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Gotowe bibliografie tematyczne / Nestin-Cre mice

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Gotowa bibliografia na temat „Nestin-Cre mice”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Nestin-Cre mice"

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Swilley, Cody, Yu Lin, Yuze Zheng, et al. "Sex-Linked Growth Disorder and Aberrant Pituitary Gene Expression in Nestin-Cre-Mediated Egr1 Conditional Knockout Mice." Biology 12, no. 7 (2023): 966. http://dx.doi.org/10.3390/biology12070966.

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Genes that regulate hormone release are essential for maintaining metabolism and energy balance. Egr1 encodes a transcription factor that regulates hormone production and release, and a decreased in growth hormones has been reported in Egr1 knockout mice. A reduction in growth hormones has also been observed in Nestin-Cre mice, a model frequently used to study the nervous system. Currently, it is unknown how Egr1 loss or the Nestin-Cre driver disrupt pituitary gene expression. Here, we compared the growth curves and pituitary gene expression profiles of Nestin-Cre-mediated Egr1 conditional kno

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do Carmo, Jussara M., Alexandre A. da Silva, Fabio N. Gava, Sydney P. Moak, Xuemei Dai, and John E. Hall. "Impact of leptin deficiency compared with neuronal-specific leptin receptor deletion on cardiometabolic regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 317, no. 4 (2019): R552—R562. http://dx.doi.org/10.1152/ajpregu.00077.2019.

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The main goal of this study was to compare the impact of total body leptin deficiency with neuronal-specific leptin receptor (LR) deletion on metabolic and cardiovascular regulation. Liver fat, diacylglycerol acyltransferase-2 (DGTA2), and CD36 protein content were measured in wild-type (WT), nervous system LR-deficient (LR/Nestin-Cre), and leptin deficient ( ob/ob) mice. Blood pressure (BP) and heart rate (HR) were recorded by telemetry, and motor activity (MA) and oxygen consumption (V̇o2) were monitored at 24 wk of age. Female and male LR/Nestin-Cre and ob/ob mice were heavier than WT mice

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Kajitani, Yusuke, Takashi Miyazawa, Tomoaki Inoue, et al. "High frequency of germline recombination in Nestin-Cre transgenic mice crossed with Glucagon-like peptide 1 receptor floxed mice." PLOS ONE 18, no. 12 (2023): e0296006. http://dx.doi.org/10.1371/journal.pone.0296006.

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The Cre-loxP strategy for tissue-specific gene inactivation has become a widely employed tool in several research studies. Conversely, inadequate breeding and genotyping without considering the potential for non-specific Cre-recombinase expression may lead to misinterpretations of results. Nestin-Cre transgenic mice, widely used for the selective deletion of genes in neurons, have been observed to have an incidence of Cre-line germline recombination. In this study, we attempted to generate neuron-specific Glucagon-like peptide 1 receptor (Glp1r) knock-out mice by crossing mice harboring the Ne

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do Carmo, Jussara M., Alexandre A. da Silva, Zhen Wang, et al. "Regulation of Blood Pressure, Appetite, and Glucose by Leptin After Inactivation of Insulin Receptor Substrate 2 Signaling in the Entire Brain or in Proopiomelanocortin Neurons." Hypertension 67, no. 2 (2016): 378–86. http://dx.doi.org/10.1161/hypertensionaha.115.06153.

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Insulin receptor substrate 2 (IRS2) is one of the 3 major leptin receptor signaling pathways, but its role in mediating the chronic effects of leptin on blood pressure, food intake, and glucose regulation is unclear. We tested whether genetic inactivation of IRS2 in the entire brain (IRS2/Nestin-cre mice) or specifically in proopiomelanocortin (POMC) neurons (IRS2/POMC-cre mice) attenuates the chronic cardiovascular, metabolic, and antidiabetic effects of leptin. Mice were instrumented with telemetry probes for measurement of blood pressure and heart rate and with venous catheters for intraven

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Singh, Pratibha, Hongge Li, and Louis M. Pelus. "Engraftment and Reconstitution of Hematopoiesis Is Dependent on Endothelial Cell Expressed Prostaglandin EP4 Receptor Signaling Mediated Regeneration of Vascular Niche." Blood 132, Supplement 1 (2018): 1293. http://dx.doi.org/10.1182/blood-2018-99-119723.

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Abstract Defining the cellular and molecular components of the bone marrow (BM) niche that regulate the homeostasis and regeneration of hematopoietic stem and progenitor cells (HSPCs) can facilitate targeted interventions to improve hematopoietic recovery after injury and enhance stem cell engraftment after transplantation. We have recently shown that BM niche prostaglandin E2 (PGE2) signaling via the EP4 receptor is crucial for hematopoietic reconstitution, as transplantation of wild-type donor cells into EP4 receptor deficient recipient mice shows reduced stem cell engraftment. However, the

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Xue, Baojian, Zhongming Zhang, Terry G. Beltz, Fang Guo, Meredith Hay, and Alan Kim Johnson. "Genetic knockdown of estrogen receptor-alpha in the subfornical organ augments ANG II-induced hypertension in female mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 6 (2015): R507—R516. http://dx.doi.org/10.1152/ajpregu.00406.2014.

