Differences in saccharin preference and genetic alterations of the Tas1r3 gene among senescence-accelerated mouse strains and their parental AKR/J strain

2014 ◽  
Vol 130 ◽  
pp. 108-112
Author(s):  
Kimie Niimi ◽  
Eiki Takahashi
Keyword(s):  
Genetic Alterations ◽  
Mouse Strains ◽  
Saccharin Preference ◽  
Senescence Accelerated Mouse

Susceptibility Alleles for Aberrant B-1 Cell Proliferation Involved in Spontaneously Occurring B-Cell Chronic Lymphocytic Leukemia in a Model of New Zealand White Mice

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3772-3779
Author(s):  
Yoshitomo Hamano ◽  
Sachiko Hirose ◽  
Akinori Ida ◽  
Masaaki Abe ◽  
Danqing Zhang ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Autoimmune Disease ◽  
B Cell ◽  
Genetic Alterations ◽  
Lymphocytic Leukemia ◽  
Chromosome 17 ◽  
Mouse Strains ◽  
Autoantibody Production ◽  
Age Related ◽  
Cell Chronic Lymphocytic Leukemia

B-cell chronic lymphocytic leukemia (B-CLL) and autoimmune disease are a related event, and genetic factors are linked to both diseases. As B-CLL is mainly of B-1 cell type that participates in autoantibody production, genetically-determined regulatory abnormalities in proliferation and/or differentiation of B-1 cells may determine their fate. We earlier found that, in H-2–congenic (NZB × NZW) F1 mice, while H-2d/z heterozygosity predisposes to autoimmune disease, H-2z/z homozygosity predisposes to B-CLL. Studies also suggested the involvement of non–H-2-linked NZW allele(s) in leukemogenesis. Using H-2–congenic NZW and B10 mouse strains, their F1 and backcross progeny, we have now identified three major NZW susceptibility loci for abnormal proliferation of B-1 cells, which form the basis of leukemogenesis; one H-2–linked locus on chromosome 17 and the other two non–H-2-linked loci, each on chromosome 13 and chromosome 17. Each susceptibility allele functioned independently, in an incomplete dominant fashion, the sum of effects determining the extent of aberrant B-1 cell frequencies. The development of leukemia was associated with age-related increase in B-1 cell frequencies in the blood. Thus, these alleles probably predispose B-1 cells to accumulate genetic alterations, giving rise to B-CLL. Potentially important candidate genes and correlation of the findings with autoimmune disease are discussed.

Susceptibility Alleles for Aberrant B-1 Cell Proliferation Involved in Spontaneously Occurring B-Cell Chronic Lymphocytic Leukemia in a Model of New Zealand White Mice

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3772-3779 ◽  
Author(s):  
Yoshitomo Hamano ◽  
Sachiko Hirose ◽  
Akinori Ida ◽  
Masaaki Abe ◽  
Danqing Zhang ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Autoimmune Disease ◽  
B Cell ◽  
Genetic Alterations ◽  
Lymphocytic Leukemia ◽  
Chromosome 17 ◽  
Mouse Strains ◽  
Autoantibody Production ◽  
Age Related ◽  
Cell Chronic Lymphocytic Leukemia

Abstract B-cell chronic lymphocytic leukemia (B-CLL) and autoimmune disease are a related event, and genetic factors are linked to both diseases. As B-CLL is mainly of B-1 cell type that participates in autoantibody production, genetically-determined regulatory abnormalities in proliferation and/or differentiation of B-1 cells may determine their fate. We earlier found that, in H-2–congenic (NZB × NZW) F1 mice, while H-2d/z heterozygosity predisposes to autoimmune disease, H-2z/z homozygosity predisposes to B-CLL. Studies also suggested the involvement of non–H-2-linked NZW allele(s) in leukemogenesis. Using H-2–congenic NZW and B10 mouse strains, their F1 and backcross progeny, we have now identified three major NZW susceptibility loci for abnormal proliferation of B-1 cells, which form the basis of leukemogenesis; one H-2–linked locus on chromosome 17 and the other two non–H-2-linked loci, each on chromosome 13 and chromosome 17. Each susceptibility allele functioned independently, in an incomplete dominant fashion, the sum of effects determining the extent of aberrant B-1 cell frequencies. The development of leukemia was associated with age-related increase in B-1 cell frequencies in the blood. Thus, these alleles probably predispose B-1 cells to accumulate genetic alterations, giving rise to B-CLL. Potentially important candidate genes and correlation of the findings with autoimmune disease are discussed.

