関: gene knockout mouse

WordNet

(genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
the syllable naming the third (mediant) note of any major scale in solmization
a blow that renders the opponent unconscious (同)KO, kayo
informal term for information; "give me the gen on your new line of computers"

PrepTutorEJDIC

遺伝子
ミ(全音階の第3音)
(ボクシングの)ノックアウト(《略》『KO,K.O.,k.o.』) / 《話》すばらしい人(物) / ノックアウトする
mouseの複数形

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1. 急性骨髄性白血病の分子遺伝学 molecular genetics of acute myeloid leukemia
2. 遺伝学およびゲノミクスのためのツール：研究用に育種された遺伝子改変マウス tools for genetics and genomics specially bred and genetically engineered mice
3. JAK3欠損を伴う重度複合型免疫不全（SCID） severe combined immunodeficiency scid with jak3 deficiency
4. 肥満への遺伝的影響と病態生理 genetic contribution and pathophysiology of obesity
5. 遺伝性ヘモクロマトーシスの遺伝学 genetics of hereditary hemochromatosis

English Journal

Integrin-linked kinase plays a key role in the regulation of angiotensin II-induced renal inflammation.

Alique M1, Civantos E1, Sanchez-Lopez E1, Lavoz C1, Rayego-Mateos S1, Rodrigues-Díez R1, García-Redondo AB1, Egido J2, Ortiz A3, Rodríguez-Puyol D4, Rodríguez-Puyol M5, Ruiz-Ortega M1.Author information 1*Cellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, Madrid, Spain.2†Renal Research Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, CIBERDEM, Madrid, Spain.3‡Dialysis Unit, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, Madrid, Spain.4§Nephrology Section, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Spain.5¶Physiology Department, Universidad de Alcalá, Madrid, Spain.AbstractILK (integrin-linked kinase) is an intracellular serine/threonine kinase involved in cell-matrix interactions. ILK dysregulation has been described in chronic renal disease and modulates podocyte function and fibrosis, whereas data about its role in inflammation are scarce. AngII (angiotensin II) is a pro-inflammatory cytokine that promotes renal inflammation. AngII blockers are renoprotective and down-regulate ILK in experimental kidney disease, but the involvement of ILK in the actions of AngII in the kidney has not been addressed. Therefore we have investigated whether ILK signalling modulates the kidney response to systemic AngII infusion in wild-type and ILK-conditional knockout mice. In wild-type mice, AngII induced an inflammatory response, characterized by infiltration of monocytes/macrophages and lymphocytes, and up-regulation of pro-inflammatory factors (chemokines, adhesion molecules and cytokines). AngII activated several intracellular signalling mechanisms, such as the NF-κB (nuclear factor κB) transcription factor, Akt and production of ROS (reactive oxygen species). All these responses were prevented in AngII-infused ILK-deficient mice. In vitro studies characterized further the mechanisms regulating the inflammatory response modulated by ILK. In cultured tubular epithelial cells ILK blockade, by siRNA, inhibited AngII-induced NF-κB subunit p65 phosphorylation and its nuclear translocation. Moreover, ILK gene silencing prevented NF-κB-related pro-inflammatory gene up-regulation. The results of the present study demonstrate that ILK plays a key role in the regulation of renal inflammation by modulating the canonical NF-κB pathway, and suggest a potential therapeutic target for inflammatory renal diseases.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jul 1;127(1):19-31. doi: 10.1042/CS20130412.
ILK (integrin-linked kinase) is an intracellular serine/threonine kinase involved in cell-matrix interactions. ILK dysregulation has been described in chronic renal disease and modulates podocyte function and fibrosis, whereas data about its role in inflammation are scarce. AngII (angiotensin II) is
PMID 24383472

Activation of inflammasomes in podocyte injury of mice on the high fat diet: Effects of ASC gene deletion and silencing.

