Genomic instability in Gadd45a-deficient mice

10.1038/13802 ◽  
1999 ◽  
Vol 23 (2) ◽  
pp. 176-184 ◽  
Author(s):  
M. Christine Hollander ◽  
M. Saeed Sheikh ◽  
Dmitry V. Bulavin ◽  
Karen Lundgren ◽  
Laura Augeri-Henmueller ◽  
...  
Keyword(s):  
Genomic Instability ◽  
Deficient Mice

Abstract 15: Inhibition of IGF-1 suppress genomic instability and epithelial lineage aberrations in the mammary gland of BRCA1 deficient mice

2012 ◽  
Author(s):  
Ignacio Fernandez-Garcia ◽  
Pietro Ameri ◽  
Mary Helen Barcellos-Hoff ◽  
David L. Kleinberg
Keyword(s):  
Mammary Gland ◽  
Genomic Instability ◽  
Deficient Mice

Increased genomic instability is not a prerequisite for shortened lifespan in DNA repair deficient mice

2006 ◽  
Vol 596 (1-2) ◽  
pp. 22-35 ◽  
Author(s):  
Martijn E.T. Dollé ◽  
Rita A. Busuttil ◽  
Ana Maria Garcia ◽  
Susan Wijnhoven ◽  
Ellen van Drunen ◽  
...  
Keyword(s):  
Dna Repair ◽  
Genomic Instability ◽  
Deficient Mice

scholarly journals The RAG-1/2 endonuclease causes genomic instability and controls CNS complications of lymphoblastic leukemia in p53/Prkdc-deficient mice

Cancer Cell ◽  
2003 ◽  
Vol 3 (1) ◽  
pp. 37-50 ◽  
Author(s):  
Rebecca A. Gladdy ◽  
Michael D. Taylor ◽  
Christine J. Williams ◽  
Ildiko Grandal ◽  
Jana Karaskova ◽  
...  
Keyword(s):  
Genomic Instability ◽  
Lymphoblastic Leukemia ◽  
Rag 1 ◽  
Deficient Mice

scholarly journals Human FANCC is hypomorphic in murine Fancc-deficient cells

Blood ◽  
2010 ◽  
Vol 116 (12) ◽  
pp. 2057-2060 ◽  
Author(s):  
Laura E. Hays ◽  
Winifred W. Keeble ◽  
Jane E. Yates ◽  
R. K. Rathbun ◽  
Tara Koretsky ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Genomic Instability ◽  
Cross Linking ◽  
Hematopoietic Stem ◽  
Cytokine Responses ◽  
Growth Inhibitory ◽  
Cross Linker ◽  
Deficient Mice

AbstractFancc suppresses cross-linker–induced genotoxicity, modulates growth-inhibitory cytokine responses, and modulates endotoxin responses. Although loss of the latter function is known to account for endotoxin-induced marrow failure in murine Fancc (mFancc)–deficient mice, some argue that cytokine and endotoxin hypersensitivities devolve simply from genomic instability. Seeking to resolve this question, we planned to ectopically express instructive human FANCC (hFANCC) mutants in murine Fancc-deficient hematopoietic stem cells. To first assure that hFANCC cDNA was competent in murine cells, we compared hFANCC and mFancc in complementation assays for cross-linking agent hypersensitivity and endotoxin hypersensitivity. We found that mFancc complemented murine Fancc-deficient cells in both assays, but that hFANCC fully suppressed only endotoxin hypersensitivity, not cross-linking agent hypersensitivity. These results support the notions that Fancc is multifunctional and that structural prerequisites for its genoprotective functions differ from those required to constrain endotoxin responses known to lead to marrow failure in Fancc-deficient mice.

787 S-Adenosylmethionine Regulates Apurinic/Apyrimidinic Endonuclease 1 Expression and Contributes to Increased Genomic Instability in Livers of Methionine Adenosyltransferase 1A Deficient Mice

2008 ◽  
Vol 134 (4) ◽  
pp. A-770
Author(s):  
Maria Lauda Tomasi ◽  
Ainhoa Iglesias-Ara ◽  
Francesco Feo ◽  
Shelly C. Lu
Keyword(s):  
Genomic Instability ◽  
Methionine Adenosyltransferase ◽  
Deficient Mice

scholarly journals Genomic Instability and Enhanced Radiosensitivity in Hsp70.1- and Hsp70.3-Deficient Mice