Evaluation of the Tg.AC Transgenic Mouse Assay for Testing the Human Carcinogenic Potential of Pharmaceuticals—Practical Pointers, Mechanistic Clues, and New Questions

2002 ◽  
Vol 21 (1) ◽  
pp. 65-79 ◽  
Author(s):  
Frank D. Sistare ◽  
Karol L. Thompson ◽  
Ronald Honchel ◽  
Joseph DeGeorge
Keyword(s):  
Transgenic Mouse ◽  
Genetic Alterations ◽  
Protocol Design ◽  
Mouse Strains ◽  
Impact Study ◽  
Multistage Process ◽  
Short Term ◽  
Tumor Induction ◽  
Carcinogenic Potential ◽  
Testing Protocols

Transgenic mouse strains with genetic alterations known to play a role in the multistage process of carcinogenesis are being used increasingly as models for evaluating the human carcinogenic potential of chemicals and Pharmaceuticals. The Tg.AC transgenic mouse is one of the strains currently being used in such alternative short-term carcinogenicity testing protocols. This review is focused on recent data from studies designed to evaluate this model's ability to discriminate carcinogens from noncarcinogens. Details relating to protocol design that can significantly impact study outcome are described. Data relating to mechanisms of chemical tumor induction in the Tg.AC model are reviewed, and questions have been formulated to encourage research to further guide appropriate future applications of this model.

scholarly journals Genetic variation responsible for mouse strain differences in integrin α2 expression is associated with altered platelet responses to collagen

Blood ◽  
2004 ◽  
Vol 103 (9) ◽  
pp. 3396-3402 ◽  
Author(s):  
Tong-Tong Li ◽  
Susana Larrucea ◽  
Shiloe Souza ◽  
Suzanne M. Leal ◽  
José A. López ◽  
...  
Keyword(s):  
Human Platelet ◽  
Strain Differences ◽  
Genetic Alterations ◽  
Mouse Strains ◽  
Lag Phase ◽  
Lod Score ◽  
Log Odds ◽  
Integrin Α2 ◽  
Mouse System ◽  
Mouse Strain Differences

Abstract As mouse models have become commonplace for studying hemostasis and thrombosis, we considered whether the mouse system had utility for assessing genetic alterations in platelet receptors. Platelets from 5 mouse strains (C57BL/6 [C57], FVB/N [FVB], BALB/c, C3H/He, and 129Sv) showed only minor differences in the expression of integrin αIIb, integrin β3, glycoprotein (GP) Ibα, or GPVI across strains. However, FVB platelets expressed approximately 50% the level of integrin α2 as platelets from other strains (P < .0001). We bred FVB mice with C57 and assessed α2 expression in FVB/C57xFVB/C57 (F2) offspring. Linkage analysis demonstrated the gene responsible for α2 levels is tightly linked to the D13mit260 marker (log odds [lod] score 6.7) near the α2 gene. FVB platelets showed reduced aggregation and a longer lag phase to collagen. FVB and C57 platelets aggregated similarly to collagen-related peptide, but FVB platelets showed a reduction in rhodocytin-induced Syk and PLCγ2 tyrosine phosphorylation. Thus, FVB platelets express half the level of α2 as other mouse strains, a trait linked to the α2 gene and seemingly responsible for reduced platelet aggregation to collagen. These strain differences serve as a useful model for the 2-fold difference in human platelet α2β1 expression and demonstrate that α2β1 participates in signaling during platelet activation. (Blood. 2004;103:3396-3402)

scholarly journals Meis1, a PBX1-related homeobox gene involved in myeloid leukemia in BXH-2 mice.

1995 ◽  
Vol 15 (10) ◽  
pp. 5434-5443 ◽  
Author(s):  
J J Moskow ◽  
F Bullrich ◽  
K Huebner ◽  
I O Daar ◽  
A M Buchberg
Keyword(s):  
Myeloid Leukemia ◽  
Leukemia Virus ◽  
Inbred Mouse ◽  
Homeobox Gene ◽  
Genetic Alterations ◽  
Tumor Formation ◽  
Mouse Strains ◽  
Control Mechanisms ◽  
Chromosome 11 ◽  
Altered Expression

