Log in

Relevant bibliographies by topics / Nestin-Cre mice

Contents

Journal articles
Book chapters

Academic literature on the topic 'Nestin-Cre mice'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Nestin-Cre mice.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Nestin-Cre mice"

1

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

3

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

5

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

8

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

10

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!