Boini KM1, Xia M2, Abais JM2, Li G2, Pitzer AL2, Gehr TW3, Zhang Y2, Li PL4.Author information 1Department of Pharmacology and Toxicology, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA. Electronic address: kmboini@vcu.edu.2Department of Pharmacology and Toxicology, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA.3Department of Internal Medicine, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA.4Department of Pharmacology and Toxicology, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA. Electronic address: pli@vcu.edu.AbstractInflammasome, an intracellular inflammatory machinery, has been reported to be involved in a variety of chronic degenerative diseases such as atherosclerosis, autoinflammatory diseases and Alzheimer's disease. The present study hypothesized that the formation and activation of inflammasomes associated with apoptosis associated speck-like protein (ASC) are an important initiating mechanism resulting in obesity-associated podocyte injury and consequent glomerular sclerosis. To test this hypothesis, Asc gene knockout (Asc(-/-)), wild type (Asc(+/+)) and intrarenal Asc shRNA-transfected wild type (Asc shRNA) mice were fed a high fat diet (HFD) or normal diet (ND) for 12weeks to produce obesity and associated glomerular injury. Western blot and RT-PCR analyses demonstrated that renal tissue Asc expression was lacking in Asc(-/-) mice or substantially reduced in Asc shRNA transfected mice compared to Asc(+/+) mice. Confocal microscopic and co-immunoprecipitation analysis showed that the HFD enhanced the formation of inflammasome associated with Asc in podocytes as shown by colocalization of Asc with Nod-like receptor protein 3 (Nalp3). This inflammasome complex aggregation was not observed in Asc(-/-) and local Asc shRNA-transfected mice. The caspase-1 activity, IL-1β production and glomerular damage index (GDI) were also significantly attenuated in Asc(-/-) and Asc shRNA-transfected mice fed the HFD. This decreased GDI in Asc(-/-) and Asc shRNA transfected mice on the HFD was accompanied by attenuated proteinuria, albuminuria, foot process effacement of podocytes and loss of podocyte slit diaphragm molecules. In conclusion, activation and formation of inflammasomes in podocytes are importantly implicated in the development of obesity-associated glomerular injury.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 May;1843(5):836-45. doi: 10.1016/j.bbamcr.2014.01.033. Epub 2014 Feb 5.
Inflammasome, an intracellular inflammatory machinery, has been reported to be involved in a variety of chronic degenerative diseases such as atherosclerosis, autoinflammatory diseases and Alzheimer's disease. The present study hypothesized that the formation and activation of inflammasomes associat
PMID 24508291

Tumor suppressor RecQL5 controls recombination induced by DNA crosslinking agents.

