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Transcriptomic changes in wild-type and Phlpp1-/- mice following KLA stimulation

ABSTRACT: Transcriptomic changes in wild-type and Phlpp1-/- mice following KLA stimulation

PROVIDER: PRJNA478064 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7439790.fastq.gz	Fastqsanger.gz
	SRR7439800.fastq.gz	Fastqsanger.gz
	SRR7439810.fastq.gz	Fastqsanger.gz
	SRR7439820.fastq.gz	Fastqsanger.gz
	SRR7439830.fastq.gz	Fastqsanger.gz

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Transcriptomic changes in wild-type and Phlpp1-/- mice following KLA stimulation

Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) of bone marrow derived macrophages from wild-type and PHLPP1 knock-out mice and how Inflammatory stimulation affects those profiles.

2019-06-01 | GSE116314 | GEO

Phlpp1 regulates endochondral ossification via the chondrocyte phospho-proteome

Project description:Appendicular growth and bone mass acquisition are controlled by a variety of growth factors, hormones, and mechanical forces in a dynamic process called endochondral ossification. Chondrocytes in the growth plate must proliferate and undergo hypertrophy to drive growth plate expansion and lay the template for bone. Pleckstrin homology (PH) domain and leucine rich repeat phosphatase 1 and 2 (Phlpp1 and Phlpp2) are protein phosphatases that regulate intracellular signaling cascades through posttranslational modification of AKT, PKC, and S6K, among others. Phlpp1 controls chondrocyte proliferation and survival and germline deletion of Phlpp1 suppresses bone lengthening. Here, we demonstrate that Phlpp2 does not regulate endochondral ossification. Phlpp2-/- mice are phenotypically indistinguishable from their wildtype (WT) littermates, with similar bone length, bone mass, and growth plate dynamics. By contrast, Phlpp1/2-/- mice are phenotypically indistinguishable from Phlpp1-/- mice. Deletion of Phlpp1 or Phlpp2 had moderate effects on the chondrocyte transcriptome and proteome compared to WT control cells. By contrast, Phlpp1-/- and Phlpp1/2-/- chondrocytes had significantly altered phospho-proteomes compared to WT and Phlpp2-/- chondrocytes. Data integration via multiomics analysis revealed that RAF-MEK-ERK signaling was altered in cells lacking Phlpp1. In conclusion, these data demonstrate that Phlpp1, but not Phlpp2, regulates endochondral ossification via the chondrocyte phospho-proteome.

2024-09-30 | GSE265773 | GEO

Phlpp1 alters the murine chondrocyte phospho-proteome during endochondral bone formation

Project description:Appendicular skeletal growth and bone mass acquisition are controlled by a variety of growth factors, hormones, and mechanical forces in a dynamic process called endochondral ossification. In long bones, chondrocytes in the growth plate proliferate and undergo hypertrophy to drive bone lengthening and mineralization. Pleckstrin homology (PH) domain and leucine rich repeat phosphatase 1 and 2 (Phlpp1 and Phlpp2) are serine/threonine protein phosphatases that regulate cell proliferation, survival, and maturation via Akt, PKC, Raf1, S6k, and other intracellular signaling cascades. Germline deletion of Phlpp1 suppresses bone lengthening in part through parathyroid hormone receptor-dependent signaling in growth plate chondrocytes. Here, we demonstrate that Phlpp2 does not regulate endochondral ossification, and we define the molecular differences between Phlpp1 and Phlpp2 in chondrocytes. Phlpp2-/- mice are phenotypically indistinguishable from their wildtype (WT) littermates, with similar bone length, bone mass, and growth plate dynamics. Deletion of Phlpp2 had moderate effects on the chondrocyte transcriptome and proteome compared to WT cells. By contrast, Phlpp1/2-/- (double knockout) mice resembled Phlpp1-/- mice phenotypically and chondrocyte phospho-proteomes of Phlpp1-/- and Phlpp1/2-/- chondrocytes were different than WT and Phlpp2-/- chondrocyte phospho-proteomes. Data integration via multiparametric analysis identified alterations in Pdpk1 and Pak1/2 signaling pathways in chondrocytes lacking Phlpp1. In conclusion, these data demonstrate that Phlpp1, but not Phlpp2, regulates endochondral ossification through multiple and complex signaling cascades.

