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Expression data of growth plate chondrocytes isolated from control or conditional Lkb1 mutant mice at postnatal day 30

ABSTRACT: We have shown that removal of Lkb1 in chondorcytes results in enchondroma-like structure in postnatal mouse long bones. To furhter understand the role of Lkb1 in this process, we performed microarrrays to compare the transcriptional profile between control and conditional Lkb1 mutant (Col2a1-Cre; Lkb1c/c) chondrocytes. Postnatal day 30 mouse growth plate chondorcytes from control and mutant mouse femurs and tibiae were isolated for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Lick Pui Lai

PROVIDER: E-GEOD-41898 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data of growth plate chondrocytes isolated from control or conditional Lkb1 mutant mice at postnatal day 30

Project description:We have shown that removal of Lkb1 in chondorcytes results in enchondroma-like structure in postnatal mouse long bones. To furhter understand the role of Lkb1 in this process, we performed microarrrays to compare the transcriptional profile between control and conditional Lkb1 mutant (Col2a1-Cre; Lkb1c/c) chondrocytes.

2013-11-14 | GSE41898 | GEO

Transcription profiling of Mus musculus gastric Lkb1 polyps vs unaffected gastric Lkb1 mucosa

Project description:Gene expression in wildtype mouse stomach wall (n=6), Lkb1+/- mouse stomach wall (n=6) and Lkb1+/- mouse gastric polyps

2010-10-06 | E-MEXP-2444 | biostudies-arrayexpress

Indian Hedgehog Signaling in the Postnatal Growth Plate

Project description:In order to characterize mRNA expression in the growth plate, we microdissected postnatal rat growth plates into their constituent zones and used microarray analysis to assess the abundences of individual transcripts. Expression patterns of PTHrP and Ihh-related genes were confirmed using real-time PCR. Using a gli1-lacZ mouse, Gli1 expression, presumably representing Ihh signaling, was visualized during pre- and postnatal development. Microdissection was used to collect individual growth plate zones from proximal tibiae of 1-wk rats and gene expression was analyzed using microarray.

2010-12-01 | E-GEOD-23432 | biostudies-arrayexpress

RNA-seq profiling of WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts

Project description:Investigating transcriptional profile of WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts untreated or stimulated with IL-1β

2023-05-11 | GSE214823 | GEO

LKB1 modulates lung cancer differentiation and metastasis

Project description:Inherited mutation in LKB1 results in the Peutz-Jeghers syndrome (PJS), characterized by intestinal hamartomas and a modestly increased frequency of gastrointestinal and breast cancer1. Somatic inactivation of LKB1 occurs in human lung adenocarcinoma2-4, but its tumor suppressor role in this tissue is unknown. Here we show that somatic Lkb1 deficiency strongly cooperates with somatic K-rasG12D activating mutation to accelerate the development of mouse lung tumorigenesis. Lkb1 deficiency in the setting of K-rasG12D mutation (K-ras Lkb1L/L) was associated with decreased tumor latency and increased tumor aggressiveness including metastasis. Furthermore, tumors from K-ras Lkb1L/L mice demonstrated histologies--squamous, adenosquamous and large cell--not seen with K-rasG12D mutation, Ink4a/Arf inactivation, or p53 inactivation alone or in combination. Experiments in vitro suggest that LKB1 suppresses lung tumorigenesis and progression through both p16INK4a-ARF-p53 dependent and independent mechanisms. These data indicate that LKB1 regulates lung tumor progression and differentiation. Keywords: cancer research To analyze the role of LKB1 in lung cancer progression and differentiation, we have dissected the lung tumors from mice with/without lkb1 loss and performed the microarray analyses to compare their gene expression pattern. In addition, we have also performed microarray analysis in both A549 and H2126 cell lines after reconsistitution of either wt-lkb1 or the kinase dead form of lkb1 (lkb1-KD) to confirm what we observed from in vivo studies.

2007-08-28 | E-GEOD-6135 | biostudies-arrayexpress

Role of growth plate Nox2 in alcoholic osteopenia

Project description:To study the role of Nox2 in ethanol toxicity on the bone growth plate chondrocytes, we generated Nox2 conditional knockout mice (CKO), in which the catalytic subunit of Nox2, Cybb, is deleted in chondrocytes using a Cre-lox system, where Cre is expressed from the Col2a1 promoter. CKO mice and floxed control mice were fed an ethanol-containing Lieber De-Carli-based diet or pair-fed a control diet for 8 weeks starting at 5-6 weeks of age. As both the Nox2 genotype and ethanol diminished the number of chondrocytes in the growth plates, we conducted an RNA-Seq analysis of the growth-plate containing regions of the femurs.

2024-05-24 | GSE234176 | GEO

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJÎº. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJÎº floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative). 6 samples for the liver-specific deletion of LKB1 corresponding to 3 KO LKB1 (Cre positive) and 3 normal liver (Cre negative). 6 samples for the liver-specific inactivation of the Notch pathway corresponding to 3 KO RbpJk (Cre positive) and 3 normal liver (Cre negative).

2015-12-08 | E-GEOD-75564 | biostudies-arrayexpress

Genome wide screen of H3K27ac enrichment in WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts

Project description:H3K27ac ChIP-seq analysis in WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts untreated or stimulated with IL-1β

2023-05-11 | GSE214822 | GEO

WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts

Project description:WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts

| PRJNA887178 | ENA

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJκ. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJκ floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative).

2015-12-08 | GSE75564 | GEO

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