Hosono Y1, Abe T2, Ishiai M3, Islam MN4, Arakawa H2, Wang W5, Takeda S6, Ishii Y7, Takata M3, Seki M8, Enomoto T9.Author information 1Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan.2IFOM, the FIRC Institute for Molecular Oncology Foundation, IFOM-IEO Campus, Via Adamello 16, 20139 Milan, Italy.3Laboratory of DNA Damage Signaling, Department of Late Effect Studies, Radiation Biology Center, Kyoto University, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.4Laboratory of Genetics, NIA, National Institutes of Health, NIH Biomedical Research Center, Baltimore, MD 21224, USA; Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA.5Laboratory of Genetics, NIA, National Institutes of Health, NIH Biomedical Research Center, Baltimore, MD 21224, USA.6Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.7Shujitsu University, School of Pharmacy, Nishigawara, Naka-ku, Okayama 703-8516, Japan.8Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan; Department of Biochemistry, Tohoku Pharmaceutical University, 4-1, Komatsushima 4-chome, Aoba-ku, Sendai, Miyagi 981-8558, Japan. Electronic address: t_eno@musashino-u.ac.jp.9Molecular Cell Biology Laboratory, Research Institute of Pharmaceutical Sciences, Faculty of Pharmacy, Musashino University, 1-1-20 Shinmachi, Nishitokyo-shi, Tokyo 202-8585, Japan. Electronic address: t_eno@musashino-u.ac.jp.AbstractRecQ family DNA helicases function in the maintenance of genome stability. Mice deficient in RecQL5, one of five RecQ helicases, show a cancer predisposition phenotype, suggesting that RecQL5 plays a tumor suppressor role. RecQL5 interacts with Rad51, a key factor in homologous recombination (HR), and displaces Rad51 from Rad51-single stranded DNA (ssDNA) filaments in vitro. However, the precise roles of RecQL5 in the cell remain elusive. Here, we present evidence suggesting that RecQL5 is involved in DNA interstrand crosslink (ICL) repair. Chicken DT40 RECQL5 gene knockout (KO) cells showed sensitivity to ICL-inducing agents such as cisplatin (CDDP) and mitomycin C (MMC) and a higher number of chromosome aberrations in the presence of MMC than wild-type cells. The phenotypes of RECQL5 KO cells resembled those of Fanconi anemia gene KO cells. Genetic analysis using corresponding gene knockout cells showed that RecQL5 is involved in the FANCD1 (BRCA2)-dependent ICL repair pathway in which Rad51-ssDNA filament formation is promoted by BRCA2. The disappearance but not appearance of Rad51-foci was delayed in RECQL5 KO cells after MMC treatment. Deletion of Rad54, which processes the Rad51-ssDNA filament in HR, in RECQL5 KO cells increased sensitivity to CDDP and further delayed the disappearance of Rad51-foci, suggesting that RecQL5 and Rad54 have different effects on the Rad51-ssDNA filament. Furthermore, the frequency and variation of CDDP-induced gene conversion at the immunoglobulin locus were increased in RECQL5 KO cells. These results suggest that RecQL5 plays a role in regulating the incidence and quality of ICL-induced recombination.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 May;1843(5):1002-12. doi: 10.1016/j.bbamcr.2014.01.005. Epub 2014 Jan 10.
RecQ family DNA helicases function in the maintenance of genome stability. Mice deficient in RecQL5, one of five RecQ helicases, show a cancer predisposition phenotype, suggesting that RecQL5 plays a tumor suppressor role. RecQL5 interacts with Rad51, a key factor in homologous recombination (HR), a
PMID 24418621

Japanese Journal

Database for exchangeable gene trap clones : Pathway and gene ontology analysis of exchangeable gene trap clone mouse lines

Araki Masatake,Nakahara Mai,Muta Mayumi [他]
Development, growth & differentiation 56(2), 161-174, 2014-02
NAID 40019987325

Generation and Characterization of Ins1-cre-driver C57BL/6N for Exclusive Pancreatic Beta Cell-specific Cre-loxP Recombination

Hasegawa Yoshikazu,Daitoku Yoko,Mizuno Seiya,Tanimoto Yoko,Mizuno-Iijima Saori,Matsuo Miki,Kajiwara Noriko,Ema Masatsugu,Oishi Hisashi,Miwa Yoshihiro,Mekada Kazuyuki,Yoshiki Atsushi,Takahashi Satoru,Sugiyama Fumihiro,Yagami Ken-ichi
Experimental Animals 63(2), 183-191, 2014
… Cre/loxP system-mediated site-specific recombination is utilized to study gene function in vivo. … Successful conditional knockout of genes of interest is dependent on the availability of Cre-driver mice. … We produced and characterized pancreatic β cell-specific Cre-driver mice for use in diabetes mellitus research. …
NAID 130003391621

Generation and Analysis of Serine Protease Inhibitor Kazal Type 3-Cre Driver Mice

Sakata Kazuya,Ohmuraya Masaki,Araki Kimi,Suzuki Chigure,Ida Satoshi,Hashimoto Daisuke,Wang Jung,Uchiyama Yasuo,Baba Hideo,Yamamura Ken-ichi
Experimental Animals 63(1), 45-53, 2014
… However, previous studies have suggested that SPINK1/Spink3 is expressed in a wide range of normal tissues and tumors, although precise characterization of its gene expression has not been described in adulthood. … In Spink3lacZ mice, β-galactosidase activity was found in acinar cells of the pancreas and kidney, as well as epithelial cells of the bronchus in the lung, but not in the gastrointestinal tract or liver. …
NAID 130003391605