Metabolic reprogramming in livers from LKB1 KO mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE192404 | GEO | 2022/01/28
REPOSITORIES: GEO
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Project description:Investigating transcriptional profile of WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts untreated or stimulated with IL-1β
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Project description:H3K27ac ChIP-seq analysis in WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts untreated or stimulated with IL-1β
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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
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). 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
Project description:Metabolic reprogramming in livers from LKB1 KO mice
| PRJNA791350 | ENA
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.
2010-12-01 | GSE24765 | GEO
Project description:Alveolar macrophages (AMs) are pivotal for maintaining lung immune homeostasis. We demonstrated that deletion of liver kinase b1 (Lkb1) in CD11c+ cells led to the greatly changed AMs abundance in lung. Transcriptomic sequencing revealed that Lkb1 inhibited the pro-inflammatory pathways, which might also contribute to the protective function of Lkb1 in AMs. We thus identified Lkb1 as a pivotal regulator to maintain immune function of AMs.
2021-03-01 | GSE167349 | GEO
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
Project description:Even though liver kinase B1 (LKB1) is commonly described as a tumor suppressor, we and others have shown that LKB1 is augmented in liver cancer. In agreement, LKB1 modulation in human hepatoma cells and mouse livers induces changes in cell proliferation and the appearance of liver neoplastic lesions in association with disruptions of energetic metabolism. After LKB1 overexpression, a surprising uncoupling between LKB1 and its downstream kinase AMP-activated protein kinase is observed as well as activation of the oncogenic Ras pathway, driven by the direct or indirect binding of LKB1 to the promoter region of the Ras activator, RASGRP3. Under these circumstances, LKB1 SUMOylation at Lys178 by SUMO-2, the main SUMO paralogue present in liver, promotes LKB1 nuclear localization, fueling hepatoma cell proliferation. Overall, SUMO-2 mediated modification of LKB1 at Lys178 is suggested as a bona fide oncogenic driver in liver cancer by regulating the nucleo-cytoplasmic shuttling of LKB1.
2018-09-11 | GSE99584 | GEO
Project description:Analysis of brown adipose tissue (BAT) isolated from wildtype (WT) and liver kinase B1 (LKB1) deletion mice (Ad/LKB1). Results provide insight into molecular mechanisms underlying paralysis of Ad/LKB1 mice
2017-11-01 | GSE89348 | GEO