Einloggen

Thematische Bibliographien / Knockin mouse model

Inhaltsverzeichnis

Zeitschriftenartikel

Auswahl der wissenschaftlichen Literatur zum Thema „Knockin mouse model“

Autor: Grafiati

Veröffentlicht am 18. Mai 2024

Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an

Wählen Sie eine Art der Quelle aus:

Machen Sie sich mit den Listen der aktuellen Artikel, Bücher, Dissertationen, Berichten und anderer wissenschaftlichen Quellen zum Thema "Knockin mouse model" bekannt.

Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.

Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.

Zeitschriftenartikel zum Thema "Knockin mouse model"

1

Savva, Isavella, Charalampos Stefanou, Myrtani Pieri, et al. "MP036A NOVEL KNOCKIN MOUSE MODEL FOR ALPORT SYNDROME." Nephrology Dialysis Transplantation 31, suppl_1 (2016): i354. http://dx.doi.org/10.1093/ndt/gfw182.06.

Der volle Inhalt der Quelle

APA, Harvard, Vancouver, ISO und andere Zitierweisen

2

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

Der volle Inhalt der Quelle

Annotation:

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.

APA, Harvard, Vancouver, ISO und andere Zitierweisen

3

de Winter, J., M. Yuen, R. Van der Pijl, 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.

Der volle Inhalt der Quelle

APA, Harvard, Vancouver, ISO und andere Zitierweisen

4

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 (2014): e115444. http://dx.doi.org/10.1371/journal.pone.0115444.

Der volle Inhalt der Quelle

APA, Harvard, Vancouver, ISO und andere Zitierweisen

5

Rose, Samuel J., Lisa H. Kriener, Ann K. Heinzer, et al. "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.

Der volle Inhalt der Quelle

APA, Harvard, Vancouver, ISO und andere Zitierweisen

6

Sundberg, J. P., C. H. Pratt, K. A. Silva, et al. "394 Card14 knockin mouse model of psoriasis and psoriatic arthritis." Journal of Investigative Dermatology 136, no. 5 (2016): S70. http://dx.doi.org/10.1016/j.jid.2016.02.428.

Der volle Inhalt der Quelle

APA, Harvard, Vancouver, ISO und andere Zitierweisen

7

Baelde, R., A. Fortes Monteiro, E. Nollet, et al. "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.

Der volle Inhalt der Quelle

APA, Harvard, Vancouver, ISO und andere Zitierweisen

8

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 (2012): 106.44. http://dx.doi.org/10.4049/jimmunol.188.supp.106.44.

Der volle Inhalt der Quelle

Annotation:

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.

APA, Harvard, Vancouver, ISO und andere Zitierweisen

9

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 (2012): 2678–91. http://dx.doi.org/10.1016/j.neurobiolaging.2012.01.002.

Der volle Inhalt der Quelle

APA, Harvard, Vancouver, ISO und andere Zitierweisen

10

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

Der volle Inhalt der Quelle

Annotation:

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.

APA, Harvard, Vancouver, ISO und andere Zitierweisen

Mehr Quellen

Wir bieten Rabatte auf alle Premium-Pläne für Autoren, deren Werke in thematische Literatursammlungen aufgenommen wurden. Kontaktieren Sie uns, um einen einzigartigen Promo-Code zu erhalten!