xu, and Ming D. Li. "Mouse Models: Knockouts/Knockins." In Addiction Medicine, 181–99. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0338-9_9.

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Bertoni, Arinna, Ignazia Prigione, Sabrina Chiesa, Isabella Ceccherini, Marco Gattorno, and Anna Rubartelli. "A Knock-In Mouse Model of Cryopyrin-Associated Periodic Syndromes." In Methods in Molecular Biology, 281–97. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3350-2_19.

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Rumney, Robin M. H., and Dariusz C. Górecki. "Knockout and Knock-in Mouse Models to Study Purinergic Signaling." In Methods in Molecular Biology, 17–43. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9717-6_2.

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Goitre, Luca, Claudia Fornelli, Alessia Zotta, Andrea Perrelli, and Saverio Francesco Retta. "Production of KRIT1-knockout and KRIT1-knockin Mouse Embryonic Fibroblasts as Cellular Models of CCM Disease." In Methods in Molecular Biology, 151–67. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0640-7_12.

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Larsen, Erik Hviid, and Jens Nørkær Sørensen. "Stationary and Nonstationary Ion and Water Flux Interactions in Kidney Proximal Tubule: Mathematical Analysis of Isosmotic Transport by a Minimalistic Model." In Reviews of Physiology, Biochemistry and Pharmacology, 101–47. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/112_2019_16.

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AbstractOur mathematical model of epithelial transport (Larsen et al. Acta Physiol. 195:171–186, 2009) is extended by equations for currents and conductance of apical SGLT2. With independent variables of the physiological parameter space, the model reproduces intracellular solute concentrations, ion and water fluxes, and electrophysiology of proximal convoluted tubule. The following were shown: Water flux is given by active Na+ flux into lateral spaces, while osmolarity of absorbed fluid depends on osmotic permeability of apical membranes. Following aquaporin “knock-out,” water uptake is not reduced but redirected to the paracellular pathway. Reported decrease in epithelial water uptake in aquaporin-1 knock-out mouse is caused by downregulation of active Na+ absorption. Luminal glucose stimulates Na+ uptake by instantaneous depolarization-induced pump activity (“cross-talk”) and delayed stimulation because of slow rise in intracellular [Na+]. Rate of fluid absorption and flux of active K+ absorption would have to be attuned at epithelial cell level for the [K+] of the absorbate being in the physiological range of interstitial [K+]. Following unilateral osmotic perturbation, time course of water fluxes between intraepithelial compartments provides physical explanation for the transepithelial osmotic permeability being orders of magnitude smaller than cell membranes’ osmotic permeability. Fluid absorption is always hyperosmotic to bath. Deviation from isosmotic absorption is increased in presence of glucose contrasting experimental studies showing isosmotic transport being independent of glucose uptake. For achieving isosmotic transport, the cost of Na+ recirculation is predicted to be but a few percent of the energy consumption of Na+/K+ pumps.

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Gu, Bin, Marina Gertsenstein, and Eszter Posfai. "Generation of Large Fragment Knock-In Mouse Models by Microinjecting into 2-Cell Stage Embryos." In Methods in Molecular Biology, 89–100. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9837-1_7.

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Parrington, John. "Next Year’s Models." In Redesigning Life, 111–32. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198766834.003.0006.

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Animal ‘models’ of health and disease have been central to biomedical science since at least when William Harvey used dogs to illustrate the fact that blood is pumped by the heart through the arteries and then through the veins back to the heart. In the 1980s, a major step forward came with the discovery of embryonic stem cells and ways to manipulate these genetically and then inject into mouse embryos, resulting in the creation of knockout and knockin mice with deletions, or more subtle changes, in specific genes. Unfortunately, it has been impossible to isolate embryonic stem cells from any other species besides mice, and more recently rats and humans. Yet rodents are far from the best animals for modelling, say the body’s metabolism or heart function and disease, or brain function and mental disorders. Instead, pigs and primates are potentially far better models for these respective areas of research. CRISPR/Cas genome editing has made it possible for the first time to create precisely genome edited versions of pigs, monkeys, and any other species that may provide a better model of specific aspects of human health and disease, than rodents. So genetically modified pigs might be used to study heart disease, but also provide hearts for human transplantation, while GM monkeys might help us better understand the biological basis of mental disorders such as depression or schizophrenia. However, this area of research is raising ethical issues about the creation of monkeys with human versions of particular genes, and how this might affect their behaviour and personality.

