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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse conditional knock out of beta-catenin by K19-CRE at E7.5

ABSTRACT: expression profile of conditional knock out of beta-catenin by K19-CRE at E7.5. Tested a wild type with two alleles of beta-catenin, a heterzyote with one deleted allele and the conditional null in the domain on cytokeratin 19 driven CRE expression

ORGANISM(S): Mus musculus

SUBMITTER: Brian Cox

PROVIDER: E-GEOD-2519 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dissecting Wnt/beta-catenin signaling during gastrulation using RNA interference in mouse embryos.

Lickert Heiko H Cox Brian B Wehrle Christian C Taketo Makoto M MM Kemler Rolf R Rossant Janet J

Development (Cambridge, England) 20050427 11

Differential gene regulation integrated in time and space drives developmental programs during embryogenesis. To understand how the program of gastrulation is regulated by Wnt/beta-catenin signaling, we have used genome-wide expression profiling of conditional beta-catenin mutant embryos. Known Wnt/beta-catenin target genes, known components of other signaling pathways, as well as a number of uncharacterized genes were downregulated in these mutants. To further narrow down the set of differentia ...[more]

PMID: 15857914

Similar Datasets

Expression profile of conditional knock out of beta-catenin by K19-CRE at E7.5

Project description:expression profile of conditional knock out of beta-catenin by K19-CRE at E7.5. Tested a wild type with two alleles of beta-catenin, a heterzyote with one deleted allele and the conditional null in the domain on cytokeratin 19 driven CRE expression Keywords: other

2005-04-13 | GSE2519 | GEO

Expression following beta-catenin stabilization in synovial sarcomagenesis

Project description:Synovial sarcoma is a deadly soft-tissue malignancy with a predilection for adolescents and young adults. Mice recapitulate synovial sarcomagenesis from expression of SS18-SSX2 in certain cells. Concomitant expression of a stabilized form of beta-catenin enhances synovial sarcomagenesis and expands the potential cells of origin. Mice bearing conditional expression of SS18-SSX2 from the Rosa26 locus and conditional excision of the 3rd exon of beta-catenin, each activated in the leg by Cre-recombinase expressed from an adeno-associated viral vector, formed large tumors at brief latency.

2015-11-04 | E-GEOD-47388 | biostudies-arrayexpress

Proteome and phosphoproteome analysis of autophagy deficient ATG5flox:CamKII-Cre and ATG5flox:VGAT-Cre conditional knockout mice

Project description:The experiment was performed to find selective targets of autophagy in different subtypes of neurons. Therefore, brain tissue of conditional knockout mice lacking autophagy protein ATG5 in inhibitory or excitatory neurons was used. Cortices (ATG5flox:CamKII-Cre) / striata (ATG5flox:VGAT-Cre) of mice were mixed with lys6 labeled brain lysates as internal controls between the samples. Samples were measured by LC-MS/MS and resulting H/L ratios were used to quantify proteomic and phosphoproteomic changes.

2022-11-15 | PXD029435 | Pride

Mus musculus

Project description:Expression profile of conditional knock out of beta-catenin by K19-CRE at E7.5

| PRJNA92057 | ENA

Gene expression in mouse whole proliferative phase wounds in response to alterations in β-Catenin levels [induced post-injury].

Project description:β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels (stabilization and downregulation) in cutaneous mouse wounds, post injury, during the proliferative phase of repair, was investigated. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction (stabilization) versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) mice were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, three days following injury, and wounds were harvested eight days post injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days, beginning at the third day after injury. Wounds were harvested eight days after wounding. This provides insight into the identities of genes modulated in response to changes in β-Catenin levels during the proliferative stage of cutaneous wound repair.

2018-12-31 | GSE50153 | GEO

Gene expression in mouse proliferative phase wounds in response to alterations in β-Catenin levels [initiated prior to injury].

Project description:β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels initiated prior to injury was investigated during the proliferative phase of repair. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction ('stabilization') versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized mice (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, four days prior to injury, and wounds were harvested eight days following injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days prior to injury. Wounds were harvested eight days after wounding. This provides insight into gene expression changes that occur during the proliferative stage of cutaneous wound repair in response to changes in β-Catenin levels initiated before/at the time of injury.

