scholarly journals Enhanced half-life of genetically engineered human IgG1 antibodies in a humanized FcRn mouse model: potential application in humorally mediated autoimmune disease

2006 ◽  
Vol 18 (12) ◽  
pp. 1759-1769 ◽  
Author(s):  
S. B. Petkova ◽  
S. Akilesh ◽  
T. J. Sproule ◽  
G. J. Christianson ◽  
H. Al Khabbaz ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Mouse Model ◽  
Half Life ◽  
Potential Application ◽  
Model Potential ◽  
Genetically Engineered ◽  
Human Igg1

VEGF165b mutant with a prolonged half-life and enhanced anti-tumor potency in a mouse model

2018 ◽  
Vol 284 ◽  
pp. 84-90 ◽  
Author(s):  
Huiyong Zhang ◽  
Enchao Jia ◽  
Wenjiao Xia ◽  
Chengui Lu ◽  
Wuling Zhu
Keyword(s):  
Mouse Model ◽  
Half Life

scholarly journals Wild-Type Hras Suppresses the Earliest Stages of Tumorigenesis in a Genetically Engineered Mouse Model of Pancreatic Cancer

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0140253 ◽  
Author(s):  
Jamie D. Weyandt ◽  
Benjamin L. Lampson ◽  
Sherry Tang ◽  
Matthew Mastrodomenico ◽  
Diana M. Cardona ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Mouse Model ◽  
Genetically Engineered ◽  
Wild Type ◽  
Genetically Engineered Mouse Model

P2-066 A genetically engineered mouse model with an enhanced beta-secretase substrate exhibits increased amyloid generation

2004 ◽  
Vol 25 ◽  
pp. S242 ◽  
Author(s):  
Adam J. Simon ◽  
Lin Chen ◽  
Eric A. Price ◽  
Min Xu ◽  
Adam Lucka ◽  
...  
Keyword(s):  
Mouse Model ◽  
Genetically Engineered ◽  
Beta Secretase ◽  
Genetically Engineered Mouse Model

scholarly journals DIPG-68. ALPHA-THALASSEMIA X-LINKED MENTAL RETARDATION PROTEIN (ATRX) LOSS-OF-FUNCTION IN A MOUSE MODEL OF DIFFUSE INTRINSIC PONTINE GLIOMA

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii300-iii300
Author(s):  
Chen Shen ◽  
David Picketts ◽  
Oren Becher
Keyword(s):  
Mouse Model ◽  
Pediatric Brain Tumor ◽  
High Grade Glioma ◽  
Genetic Alterations ◽  
Genetically Engineered ◽  
Tumor Incidence ◽  
Loss Of Function ◽  
Nestin Expression ◽  
Genetically Engineered Mouse Model ◽  
Clinical Cases

Abstract Diffuse Intrinsic Potine Glioma (DIPG) is a rare pediatric brain tumor for which no cure or efficacious therapies exist. Previous discoveries have revealed that, DIPG harbors distinct genetic alterations, when compared with adult high-grade glioma (HGG) or even with non-DIPG pediatric HGGs. ATRX alteration is found in 9% of clinical cases of DIPG, and significantly overlaps with H3.3K27M mutation and p53 loss, the two most common genetic changes in DIPG, found in 80% and 77% clinical cases, respectively. Here we developed genetically engineered mouse model of brainstem glioma using the RCAS-Tv-a system by targeting PDGF-B overexpression, p53 loss, H3.3K27M mutation and ATRX loss-of function to Nestin-expression brainstem progenitor cells of the neonatal mouse. Specifically, we used Nestin-Tv-a; p53 floxed; ATRX heterozygous female and Nestin-Tv-a; p53 floxed; ATRX floxed male breeders, generated offsprings with ATRX loss of function (n=18), ATRX heterozygous females (n=6), and ATRX WT (n=10). Median survial of the three groups are 65 days, 88 days and 51 days, respectively. Also, ATRX null mice is lower in tumor incidence (44.4%), compared with ATRX WT (80%). We evaluated the pathological features of DIPG with or without ATRX alteration, RNA-seq is performed to identify differentially expressed genes between ATRX WT and loss-of-function. In conclution, this study generated the first genetically modified mouse model studying ATRX loss-of-function in DIPG, and suggested that ATRX loss-of-function in DIPG may slow down tumorigenesis and decrease tumor incidence.

