Close Encounters: RIDGEs, Hyperacetylated Chromatin, Radiation Breakpoints and Genes Differentially Expressed in Tumors Cluster at Specific Human Chromosome Regions

2010 ◽  
Vol 128 (1-3) ◽  
pp. 17-27 ◽  
Author(s):  
G.A. Folle ◽  
P. Liddle ◽  
L. Lafon-Hughes ◽  
M.V. Di Tomaso
Keyword(s):  
Human Chromosome ◽  
Differentially Expressed ◽  
Close Encounters ◽  
Chromosome Regions

scholarly journals The Use of Mouse Models for Understanding the Biology of Down Syndrome and Aging

2012 ◽  
Vol 2012 ◽  
pp. 1-20 ◽  
Author(s):  
Guido N. Vacano ◽  
Nathan Duval ◽  
David Patterson
Keyword(s):  
Down Syndrome ◽  
Human Chromosome ◽  
Mouse Models ◽  
Targeted Mutagenesis ◽  
Chromosome 21 ◽  
Practical Reasons ◽  
Future Directions ◽  
Human Chromosome 21 ◽  
Biology Of Aging ◽  
Chromosome Regions

Down syndrome is a complex condition caused by trisomy of human chromosome 21. The biology of aging may be different in individuals with Down syndrome; this is not well understood in any organism. Because of its complexity, many aspects of Down syndrome must be studied either in humans or in animal models. Studies in humans are essential but are limited for ethical and practical reasons. Fortunately, genetically altered mice can serve as extremely useful models of Down syndrome, and progress in their production and analysis has been remarkable. Here, we describe various mouse models that have been used to study Down syndrome. We focus on segmental trisomies of mouse chromosome regions syntenic to human chromosome 21, mice in which individual genes have been introduced, or mice in which genes have been silenced by targeted mutagenesis. We selected a limited number of genes for which considerable evidence links them to aspects of Down syndrome, and about which much is known regarding their function. We focused on genes important for brain and cognitive function, and for the altered cancer spectrum seen in individuals with Down syndrome. We conclude with observations on the usefulness of mouse models and speculation on future directions.

Identification of a gene on human chromosome 8q11 that is differentially expressed during prostate-cancer progression

1999 ◽  
Vol 83 (4) ◽  
pp. 506-511 ◽  
Author(s):  
Glenn T.G. Chang ◽  
Nita Tapsi ◽  
Martine Steenbeek ◽  
Leen J. Blok ◽  
Wytske M. van Weerden ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Human Chromosome ◽  
Cancer Progression ◽  
Differentially Expressed ◽  
Prostate Cancer Progression

Identification of human chromosome regions by aid of computerized pattern analysis

1972 ◽  
Vol 70 (2) ◽  
pp. 475-478 ◽  
Author(s):  
A. Møller ◽  
H. Nilsson ◽  
T. Caspersson ◽  
G. Lomakka
Keyword(s):  
Human Chromosome ◽  
Pattern Analysis ◽  
Chromosome Regions

Strain-specific modifier genes of Cecr2-associated exencephaly in mice: genetic analysis and identification of differentially expressed candidate genes

2012 ◽  
Vol 44 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Megan K. Kooistra ◽  
Renee Y. M. Leduc ◽  
Christine E. Dawe ◽  
Nicholas A. Fairbridge ◽  
Jay Rasmussen ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Human Chromosome ◽  
Stop Codon ◽  
Modifier Gene ◽  
Modifier Genes ◽  
Differentially Expressed ◽  
Whole Genome ◽  
Chromosome 19 ◽  
Neural Tubes ◽  
Congenic Lines

Although neural tube defects (NTDs) are common in humans, little is known about their multifactorial genetic causes. While most mouse models involve NTDs caused by a single mutated gene, we have previously described a multigenic system involving susceptibility to NTDs. In mice with a mutation in Cecr2, the cranial NTD exencephaly shows strain-specific differences in penetrance, with 74% penetrance in BALB/cCrl and 0% penetrance in FVB/N. Whole genome linkage analysis showed that a region of chromosome 19 was partially responsible for this difference in penetrance. We now reveal by genetic analysis of three subinterval congenic lines that the chromosome 19 region contains more than one modifier gene. Analysis of embryos showed that although a Cecr2 mutation causes wider neural tubes in both strains, FVB/N embryos overcome this abnormality and close. A microarray analysis comparing neurulating female embryos from both strains identified differentially expressed genes within the chromosome 19 region, including Arhgap19, which is expressed at a lower level in BALB/cCrl due to a stop codon specific to that substrain. Modifier genes in this region are of particular interest because a large portion of this region is syntenic to human chromosome 10q25, the site of a human susceptibility locus.

Genetic linkage studies in familial frontal epilepsy: Exclusion of the human chromosome regions homologous to the El-1 mouse locus

1995 ◽  
Vol 22 (3) ◽  
pp. 227-233 ◽  
Author(s):  
I. Lopes-Cendes ◽  
H.A. Phillips ◽  
I.E. Scheffer ◽  
J.C. Mulley ◽  
R. Desbiens ◽  
...  
Keyword(s):  
Human Chromosome ◽  
Genetic Linkage ◽  
Linkage Studies ◽  
Frontal Epilepsy ◽  
Chromosome Regions

A cosmid library specific for human Chromosome regions 6p21.3 and 6q27

1993 ◽  
Vol 4 (9) ◽  
pp. 493-498 ◽  
Author(s):  
Vivienne P. Shortle ◽  
Patrizia Malaspina ◽  
Margaret Fox ◽  
James S. Dooley ◽  
Armin Volz ◽  
...  
Keyword(s):  
Human Chromosome ◽  
Cosmid Library ◽  
Chromosome Regions
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