Leukemia results from the accumulation of multiple genetic alterations that disrupt the control mechanisms of normal growth and differentiation. The use of inbred mouse strains that develop leukemia has greatly facilitated the identification of genes that contribute to the neoplastic transformation of hematopoietic cells. BXH-2 mice develop myeloid leukemia as a result of the expression of an ecotropic murine leukemia virus that acts as an insertional mutagen to alter the expression of cellular proto-oncogenes. We report the isolation of a new locus, Meis1, that serves as a site of viral integration in 15% of the tumors arising in BXH-2 mice. Meis1 was mapped to a distinct location on proximal mouse chromosome 11, suggesting that it represents a novel locus. Analysis of somatic cell hybrids segregating human chromosomes allowed localization of MEIS1 to human chromosome 2p23-p12, in a region known to contain translocations found in human leukemias. Northern (RNA) blot analysis demonstrated that a Meis1 probe detected a 3.8-kb mRNA present in all BXH-2 tumors, whereas tumors containing integrations at the Meis1 locus expressed an additional truncated transcript. A Meis1 cDNA clone that encoded a novel member of the homeobox gene family was identified. The homeodomain of Meis1 is most closely related to those of the PBX/exd family of homeobox protein-encoding genes, suggesting that Meis1 functions in a similar fashion by cooperative binding to a distinct subset of HOX proteins. Collectively, these results indicate that altered expression of the homeobox gene Meis1 may be one of the events that lead to tumor formation in BXH-2 mice.

Alterations in the number of motoneurons containing immunoreactive calcitonin gene-related peptide(CGRP)& choline acetyltransferase(ChAT) in the cervical spinal cord of the wobbler mouse during the development of the motoneuron disease

1995 ◽  
Vol 53 ◽  
pp. 970-971
Author(s):  
L. Vacca-Galloway ◽  
Y.Q. Zhang ◽  
P. Bose ◽  
S.H. Zhang
Keyword(s):  
Spinal Cord ◽  
Early Stage ◽  
Cervical Spinal Cord ◽  
Wild Type Mouse ◽  
Reflex Response ◽  
Mouse Strains ◽  
Behavioral Tests ◽  
Wobbler Mouse ◽  
Stage 4 ◽  
Stage 1

The Wobbler mouse (wr) has been studied as a model for inherited human motoneuron diseases (MNDs). Using behavioral tests for forelimb power, walking, climbing, and the “clasp-like reflex” response, the progress of the MND can be categorized into early (Stage 1, age 21 days) and late (Stage 4, age 3 months) stages. Age-and sex-matched normal phenotype littermates (NFR/wr) were used as controls (Stage 0), as well as mice from two related wild-type mouse strains: NFR/N and a C57BI/6N. Using behavioral tests, we also detected pre-symptomatic Wobblers at postnatal ages 7 and 14 days. The mice were anesthetized and perfusion-fixed for immunocytochemical (ICC) of CGRP and ChAT in the spinal cord (C3 to C5).Using computerized morphomety (Vidas, Zeiss), the numbers of IR-CGRP labelled motoneurons were significantly lower in 14 day old Wobbler specimens compared with the controls (Fig. 1). The same trend was observed at 21 days (Stage 1) and 3 months (Stage 4). The IR-CGRP-containing motoneurons in the Wobbler specimens declined progressively with age.

High performance Nanogold™-in situ hybridzation and its use in the detection of hybridized and PCR-amplified microscopical preparations

1996 ◽  
Vol 54 ◽  
pp. 896-897
Author(s):  
G. W. Hacker ◽  
I. Zehbe ◽  
J. Hainfeld ◽  
A.-H. Graf ◽  
C. Hauser-Kronberger ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Messenger Rna ◽  
High Performance ◽  
Detection System ◽  
Direct Methods ◽  
Genetic Alterations ◽  
Chain Reaction ◽  
Protein Encoding ◽  
Polymerase Chain

In situ hybridization (ISH) with biotin-labeled probes is increasingly used in histology, histopathology and molecular biology, to detect genetic nucleic acid sequences of interest, such as viruses, genetic alterations and peptide-/protein-encoding messenger RNA (mRNA). In situ polymerase chain reaction (PCR) (PCR in situ hybridization = PISH) and the new in situ self-sustained sequence replication-based amplification (3SR) method even allow the detection of single copies of DNA or RNA in cytological and histological material. However, there is a number of considerable problems with the in situ PCR methods available today: False positives due to mis-priming of DNA breakdown products contained in several types of cells causing non-specific incorporation of label in direct methods, and re-diffusion artefacts of amplicons into previously negative cells have been observed. To avoid these problems, super-sensitive ISH procedures can be used, and it is well known that the sensitivity and outcome of these methods partially depend on the detection system used.

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