Abstract 215: The Role of Titin in Cardiac Function: Studies in Two Genetically Engineered Mouse Models With Disparate Titin’s Size

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Mei Methawasin ◽  
Kirk R Hutchinson ◽  
John E Smith ◽  
Henk L Granzier
Keyword(s):  
Mouse Model ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Exercise Capacity ◽  
Mouse Models ◽  
Wheel Running ◽  
Left Ventricular ◽  
Genetically Engineered ◽  
Passive Stiffness ◽  
Genetically Engineered Mouse Models

Titin, a myofilament that acts as a molecular spring in the sarcomere, is considered the main contributor to passive stiffness of cardiomyocytes and is responsible for cardiac diastolic function. Increased titin stiffness is related to diastolic dysfunction and HFpEF (Heart Failure with preserved Ejection Fraction). Alteration in size of titin’s spring region leads to changes in cardiomyocyte and left ventricular (LV) chamber stiffness. We tested the effect of alteration in titin’s size in two genetically engineered mouse models. We investigated the effect of shortening titin’s spring region in a mouse model in which I-band/A-band region of titin’s spring has been deleted (TtnΔIAjxn ), in comparison to the effect of lengthening titin’s spring region in a mouse model deficient in titin splicing factor (Rbm20ΔRRM). Integrative approaches were used from single cardiomyocyte mechanics to pressure-volume analysis and exercise study. Study of skinned LV cardiomyocytes revealed that cellular passive stiffness was inversely related to the size of titin. Cellular passive stiffness was increased in TtnΔIAjxn homozygous (-/-) (~ 110 % higher than wildtype (WT)) and was reduced in a graded manner in Rbm20ΔRRM heterozygous (+/-) and -/- cardiomyocytes (~61% and ~87% less than WT). This effect was carried through at the LV chamber level which could be demonstrated in pressure volume (PV) analysis as an increased end-diastolic pressure-volume relationship (EDPVR) in TtnΔIAjxn -/- (~110% higher than WT’s hearts) and reduced EDPVR in Rbm20ΔRRM +/- and -/- (~57% and ~48% less than WT’s hearts). Free-wheel running studies revealed a running deficiency in TtnΔIAjxn -/- mice but an increase in exercise capacity in Rbm20ΔRRM +/– mice. Conclusions: Functional studies from the cellular to in-vivo LV chamber levels showed that mice with shortening of titin’s spring region had increased LV stiffness, diastolic dysfunction and reduced exercise capacity, while mice with lengthening titin’s spring region had compliant LV and increased exercise capacity. Thus, our work supports titin’s important roles in LV diastolic function and suggests that modification of the size of titin’s spring region could be a potential therapeutic strategy for HFpEF.

240 - Genetically Engineered E. Coli Nissle Attenuates Hyperammonemia in a Mouse Model of Hepatic Encephalopathy by Metabolizing Gut Ammonia and Increasing Urea Production

2018 ◽  
Vol 154 (6) ◽  
pp. S-1078 ◽  
Author(s):  
Yossi Dagon ◽  
Yves Millet ◽  
Lauren Renaud ◽  
Binh Ha ◽  
Denise Wong ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Mouse Model ◽  
Genetically Engineered ◽  
E Coli ◽  
Urea Production

scholarly journals Electron exchange model potential: Application to positronium-helium scattering

1999 ◽  
Vol 59 (1) ◽  
pp. 363-370 ◽  
Author(s):  
P. K. Biswas ◽  
Sadhan K. Adhikari
Keyword(s):  
Potential Application ◽  
Model Potential ◽  
Exchange Model ◽  
Electron Exchange ◽  
Helium Scattering
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