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Dynamic chromatin accessibility landscape changes following interleukin-1 stimulation

Project description:Dynamic chromatin accessibility landscape changes following interleukin-1 stimulation

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Dynamic chromatin accessibility landscape changes following interleukin-1 stimulation

Project description:Dynamic chromatin accessibility landscape changes following interleukin-1 stimulation

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PHLPP1 Cut&Tag profiling of untreatment (UT) and IL-4 treated alveolar macrophage

Project description:Purpose: To transcriptome widely reveal genes regulation by PHLPP1, we performed Cleavage Under Targets and Tagmentation (CUT&Tag) analysis of wild-type (WT) AMs. Methods: Mouse AMs were generated from bronchoalveolar lavage fluid (BALF). AMs were stained to confirm the surface expression of CD11C and Siglec-F. Cells with purity >97.5% were used for subsequent experiments. WT AMs were stimulated with IL-4 (20ng/ml) for 4 hours. Results: We carried out a CUT&Tag assay using antibodies against PHLPP1,and found the global influence of PHLPP1 in regulating genes for pro-fibrosis macrophage effector function.

2025-12-10 | GSE284011 | GEO

Changes in H3K27ac following LPS stimulation in pharyngeal epithelial cells

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Identification of PHLPP1 as a tumor suppressor reveals the role of feedback compensation in PTEN-mutant prostate cancer progression

Project description:Hyper-activation of the PI 3-Kinase/ AKT pathway is a driving force of many cancers. Here we identify the AKT-inactivating phosphatase PHLPP1 as a prostate tumor suppressor. We show that Phlpp1-loss causes neoplasia and, upon partial Pten-loss, carcinoma in mouse prostate. This genetic setting initially triggers a growth suppressive response via p53 and the Phlpp2 ortholog, and reveals spontaneous Trp53 inactivation as a condition for full-blown disease. Surprisingly, the co-deletion of PTEN and PHLPP1 in patient samples is highly restricted to metastatic disease and tightly correlated to deletion of TP53 and PHLPP2. These data establish a conceptual framework for progression of PTEN-mutant prostate cancer to life-threatening disease. To better assess the role of Phlpp in prostate we performed micorarray analysis of gene expression in the WT and Pten+/-; Phlpp1-/- mice.

2011-08-16 | E-GEOD-30987 | biostudies-arrayexpress

Effects of dexamethasone and KLA on HepG2 gene expression

Project description:In this study, we exposed HepG2 cells to synthetic glucocorticoid dexamethasone (Dex), Kdo2-Lipid A (KLA), or both (DexKLA) for 24 hours and conducted RNA-seq analysis to investigate the impact of exposures on gene expression. We aimed to elucidate how Dex and KLA disrupt, misregulate, or interfere with inflammatory and metabolic pathways at the transcriptional level. By analyzing the differential gene expression profiles, we sought to identify affected specific pathways and genes, providing insight into the underlying molecular mechanisms.

2025-04-11 | GSE278602 | GEO

Human Beta-Defensin 3 attenuates the pro-inflammatory effects of KDO2-Lipid A (KLA) at 6 hour

Project description:We examine the global effect of hBD3 on transcription in TLR4-stimulated macrophages and for the first time show that hBD3 inhibits the transcription of critical pro-inflammatory genes. Among the repressed genes we detect significant enrichment of groups involved in the positive regulation of NFkappaB including components of Toll-like receptor signaling pathways. Total RNA obtained from bone marrow derived macrophages (BMDM) that have been subjected to 6 hour treatment with KLA, KLA&hBD3, hBD3 or untreated. There are 3 biological replicates per group.

2012-01-01 | E-GEOD-25871 | biostudies-arrayexpress

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