scholarly journals Toward pharmacogenetic SLCO1B1‐guided dosing of methotrexate in arthritis using a murine Slco1b2 knockout model

2021 ◽  
Author(s):  
Zachary L. Taylor ◽  
Lauren E. Thompson ◽  
Heather Bear ◽  
Tomoyuki Mizuno ◽  
Alexander A. Vinks ◽  
...  
Keyword(s):  
Knockout Model

scholarly journals AAV Gene Therapy Prevents and Reverses Heart Failure in a Murine Knockout Model of Barth Syndrome

2020 ◽  
Vol 126 (8) ◽  
pp. 1024-1039 ◽  
Author(s):  
Suya Wang ◽  
Yifei Li ◽  
Yang Xu ◽  
Qing Ma ◽  
Zhiqiang Lin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Gene Therapy ◽  
Barth Syndrome ◽  
Knockout Model

Test of the Cluster Knockout Model Using the ReactionLi6(p,pα)d.

1969 ◽  
Vol 22 (9) ◽  
pp. 442-442
Author(s):  
P. G. Roos ◽  
Hogil Him ◽  
Mahavir Jain ◽  
H. D. Holmgren
Keyword(s):  
Knockout Model

scholarly journals Susceptibility to diet induced obesity at thermoneutral conditions is independent of UCP1

2021 ◽  
Author(s):  
Sebastian Dieckmann ◽  
Akim Strohmeyer ◽  
Monja Willershaeuser ◽  
Stefanie Maurer ◽  
Wolfgang Wurst ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Knockout Mice ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
Exon 2 ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Knockout Model

Objective Activation of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) upon cold stimulation leads to substantial increase in energy expenditure to defend body temperature. Increases in energy expenditure after a high caloric food intake, termed diet-induced thermogenesis, are also attributed to BAT. These properties render BAT a potential target to combat diet-induced obesity. However, studies investigating the role of UCP1 to protect against diet-induced obesity are controversial and rely on the phenotyping of a single constitutive UCP1-knockout model. To address this issue, we generated a novel UCP1-knockout model by Cre-mediated deletion of Exon 2 in the UCP1 gene. We studied the effect of constitutive UCP1 knockout on metabolism and the development of diet-induced obesity. Methods UCP1 knockout and wildtype mice were housed at 30°C and fed a control diet for 4-weeks followed by 8-weeks of high-fat diet. Body weight and food intake were monitored continuously over the course of the study and indirect calorimetry was used to determine energy expenditure during both feeding periods. Results Based on Western blot analysis, thermal imaging and noradrenaline test, we confirmed the lack of functional UCP1 in knockout mice. However, body weight gain, food intake and energy expenditure were not affected by deletion of UCP1 gene function during both feeding periods. Conclusion Conclusively, we show that UCP1 does not protect against diet-induced obesity at thermoneutrality. Further we introduce a novel UCP1-KO mouse enabling the generation of conditional UCP1-knockout mice to scrutinize the contribution of UCP1 to energy metabolism in different cell types or life stages.

scholarly journals Nanoparticle‐mediated rhodopsin cDNA but not intron‐containing DNA delivery causes transgene silencing in a rhodopsin knockout model

2015 ◽  
Vol 30 (3) ◽  
pp. 1076-1086 ◽  
Author(s):  
Min Zheng ◽  
Rajendra N. Mitra ◽  
Nazar A. Filonov ◽  
Zongchao Han
Keyword(s):  
Dna Delivery ◽  
Transgene Silencing ◽  
Knockout Model

scholarly journals In vivo roles of factor XII

Blood ◽  
2012 ◽  
Vol 120 (22) ◽  
pp. 4296-4303 ◽  
Author(s):  
Thomas Renné ◽  
Alvin H. Schmaier ◽  
Katrin F. Nickel ◽  
Margareta Blombäck ◽  
Coen Maas
Keyword(s):  
Thrombus Formation ◽  
Coagulation Factor ◽  
Special Focus ◽  
Factor Xii ◽  
Excessive Bleeding ◽  
Charged Surfaces ◽  
Factor Xiia ◽  
Knockout Model

Abstract Coagulation factor XII (FXII, Hageman factor, EC = 3.4.21.38) is the zymogen of the serine protease, factor XIIa (FXIIa). FXII is converted to FXIIa through autoactivation induced by “contact” to charged surfaces. FXIIa is of crucial importance for fibrin formation in vitro, but deficiency in the protease is not associated with excessive bleeding. For decades, FXII was considered to have no function for coagulation in vivo. Our laboratory developed the first murine knockout model of FXII. Consistent with their human counterparts, FXII−/− mice have a normal hemostatic capacity. However, thrombus formation in FXII−/− mice is largely defective, and the animals are protected from experimental cerebral ischemia and pulmonary embolism. This murine model has created new interest in FXII because it raises the possibility for safe anticoagulation, which targets thrombosis without influence on hemostasis. We recently have identified platelet polyphosphate (an inorganic polymer) and mast cell heparin as in vivo FXII activators with implications on the initiation of thrombosis and edema during hypersensitivity reactions. Independent of its protease activity, FXII exerts mitogenic activity with implications for angiogenesis. The goal of this review is to summarize the in vivo functions of FXII, with special focus to its functions in thrombosis and vascular biology.

A mouse gene knockout model for juvenile ceroid-lipofuscinosis (batten disease)

1999 ◽  
Vol 57 (4) ◽  
pp. 551-556 ◽  
Author(s):  
Martin L. Katz ◽  
Hisashi Shibuya ◽  
Po-Ching Liu ◽  
Satbir Kaur ◽  
Chun-Lan Gao ◽  
...  
Keyword(s):  
Gene Knockout ◽  
Batten Disease ◽  
Mouse Gene ◽  
Ceroid Lipofuscinosis ◽  
Knockout Model

scholarly journals Evaluation of the role of IKAChin atrial fibrillation using a mouse knockout model

2001 ◽  
Vol 37 (8) ◽  
pp. 2136-2143 ◽  
Author(s):  
Pramesh Kovoor ◽  
Kevin Wickman ◽  
Colin T Maguire ◽  
William Pu ◽  
Josef Gehrmann ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Mouse Knockout ◽  
Knockout Model
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