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Corbett, Brian, and Jeannie Chin. "Mouse models in bioscience research." In Tools and Techniques in Biomolecular Science. Oxford University Press, 2013. http://dx.doi.org/10.1093/hesc/9780199695560.003.0019.

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This chapter looks at mouse models, which play a critical part in answering important questions in biological and biomedical research, especially in probing the role of genes in vivo . Mice are mammalian and have fundamental anatomy that is comparable to that of humans, making research in mouse models more easily translatable to human conditions. The chapter covers different types of genetic manipulation in mice, touching on the various types of genetically engineered mice such as transgenic, knockin, knockout, and conditional knockout mice, as well as mice with inducible or repressible gene expression. The chapter provides an overview of their applications in research and outlines key considerations in the use of each.

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Liu, Wei, Xin Wang, and Elizabeth J. Cartwright. "Transgenesis." In Molecular Biology and Biotechnology, 155–90. 7th ed. The Royal Society of Chemistry, 2021. http://dx.doi.org/10.1039/9781788017862-00155.

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Transgenesis is a term to describe an array of techniques used to modify the genomes of intact organisms including those of plants, insects, invertebrates, amphibians, fish and small and large mammals. To increase our knowledge of human health and disease, it is essential that we elucidate the function of the 21 000 genes in the mammalian genome. The mouse is the most commonly used mammalian model in which to explore gene function owing to the relative ease with which its genome can be modified. In the mouse, gene function can be altered in a number of ways, including over-expressing a gene, expressing a foreign gene, knocking out or deleting single or multiple genes, introducing point mutations and altering gene expression in a specific tissue or at a specific point in time. This chapter describes how the different techniques are used to introduce this wide range of gene modifications.

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Levy, Isaac, Matthew Starost, Evan Ball, Fabio Rueda Faucz, Spyros Koliavasillis, Anelia Horvath, Kitman Tsang, et al. "Phosphodiesterase 11A (Pde11a) Expression in Mouse Tissues and Characterization of a Pde11a Mouse Knock-Out Model." In BASIC/TRANSLATIONAL - Development & Epigenetics of Steroid Biology & Neoplasia, P1–41—P1–41. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.p2.p1-41.

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Conference papers on the topic "Knockin mouse model"

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Ma, Hechun, Yi Li, Ping Yang, Renxing Zhang, Dongxiao Feng, Jian Fei, Ruilin Sun, and Daniel X. He. "14 Humanized TFR1/CD71 knockin mouse model enables in vivo assessment of TFR1-targeted antibody therapies for cancer and beyond to across the blood-brain barrier." In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0014.

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Mahmoud, Ahmed M., Bunyen Teng, S. Jamal Mustafa, and Osama M. Mukdadi. "High-Frequency Ultrasound Tissue Classification of Atherosclerotic Plaques in an APOE-KO Mouse Model Using Spectral Analysis." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-13061.

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Small animal models have been widely used in cardiovascular research when studying the development and treatment of different diseases. This kind of research has promoted the development of noninvasive techniques to assess cardiac tissue and blood vessels of small animals. Recently, we have developed a high-frequency ultrasound imaging system for small animals, in particular, mouse and rat models. In this work, we aim to elucidate the usefulness of using spectral analysis of the received radiofrequency (RF) ultrasound signals to extract quantitative parameters to assess mechanical properties of cardiac and vascular tissues. A custom system that employs high-frequency single-element ultrasound transducers (30–120 MHz) is used for scanning. Various signal and image processing techniques are applied on the received ultrasound signals to reconstruct high resolution B-mode and spectral images. In vitro imaging of isolated heart and vessels of APOE-KO “knock-out” mouse model with atherosclerosis was performed. Power spectral densities (PSD) of RF signals were evaluated within various regions of interests (ROI) including degassed water, normal cardiac tissue, and cardiac tissue with atheroma. Various parameters were extracted from the power spectrum such as the maximum power (Pmax), the frequency at maximum power (Fpeak), and the variance of power spectrum (Pvar). Results of the preliminary spectral analysis indicated larger values for the Pmax, Fpeak, and Pvar parameters for ROI contains atheroma than other regions. For example using the envelop data, the normalized maximum power (Pmax) value for cardiac tissue with atheroma was 0.0 ± 0.789 (dB), whereas for normal tissues it was about −13.71± 0.267 (dB). These results suggest the use spectral images as a quantitative method when assessing mouse hearts and blood vessels noninvasively.

