Generation and Characterization of Apolipoprotein Cl-Deficient Mice

1995 ◽  
pp. 317-322
Author(s):  
Marten H. Hofker ◽  
Janine H. Ree ◽  
Walther J. A. A. Broeck ◽  
Jan M. A. Deursen ◽  
Hans Boom ◽  
...  
Keyword(s):  
2001 ◽  
Vol 120 (5) ◽  
pp. A523-A523
Author(s):  
A BURICH ◽  
R HERSHBERG ◽  
K WAGGIE ◽  
W ZENG ◽  
J VINEY ◽  
...  

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
K Hochrath ◽  
S Hillebrandt ◽  
F Lammert ◽  
B Rathkolb ◽  
H Fuchs ◽  
...  

2009 ◽  
Vol 36 (S 02) ◽  
Author(s):  
C Ganos ◽  
U Schumacher ◽  
U Borgmeyer ◽  
I Hermans-Borgmeyer ◽  
D Lorke

2006 ◽  
Vol 26 (6) ◽  
pp. 2317-2326 ◽  
Author(s):  
Ivan del Barco Barrantes ◽  
Ana Montero-Pedrazuela ◽  
Ana Guadaño-Ferraz ◽  
Maria-Jesus Obregon ◽  
Raquel Martinez de Mena ◽  
...  

ABSTRACT dickkopf (dkk) genes encode a small family of secreted Wnt antagonists, except for dkk3, which is divergent and whose function is poorly understood. Here, we describe the generation and characterization of dkk3 mutant mice. dkk3-deficient mice are viable and fertile. Phenotypic analysis shows no major alterations in organ morphology, physiology, and most clinical chemistry parameters. Since Dkk3 was proposed to function as thyroid hormone binding protein, we have analyzed deiodinase activities, as well as thyroid hormone levels. Mutant mice are euthyroid, and the data do not support a relationship of dkk3 with thyroid hormone metabolism. Altered phenotypes in dkk3 mutant mice were observed in the frequency of NK cells, immunoglobulin M, hemoglobin, and hematocrit levels, as well as lung ventilation. Furthermore, dkk3-deficient mice display hyperactivity.


2002 ◽  
Vol 22 (10) ◽  
pp. 3509-3517 ◽  
Author(s):  
Hitoshi Okada ◽  
Woong-Kyung Suh ◽  
Jianping Jin ◽  
Minna Woo ◽  
Chunying Du ◽  
...  

ABSTRACT The mitochondrial proapoptotic protein Smac/DIABLO has recently been shown to potentiate apoptosis by counteracting the antiapoptotic function of the inhibitor of apoptosis proteins (IAPs). In response to apoptotic stimuli, Smac is released into the cytosol and promotes caspase activation by binding to IAPs, thereby blocking their function. These observations have suggested that Smac is a new regulator of apoptosis. To better understand the physiological function of Smac in normal cells, we generated Smac-deficient (Smac−/− ) mice by using homologous recombination in embryonic stem (ES) cells. Smac−/− mice were viable, grew, and matured normally and did not show any histological abnormalities. Although the cleavage in vitro of procaspase-3 was inhibited in lysates of Smac−/− cells, all types of cultured Smac−/− cells tested responded normally to all apoptotic stimuli applied. There were also no detectable differences in Fas-mediated apoptosis in the liver in vivo. Our data strongly suggest the existence of a redundant molecule or molecules capable of compensating for a loss of Smac function.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shih-Ching Lo ◽  
Kimberly Scearce-Levie ◽  
Morgan Sheng

Author(s):  
Yoshi-nobu Harada ◽  
Naoko Shiomi ◽  
Masahito Ikawa ◽  
Masaru Okabe ◽  
Sciichi Hirota ◽  
...  
Keyword(s):  

Author(s):  
Lia Kwee ◽  
Daniel K. Burns ◽  
John M. Rumberger ◽  
Chris Norton ◽  
Barry Wolitzky ◽  
...  
Keyword(s):  

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