Expression and Localization of Bestrophin during Normal Mouse Development

2003 ◽  
Vol 44 (8) ◽  
pp. 3622 ◽  
Author(s):  
Benjamin Bakall ◽  
Lihua Y. Marmorstein ◽  
George Hoppe ◽  
Neal S. Peachey ◽  
Claes Wadelius ◽  
...  
Keyword(s):  
Normal Mouse ◽  
Mouse Development

gli, a zinc finger transcription factor and oncogene, is expressed during normal mouse development

1993 ◽  
Vol 196 (2) ◽  
pp. 91-102 ◽  
Author(s):  
David Walterhouse ◽  
Maqbool Ahmed ◽  
Diane Slusarski ◽  
Julie Kalamaras ◽  
Diane Boucher ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Normal Mouse ◽  
Mouse Development ◽  
Zinc Finger Transcription Factor

scholarly journals Sumo-1 Function Is Dispensable in Normal Mouse Development

2008 ◽  
Vol 28 (17) ◽  
pp. 5381-5390 ◽  
Author(s):  
Fu-Ping Zhang ◽  
Laura Mikkonen ◽  
Jorma Toppari ◽  
Jorma J. Palvimo ◽  
Irma Thesleff ◽  
...  
Keyword(s):  
Normal Mouse ◽  
Wild Type Mouse ◽  
Wild Type ◽  
Mouse Development ◽  
Palate Development ◽  
Mouse Embryo Fibroblasts ◽  
Wild Type Mefs ◽  
And Function ◽  
Old Mice

ABSTRACT To elucidate SUMO-1 functions in vivo, we targeted by homologous recombination the last three exons of the murine Sumo-1 gene. Sumo-1 mRNA abundance was reduced to one-half in heterozygotes and was undetectable in Sumo-1 −/− mice, and SUMO-1-conjugated RanGAP1 was detectable in wild-type mouse embryo fibroblasts (MEFs) but not in Sumo-1 −/− MEFs, indicating that gene targeting yielded Sumo-1-null mice. Sumo-1 mRNA is expressed in all tissues of wild-type mice, and its abundance is highest in the testis, brain, lungs, and spleen. Sumo-2 and Sumo-3 mRNAs are also expressed in all tissues, but their abundance was not upregulated in Sumo-1-null mice. The development and function of testis are normal in the absence of Sumo-1, and Sumo-1 − / − mice of both sexes are viable and fertile. In contrast to a previous report (F. S. Alkuraya et al., Science 313:1751, 2006), we did not observe embryonic or early postnatal demise of Sumo-1-targeted mice; genotypes of embryos and 21-day-old mice were of predicted Mendelian ratios, and there was no defect in lip and palate development in Sumo-1 +/− or Sumo-1 −/− embryos. The ability of Sumo-1 −/− MEFs to differentiate into adipocyte was not different from that of wild-type MEFs. Collectively, our results support the notion that most, if not all, SUMO-1 functions are compensated for in vivo by SUMO-2 and SUMO-3.

c-Jun is essential for normal mouse development and hepatogenesis

Nature ◽  
1993 ◽  
Vol 365 (6442) ◽  
pp. 179-181 ◽  
Author(s):  
Frank Hilberg ◽  
Adriano Aguzzi ◽  
Norma Howells ◽  
Erwin F. Wagner
Keyword(s):  
Normal Mouse ◽  
Mouse Development

scholarly journals Erratum: c-Jun is essential for normal mouse development and hepatogenesis

Nature ◽  
1993 ◽  
Vol 366 (6453) ◽  
pp. 368-368 ◽  
Author(s):  
Frank Hilberg ◽  
Adriano Aguzzi ◽  
Norma Howells ◽  
Erwin F. Wagner
Keyword(s):  
Normal Mouse ◽  
Mouse Development

scholarly journals Goosecoid-like (GSCL), a candidate gene for velocardiofacial syndrome, is not essential for normal mouse development

1998 ◽  
Vol 7 (12) ◽  
pp. 1841-1849 ◽  
Author(s):  
B. Saint-Jore ◽  
A. Puech ◽  
J. Heyer ◽  
Q. Lin ◽  
C. Raine ◽  
...  
Keyword(s):  
Candidate Gene ◽  
Normal Mouse ◽  
Velocardiofacial Syndrome ◽  
Mouse Development

scholarly journals Gadd45γ Is Dispensable for Normal Mouse Development and T-Cell Proliferation

2001 ◽  
Vol 21 (9) ◽  
pp. 3137-3143 ◽  
Author(s):  
Angelika Hoffmeyer ◽  
Roland Piekorz ◽  
Richard Moriggl ◽  
James N. Ihle
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Normal Mouse ◽  
Interleukin 2 ◽  
Family Members ◽  
Growth Control ◽  
Physiological Role ◽  
T Cell Proliferation ◽  
Mouse Development ◽  
Peripheral T Cells

ABSTRACT Gadd45γ, a family member of the growth arrest and DNA damage-inducible gene family 45 (Gadd45), is strongly induced by interleukin-2 (IL-2) in peripheral T cells. While in most tissues all Gadd45 family members are expressed, Gadd45γ is the only member that is induced by IL-2. Here we show that the IL-2-induced expression of Gadd45γ is dependent on a signaling pathway mediated by the tyrosine kinase Jak3 and the transcription factors Stat5a and Stat5b (signal transducer and activator of transcription). Previous studies with ectopically overexpressed Gadd45γ in various cell lines implicated its function in negative growth control. To analyze the physiological role of Gadd45γ we used homologous recombination to generate mice lacking Gadd45γ. Gadd45γ-deficient mice develop normally, are indistinguishable from their littermates, and are fertile. Furthermore, hematopoiesis in mice lacking Gadd45γ is not impaired and Gadd45γ-deficient T lymphocytes show normal responses to IL-2. These data demonstrate that Gadd45γ is not essential for normal mouse development and hematopoiesis, possibly due to functional redundancy among the Gadd45 family members. Gadd45γ is also dispensable for IL-2-induced T-cell proliferation.

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