scholarly journals Generation and Characterization of dickkopf3 Mutant Mice

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.

2003 ◽  
Vol 23 (22) ◽  
pp. 8216-8225 ◽  
Author(s):  
Mélanie Lebel ◽  
Pooja Agarwal ◽  
Chi Wa Cheng ◽  
M. Golam Kabir ◽  
Toby Y. Chan ◽  
...  

ABSTRACT The Iroquois homeobox (Irx) genes have been implicated in the specification and patterning of several organs in Drosophila and several vertebrate species. Misexpression studies of chick, Xenopus, and zebra fish embryos have demonstrated that Irx genes are involved in the specification of the midbrain-hindbrain boundary. All six murine Irx genes are expressed in the developing heart, suggesting that they might possess distinct functions during heart development, and a role for Irx4 in normal heart development has been recently demonstrated by gene-targeting experiments. Here we describe the generation and phenotypic analysis of an Irx2-deficient mouse strain. By targeted insertion of a lacZ reporter gene into the Irx2 locus, we show that lacZ expression reproduces most of the endogenous Irx2 expression pattern. Despite the dynamic expression of Irx2 in the developing heart, nervous system, and other organs, Irx2-deficient mice are viable, are fertile, and appear to be normal. Although chick Irx2 has been implicated in the development of the midbrain-hindbrain region, we show that Irx2-deficient mice develop a normal midbrain-hindbrain boundary. Furthermore, Irx2-deficient mice have normal cardiac morphology and function. Functional compensation by other Irx genes might account for the absence of a phenotype in Irx2-deficient mice. Further studies of mutant mice of other Irx genes as well as compound mutant mice will be necessary to uncover the functional roles of these evolutionarily conserved transcriptional regulators in development and disease.


2001 ◽  
Vol 265 (3) ◽  
pp. 944-949 ◽  
Author(s):  
Kiyoshi Yamauchi ◽  
Jun-ichiro Nakajima ◽  
Hiroaki Hayashi ◽  
Akihiko Hara ◽  
Kohei Yamauchi

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

Tick-borne encephalitis virus (TBEV) was isolated for the first time in Sweden in 1958 (from ticks and from 1 tick-borne encephalitis [TBE] patient).1 In 2003, Haglund and colleagues reported the isolation and antigenic and genetic characterization of 14 TBEV strains from Swedish patients (samples collected 1991–1994).2 The first serum sample, from which TBEV was isolated, was obtained 2–10 days after onset of disease and found to be negative for anti-TBEV immunoglobulin M (IgM) by enzyme-linked immunosorbent assay (ELISA), whereas TBEV-specific IgM (and TBEV-specific immunoglobulin G/cerebrospinal fluid [IgG/CSF] activity) was demonstrated in later serum samples taken during the second phase of the disease.


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