2018-12-31 | GSE50152 | GEO

Mammary tumors from K14-cre; ApcCKO/+ mice vs control mammary glands

Project description:Many components of Wnt/β-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of β-catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of β-catenin signaling optimal for mammary tumor development.

2009-02-10 | GSE14753 | GEO

Transcription profiling of mouse liver in conditional knockouts of the tumor suppressor gene Apc identifies Wnt/bet-catenin signaling activation in hepatocytes

Project description:A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). Conditional Knockout mouse model for the tumor suppressor gene Ap, Apc 2lox. The disruption of the Apc gene is realized by injection of an adenovirus encoding the Cre recombinase (AdCre). Homozygous animals injected with a high dose of AdCre showed an activation of the Wnt/beta-catenin signaling in most of the hepatocytes and develop an hepatomegaly and die soon after. Analysis of gene up- and down regulation for liver-indicible APC disruption.

2006-03-13 | E-TABM-81 | biostudies-arrayexpress

Investigate the role of Wnt/beta-catenin signaling in development of the exocrine pancreas

Project description:beta-catenin is an essential mediator of canonical Wnt signaling and a central component of the cadherin-catenin epithelial adhesion complex. Dysregulation of beta-catenin expression has been described in pancreatic neoplasia. Newly published studies have suggested that beta-catenin is critical for normal pancreatic development although these reports reached somewhat different conclusions. In addition, the molecular mechanisms by which loss of beta-catenin affects pancreas development are not well understood. The goals of this study then were; 1] to further investigate the role of beta-catenin in pancreatic development using a conditional knockout approach and 2] to identify possible mechanisms by which loss of beta-catenin disrupts pancreatic development. A Pdx1-cre mouse line was used to delete a floxed beta-catenin allele specifically in the developing pancreas, and embryonic pancreata were studied by immunohistochemistry and microarray analysis. Keywords: Time course

2007-04-04 | GSE7430 | GEO

Transcription profiling of mouse pancreas at embryonic days 14.5 and 16.5 from animals lacking beta-catenin, a mediator of Wnt signaling and a component of the cadherin-catenin epithelial adhesion complex

Project description:Beta-catenin is an essential mediator of canonical Wnt signaling and a central component of the cadherin-catenin epithelial adhesion complex. Dysregulation of beta-catenin expression has been described in pancreatic neoplasia. Newly published studies have suggested that beta-catenin is critical for normal pancreatic development although these reports reached somewhat different conclusions. In addition, the molecular mechanisms by which loss of beta-catenin affects pancreas development are not well understood. The goals of this study then were; 1] to further investigate the role of beta-catenin in pancreatic development using a conditional knockout approach and 2] to identify possible mechanisms by which loss of beta-catenin disrupts pancreatic development. A Pdx1-cre mouse line was used to delete a floxed beta-catenin allele specifically in the developing pancreas, and embryonic pancreata were studied by immunohistochemistry and microarray analysis. Experiment Overall Design: Parameter: embryonic pancreas from wild type and Pdx1Cre/+; beta-cateninflox/flox Experiment Overall Design: Sample type: RNA Experiment Overall Design: Source name: Embryonic day 14.6 and 16.5 pancreas Experiment Overall Design: Organism: Mus Musculus Experiment Overall Design: Strain: Derived from an intercross of Pdx1Cre/+ ; beta-cateninflox/+ mice. Experiment Overall Design: Extracted molecule:Total RNA Experiment Overall Design: In the study, we hybridized RNA from Embryonic day 14.6 and 16.5 pancreas of wild type (WT) control and Pdx1Cre/+; beta-cateninflox/floxÂ beta-catenin null in the pancreas) embryonic pancreas to Affymetrix MOE430 2.0 GeneChip® arrays containing 45,101 well characterized mouse genes/ESTs.

2007-12-13 | E-GEOD-7430 | biostudies-arrayexpress

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