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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.

ORGANISM(S): Mus musculus

PROVIDER: GSE41898 | GEO | 2013/11/14

SECONDARY ACCESSION(S): PRJNA178418

REPOSITORIES: GEO

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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. 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.

2013-11-14 | E-GEOD-41898 | biostudies-arrayexpress

Gene expression profiles of Lkb1 WT and KO hematopoietic stem cells (HSCs)

Project description:LKB1 encodes a Ser/Thr kinase and acts as an evolutionarily conserved sensor of cellular energy status in eukaryotic cells. LKB1 functions as the major upstream kinase to phosphorylate AMPK and 12 other AMPK-related kinases, which is required for their activation in many cellular contexts. Once activated, AMPK and AMPK-related kinases phosphorylate a diverse array of downstream effectors to switch on ATP-generating catabolic processes and switch off ATP-consuming anabolic processes, thus restoring energy balance during periods of energetic stress. To study the role and mechanisms of Lkb1 in the regulation of hematopoietic stem cell (HSC) biology, we performed transcriptome analysis of sorted LSK (Lin-, Sca-1+, c-Kit+) cells from Lkb1 WT and KO bone marrows at 1 day post-completing tamoxifen injection (DPI). To identify more proximal molecular effects, we chose 1 DPI due to the modest phenotypes in Lkb1 KO mice, yet documentation of efficient Lkb1 deletion in LSK cells at this very early time point. We treated Lkb1 L/L rosa26CreERT2 and Lkb1 L/L mice (C57BL/Ka-CD45.2:Thy-1.1 background) with Tamoxifen for 5 days to somatically delete Lkb1 in adult mice, and generated Lkb1 WT and KO mice. At 1 DPI, we prepared single-cell suspensions from bone marrow (from femoral and tibial bones), and stained and sorted LSK populations using FACSAria (Becton Dickinson, Mountain View, CA). The RNA was extracted from sorted LSK cells, amplified and subjected to gene profiling. The samples include 3 Lkb1 WT (Lkb1 WT 5-7) and 4 Lkb1 KO (Lkb1 KO 4-7) replicates.

2010-12-01 | E-GEOD-24765 | biostudies-arrayexpress

Col2a1-Cre Idh1LSL/+ embryonic growth plate chondrocytes

Project description:Col2a1-Cre Idh1LSL/+ embryonic growth plate chondrocytes

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Single cell RNAseq analysis of Col2a1+ growth plate chondrocytes

Project description:Single cell RNAseq analysis of Col2a1+ growth plate chondrocytes

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WT versus Girk3-/- Chondrocytes

Project description:Long bones are formed and repaired through the process of endochondral ossification. Activation of G protein coupled receptor (GPCR) signaling regulates skeletal development and long bone growth. G protein-coupled Inward-Rectifying potassium (K+) channel (GIRK) genes are key functional components of the GPCR in excitable tissues (e.g., neurons and cardiomyocytes) but their roles in the non-excitable cells that directly contribute to endochondral bone formation have not been studied. In this study we analyzed skeletal phenotypes of Girk2-/-, Girk3-/- and Girk2/3-/- mice. Bones from 12-week-old Girk2-/- mice were normal in length, but femurs and tibiae from Girk3-/- and Girk2/3-/- mice were longer. Epiphyseal chondrocytes from five-day-old Girk3-/- mice expressed higher levels of genes involved in collagen chain trimerization and collagen fibril assembly and lower levels of VEGF receptors and produced larger micromasses than wildtype chondrocytes in vitro. Girk3-/- chondrocytes were also more responsive to the GPCR ligand, dynorphin, as evidenced by greater cAMP and pCREB expression, greater GAG production, and upregulation of Col2a1 and Sox9 transcripts. Imaging studies showed that Kdr (Vegfr2) and endomucin expression was dramatically reduced in bones from young Girk3-/- mice, supporting a role for delayed vasculogenesis during postnatal growth. Together these data identify Girk3 as a GPCR effector that controls bone lengthening.

2022-03-31 | GSE192933 | 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

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

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

Expression data from wt, Lkb1 conditional knock out and LPS treated DC

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2018-10-29 | GSE117286 | GEO

LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

Project description:LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

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