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Wan, William, and Rudolph L. Gleason. "Collagen Fiber Angle Quantification of Carotid Arteries From Fibulin-5 Null Mice." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53685.

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Recent studies have revealed that carotid arteries from fibulin-5 (fbln5) null mice exhibit altered biomechanical and microstructural properties [1–2]. While the previous studies outline quantitative differences in mechanical properties of arteries from fbln5 null and wildtype mice, physical microstructural differences have yet to be quantified. Measurement of microstructural parameters will provide a crucial link between previously quantified mechanical properties and biological effects of knocking out the fbln5 gene. Characterizing microstructural properties will also provide experimental data to validate structurally-motivated constitutive relations and growth and remodeling models [3–4]. In this study, we quantified collagen fiber orientation in carotid arteries from fbln5 null and wildtype mice; collagen in mouse carotid arteries were imaged using multiphoton microscopy and analyzed using a fast Fourier transform algorithm.

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Xiong, Shunbin, Yun Zhang, and Guillermina Lozano. "Abstract B07: Gain of function activities of p53R245W in a conditional knock-in mouse model." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-b07.

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Bertoni, Arinna, Sonia Carta, Chiara Baldovini, Federica Penco, Enrica Balza, Silvia Borghini, Marco DI Duca, et al. "OP0106 A NOVEL KNOCK-IN MOUSE MODEL OF CAPS THAT DEVELOPS AMYLOIDOSIS: THERAPEUTIC EFFICACY OF PROTON PUMP INHIBITORS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5727.

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Yoshida, Kyoko, Claire Reeves, Jan Kitajewski, Ronald Wapner, Joy Vink, Michael Fernandez, and Kristin Myers. "Anthrax Toxin Receptor 2 Knock-Out and Wild Type Mouse Cervix Exhibit Time-Dependent Mechanical Properties." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80732.

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The cervix plays a critical role during pregnancy, acting as a mechanical barrier to keep the fetus inside the uterus until term. In a normal pregnancy, it is hypothesized that the cervix gradually softens until uterine contractions occur. At this point, the cervix dramatically ripens and dilates for delivery. Similar to other collagenous tissues, the extracellular matrix (ECM) is the load-bearing component of cervical tissue. It is composed mainly of a cross-linked network of fibril forming collagen, types I and III, embedded in a viscous proteoglycan ground substance. Studies conducted on animal models suggest that during normal maturation, a shift in ECM components facilitate cervical softening. However, quantitative cervical softness measurements (i.e. material properties) of these previous studies are ill-defined, limiting the comparative ability of the outcome values. Therefore, our goal is to quantify sensitive and specific time-dependent material properties utilizing mouse models of normal and abnormal pregnancy. Our aim is to discern the role of ECM maintenance in cervical softening.

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Diaz Martinez, Myriam, Masoud Ghamari-Langroudi, Aliya Gifford, Roger Cone, and E. B. Welch. "Automated pipeline to analyze non-contact infrared images of the paraventricular nucleus specific leptin receptor knock-out mouse model." In SPIE Medical Imaging, edited by Barjor Gimi and Robert C. Molthen. SPIE, 2015. http://dx.doi.org/10.1117/12.2082102.

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Hilhorst, Maria H., Liesbeth Houkes, Hanneke Korsten, Monique Mommersteeg, Jan Trapman, and Rob Ruijtenbeek. "Abstract 4046: Direct detection of AKT/PKB activity in a Pten knock out mouse model using dynamic peptide microarrays." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4046.

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Song, Ihn Young, Atul Kumar, Reyno Delrosario, Jian-Hua Mao, and Allan Balmain. "Abstract LB-258: The human Aurora-A kinase Phe31Ile polymorphism affects cancer susceptibility in a knock-in mouse model." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-258.

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Hummel, S., L. Slemann, J. Gnoerich, L. H. Kunze, G. Biechele, P. E. Sanchez, C. Haass, et al. "F-18-florbetaben-PET shows distinct distribution patterns of β-amyloid in different knock-in AD mouse models." In 60. Jahrestagung der Deutschen Gesellschaft für Nuklearmedizin. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1746038.

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