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The present study tested the hypotheses that 1) ERα in the brain plays a key role in the estrogen-protective effects against ANG II-induced hypertension, and 2) that the subfornical organ (SFO) is a key site where ERα mediates these protective actions. In this study, a “floxed” ERα transgenic mouse line (ERαflox) was used to create models in which ERα was knocked down in the brain or just in the SFO. Female mice with ERα ablated in the nervous system (Nestin-ERα− mice) showed greater increases in blood pressure (BP) in response to ANG II. Furthermore, females with ERα knockdown specifically in

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Wang, Xueqiao, Xiaoqing Zheng, Juanlian Zhang, et al. "Physiological functions of ferroportin in the regulation of renal iron recycling and ischemic acute kidney injury." American Journal of Physiology-Renal Physiology 315, no. 4 (2018): F1042—F1057. http://dx.doi.org/10.1152/ajprenal.00072.2018.

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Renal iron recycling preserves filtered iron from urinary excretion. However, it remains debated whether ferroportin (FPN), the only known iron exporter, is functionally involved in renal iron recycling and whether renal iron recycling is required for systemic iron homeostasis. We deleted FPN in whole nephrons by use of a Nestin-Cre and in the distal nephrons and collecting ducts, using a Ksp-Cre, and investigated its impacts on renal iron recycling and systemic iron homeostasis. FPN deletion by Nestin-Cre, but not by Ksp-Cre, caused excess iron retention and increased ferritin heavy chain (FT

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Jia, Junshuang, Xiaolin Lin, Xia Lin, et al. "R/L, a double reporter mouse line that expresses luciferase gene upon Cre-mediated excision, followed by inactivation of mRFP expression." Genome 59, no. 10 (2016): 816–26. http://dx.doi.org/10.1139/gen-2016-0090.

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The Cre/loxP system has become an important tool for the conditional gene knockout and conditional gene expression in genetically engineered mice. The applications of this system depend on transgenic reporter mouse lines that provide Cre recombinase activity with a defined cell type-, tissue-, or developmental stage-specificity. To develop a sensitive assay for monitoring Cre-mediated DNA excisions in mice, we generated Cre-mediated excision reporter mice, designated R/L mice (R/L: mRFP(monomeric red fluorescent protein)/luciferase), express mRFP throughout embryonic development and adult stag

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Aamir, Zoya, Melissa Galati, Emma Gattoni, et al. "BIOL-18. NEWLY DEVELOPED REPLICATION REPAIR DEFICIENT (RRD) MOUSE MODELS PROVIDE INSIGHTS INTO MEDULLOBLASTOMA/GLIOMAGENESIS AND RESPONSE TO IMMUNOTHERAPY." Neuro-Oncology 25, Supplement_1 (2023): i9—i10. http://dx.doi.org/10.1093/neuonc/noad073.037.

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Abstract Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-resistant, but respond favorably to immune checkpoint inhibition (ICI). Representative immunocompetent animal models are urgently needed for 3 recently identified subgroups based on specific somatically-acquired mutations, survival, and immunotherapy response (RRD1: MMRD with POLE mutations, RRD2: M

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Galati, Melissa, Li Li, Sumedha Sudhaman, et al. "MODL-25. REPLICATION REPAIR DEFICIENT MOUSE MODELS PROVIDE INSIGHT ON HYPERMUTANT BRAIN TUMOURS, MECHANISMS OF IMMUNE EVASION, AND COMBINATORIAL IMMUNOTHERAPY." Neuro-Oncology 22, Supplement_3 (2020): iii416. http://dx.doi.org/10.1093/neuonc/noaa222.598.

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Abstract Replication repair deficiency (RRD) is the leading cause of hypermutant brain tumours in children. RRD is caused by defects in one of four mismatch repair (MMR) genes and mutations in POLE or POLD1. Such tumours are resistant to common therapeutic agents and animal models are needed to study RRD in vivo and test novel therapies like immune checkpoint inhibitors (ICIs). To model RRD brain tumours specifically, we engineered a Pole mutant mouse model harbouring the S459F mutation (PoleS459F). We combined PoleS459F mice with conditional Msh2 knockout (Msh2LoxP) and Nestin-cre mice. All N

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Części książek na temat "Nestin-Cre mice"

1

Omais, Saad, Nour N. Halaby, Karl John Habashy, Carine Jaafar, Anthony T. Bejjani, and Noël Ghanem. "Histological Assessment of Cre-loxP Genetic Recombination in the Aging Subventricular Zone of Nestin-CreERT2/Rosa26YFP Mice." In Stem Cells and Aging. Springer New York, 2019. http://dx.doi.org/10.1007/7651_2019_214.

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