2004 ◽  
Vol 24 (2) ◽  
pp. 899-911 ◽  
Author(s):  
Clayton R. Hunt ◽  
David J. Dix ◽  
Girdhar G. Sharma ◽  
Raj K. Pandita ◽  
Arun Gupta ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Genomic Instability ◽  
Cell Killing ◽  
Embryonic Fibroblasts ◽  
Shock Proteins ◽  
Hsp Genes ◽  
First Time ◽  
Deficient Mice

ABSTRACT Heat shock proteins (HSPs) are highly conserved among all organisms from prokaryotes to eukaryotes. In mice, the HSP genes Hsp70.1 and Hsp70.3 are induced by both endogenous and exogenous stressors, such as heat and toxicants. In order to determine whether such proteins specifically influence genomic instability, mice deficient for Hsp70.1 and Hsp70.3 (Hsp70.1/3−/− mice) were generated by gene targeting. Mouse embryonic fibroblasts (MEFs) prepared from Hsp70.1/3−/− mice did not synthesize Hsp70.1 or Hsp70.3 after heat-induced stress. While the Hsp70.1/3−/− mutant mice were fertile, their cells displayed genomic instability that was enhanced by heat treatment. Cells from Hsp70.1/3−/− mice also display a higher frequency of chromosome end-to-end associations than do control Hsp70.1/3+/+ cells. To determine whether observed genomic instability was related to defective chromosome repair, Hsp70.1/3−/− and Hsp70.1/3+/+ fibroblasts were treated with ionizing radiation (IR) alone or heat and IR. Exposure to IR led to more residual chromosome aberrations, radioresistant DNA synthesis (a hallmark of genomic instability), increased cell killing, and enhanced IR-induced oncogenic transformation in Hsp70.1/3−/− cells. Heat treatment prior to IR exposure enhanced cell killing, S-phase-specific chromosome damage, and the frequency of transformants in Hsp70.1/3−/− cells in comparison to Hsp70.1/3+/+ cells. Both in vivo and in vitro studies demonstrate for the first time that Hsp70.1 and Hsp70.3 have an essential role in maintaining genomic stability under stress conditions.

scholarly journals Loss of caspase-2 augments lymphomagenesis and enhances genomic instability in Atm-deficient mice

2013 ◽  
Vol 110 (49) ◽  
pp. 19920-19925 ◽  
Author(s):  
J. Puccini ◽  
S. Shalini ◽  
A. K. Voss ◽  
M. Gatei ◽  
C. H. Wilson ◽  
...  
Keyword(s):  
Genomic Instability ◽  
Caspase 2 ◽  
Deficient Mice

Comparison of localization of metallothionein in tissues of metallothionein-deficient mice

1995 ◽  
Vol 53 ◽  
pp. 1042-1043
Author(s):  
H. Nishimura ◽  
R Nishimura ◽  
D.L. Adelson ◽  
A.E. Michaelska ◽  
K.H.A. Choo ◽  
...  
Keyword(s):  
Metal Binding ◽  
Immunohistochemical Staining ◽  
Squamous Epithelium ◽  
Rabbit Antiserum ◽  
Slight Modification ◽  
Positive Control ◽  
Heavy Metal Binding ◽  
Critical Organ ◽  
Metal Binding Protein ◽  
Deficient Mice

Metallothionein (MT), a cysteine-rich heavy metal binding protein, has several isoforms designated from I to IV. Its major isoforms, I and II, can be induced by heavy metals like cadmium (Cd) and, are present in various organs of man and animals. Rodent testes are a critical organ to Cd and it is still a controversial matter whether MT exists in the testis although it is clear that MT is not induced by Cd in this tissue. MT-IV mRNA was found to localize within tongue squamous epithelium. Whether MT-III is present mainly glial cells or neurons has become a debatable topic. In the present study, we have utilized MT-I and II gene targeted mice and compared MT localization in various tissues from both MT-deficient mice and C57Black/6J mice (C57BL) which were used as an MT-positive control. For MT immunostaining, we have used rabbit antiserum against rat MT-I known to cross-react with mammalian MT-I and II and human MT-III. Immunohistochemical staining was conducted by the method described in the previous paper with a slight modification after the tissues were fixed in HistoChoice and embedded in paraffin.

Alterations during Positive Selection in the Thymus of nackt CD4-Deficient Mice

2000 ◽  
Vol 52 (6) ◽  
pp. 555-562 ◽  
Author(s):  
I. Nepomnaschy ◽  
G. Lombardi ◽  
P. Bekinschtein ◽  
P. Berguer ◽  
V. Francisco ◽  
...  
Keyword(s):  
Positive Selection ◽  
Deficient Mice
Sign in / Sign up

Export Citation Format

Share Document