From ea46f42ee640928b92947bfb204c41a482d80937 Mon Sep 17 00:00:00 2001 From: root Date: Tue, 8 May 2012 18:39:56 -0500 Subject: Add all the source codes into the github. --- web/dbdoc/SUH_Liv_RMA_0611.html | 362 ++++++++++++++++++++++++++++++++++++++++ 1 file changed, 362 insertions(+) create mode 100755 web/dbdoc/SUH_Liv_RMA_0611.html (limited to 'web/dbdoc/SUH_Liv_RMA_0611.html') diff --git a/web/dbdoc/SUH_Liv_RMA_0611.html b/web/dbdoc/SUH_Liv_RMA_0611.html new file mode 100755 index 00000000..151ea4ce --- /dev/null +++ b/web/dbdoc/SUH_Liv_RMA_0611.html @@ -0,0 +1,362 @@ + + + +SUH BXD Liver Affy Mouse Gene 1.0 ST (Jun11) RMA ** + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + +
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SUH BXD Liver Affy Mouse Gene 1.0 ST (Jun11) RMA **modify this page

+ +Accession number: GN325

+ + +

Saarland University Homburg (SUH) Carbon Tetrachloride-Treated BXD Mouse Affymetrix Mouse Gene 1.0 ST Array data set + +

This experimental liver gene expression data set (~100 Affymetrix exon-type arrays), was generated by Frank Lammert, Sonja Hillebrandt, Rabea Hall, and colleagues at the Saarland University Medical Center in Homburg, Germany. This work is part of the German Network for Systems Genetics (GeNeSys). + +

Expression data after carbon tetrachloride treatment (CCl4, also known as Halon, Freon, carbon tet, or tetrachloromethane) were generated using RNA sample from 30 BXD strains, both parental strains (C57BL/6J, DBA/2J), and B6D2 F1 hybrids. The great majority of cases were females and were treated with carbon tetrachloride injections over a six week period. Three arrays were run for each strain using independent liver samples. + +

PURPOSE: The overall goal of the project is to understand the etiology of liver fibrogenesis using carbon tetracholoride as a toxin and inducer of liver disease. Liver fibrogenesis, or scarring of the liver, is the common end-stage of chronic liver diseases, in particular after chronic viral infections. In Germany along complications associated with liver fibrosis cause approximately 10,000 deaths per year. In the past decade key molecular pathomechanisms of hepatic fibrogenesis due to chronic viral infections have been identified. Activated hepatic stellate cells (HSCs) drive the process of de novo deposition of abnormal extracellular matrix, which is modulated by complex interactions between cytokines, receptors, and matrix components. + +

Several studies have demonstrated that the course and progression of the fibrogenic response to chronic liver injury is highly variability among individuals. This marked variabilityhas been attributed to etiology, age, gender, and environmental factors. In humans these genetic disease fibrosis predisposition factors have not yet to be studied systematically. + +

Our group recently identified a gene variant that contributes to liver fibrogenesis by using QTL mapping in an experimental crosses between fibrosis-susceptible and resistant strains of mice (Hillebrandt et al., 2005). We demonstrated that sequence differences in the HC gene that encodes complement factor C5 (also known as hemolytic complement), are responsible for this strain difference. Common haplotype-tagging polymorphisms of the human HC gene were shown to be associated with advanced fibrosis in chronic hepatitis C virus infection. Thus, the mouse analysis led to the identification of an unknown gene underlying human susceptibility to liver fibrosis, supporting the idea that HC has a causal role in chronic inflammatory disorders and organ fibrogenesis across species. + +

As part of the GeNeSys program we have studied liver fibrogenesis in the BXD family of strains as a model for chronic liver injury. This expression data set is used to map complex genetic traits that modulate gene expression and determine gene networks during liver fibrogenesis in GRPs. + +

The following assays are complete or are in progress: + +

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  1. Liver fibrosis studies: Phenotyping protocols include standard histology, morphometry, biochemical quantification of hepatic collagen contents, serum surrogate markers of fibrosis, immunohistochemistry, and expression profiling of proinflammatory and profibrogenic genes by qRT-PCR and Affymetrix microarrays (this data set). + + +
  2. Characterization of liver cells: Liver immune cell fractions will be isolated and sorted according to SOPs developed in the Lammert laboratory. In addition, in cooperation with the technology platforms of the HepatoSys Network of Excellence, we will characterize primary HSCs that play critical roles in liver fibrogenesis with respect to proinflammatory responses during chronic liver inflammation. + +
+ + +

PROTOCOL for carbon tetrachloride (CCl4) treatment (parental strains, F1, and BXD lines). Animals were injected with CCl4 (12 x 0.7 mg/kg ip) over a 6-week period on days 1 and 4 of each week. Intraperitoneal injections were begun between the ages of 6-8 weeks. Animals were sacrificed after 6 weeks of treatment at 12 to 14 weeks of age. Untreated control mice from only the two parental strains were also sacrificed at 12-14 weeks of age + +

+Tissue: Livers were snap frozen in liquid nitrogen immediately after harvesting. RNA was extracted and submitted to the UTHSC Molecular Resource Core for expression profiling. Expression data were generated by Lorne Rose, William Taylor and colleagues. Data were entered into GeneNetwork by Arthur Centeno, June 17, 2011. Data were quality controlled by R. W. Williams.

+ +

QC Results: This data set consists of expression data for 33 strains. A total of 166 probe sets are associated with LOD scores above 10 and the highest linkage score of 22 for Rpl3 (probe set 10430669). Strain distribution patterns of eQTLs with a Mendelian expression pattern match those of their closest markers perfectly, verifying that there are no errors of strain assignment in this data set. + +

Analysis of XIST probe set 1060617 confirms that most strains are purely female. However, only males were available for BXD1 and BXD6. BXD28 and BXD33 data are based on the average of two female samples and one male sample. All other strains are purely female. + +

Data were analyzed by Rabea Hall and Dr. Frank Lammert at the Universitätsklinikum des Saarlandes in Homburg, Germany. + +

Contacts: rabea.hall at uks.eu, Rabea.Hall at uniklinikum-saarland.de, and frank.lammert at uks.eu + + + + +

Table updated 7-19-2011

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IndexSample IDStrain IDTreatment
1504B6D2F1 CCl4
2506B6D2F1CCl4
3508B6D2F1CCl4
4414C57BL/6JCCl4
5488C57BL/6JCCl4
6489C57BL/6JCCl4
7B6J1 C57BL/6Juntreated control
8B6J2 C57BL/6Juntreated control
9B6J3 C57BL/6Juntreated control
10449DBA/2JCCl4
11450DBA/2JCCl4
12451DBA/2JCCl4
13219.1DBA/2Juntreated control
14219.2DBA/2Juntreated control
15219.3DBA/2Juntreated control
16276BXD1CCl4
17278BXD1CCl4
18279BXD1CCl4
19353BXD2CCl4
20357BXD2CCl4
21358BXD2CCl4
22272BXD6CCl4
23273BXD6CCl4
24274BXD6CCl4
25405BXD11CCl4
26406BXD11CCl4
27408BXD11CCl4
28239BXD12CCl4
29240BXD12CCl4
30241BXD12CCl4
31553BXD13CCl4
32554BXD13CCl4
33555BXD13CCl4
34249BXD14CCl4
35250BXD14CCl4
36288BXD14CCl4
37191BXD19CCl4
38644BXD19CCl4
39645BXD19CCl4
40442BXD24aCCl4
41443BXD24aCCl4
42444BXD24aCCl4
43216BXD27CCl4
44218BXD27CCl4
45290BXD27CCl4
4628BXD28CCl4
4771BXD28CCl4
48129BXD28CCl4
49219BXD31CCl4
50220BXD31CCl4
51231BXD31CCl4
52549BXD32CCl4
53550BXD32CCl4
54551BXD32CCl4
55139BXD33CCl4
56140BXD33CCl4
57559BXD33CCl4
58132BXD34CCl4
59146BXD34CCl4
60147BXD34CCl4
61293BXD39CCl4
62597BXD39CCl4
63599BXD39CCl4
64154BXD40CCl4
65570BXD40CCl4
66572BXD40CCl4
67361BXD42CCl4
68362BXD42CCl4
69373BXD42CCl4
70428BXD43CCl4
71429BXD43CCl4
72556BXD43CCl4
73472BXD51CCl4
74473BXD51CCl4
75474BXD51CCl4
76533BXD55CCl4
77534BXD55CCl4
78535BXD55CCl4
79519BXD62CCl4
80520BXD62CCl4
81521BXD62CCl4
82463BXD65CCl4
83464BXD65CCl4
84465BXD65CCl4
85327BXD69CCl4
86346BXD69CCl4
87347BXD69CCl4
88614BXD73CCl4
89616BXD73CCl4
90619BXD73CCl4
91395BXD75CCl4
92482BXD75CCl4
93483BXD75CCl4
94317BXD87CCl4
95319BXD87CCl4
96322BXD87CCl4
97374BXD90CCl4
98388BXD90CCl4
99389BXD90CCl4
100402BXD96CCl4
101403BXD96CCl4
102404BXD96CCl4
103584BXD98CCl4
104585BXD98CCl4
105607BXD98CCl4
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+ + CITG + + Service initiated June 15, 2001. Site by + Xiaodong Zhou, + Lei Yan, + Ning Liu, + Zachary Sloan, + Rudi Alberts, + Arthur Centeno, Jintao Wang, Lu Lu, Kenneth Manly, Robert W. Williams, and colleagues. + + + Python Powered + + + Registered with Nif +
+ + GeneNetwork support from: + +
+      +
+
+ + + + + + + + + + -- cgit v1.2.3