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Differences in gene expression between murine Fnip1-null pre-B cells and wild type pre-B cells.

ABSTRACT: Analysis of gene expression in FACs-sorted pre-B cells derived from Fnip1-null and normal wildtype littermate mice. 3 arrays from 3 different mice per genotype were utilized to generate the expression data (mouse WG-6 v.2.0 beadchip (Illumina Inc, San Diego CA)) and statistics. P-values are shown.

ORGANISM(S): Mus musculus

PROVIDER: GSE37687 | GEO | 2012/05/02

SECONDARY ACCESSION(S): PRJNA162859

REPOSITORIES: GEO

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Differences in gene expression between murine Fnip1-null pre-B cells and wild type pre-B cells.

Project description:Analysis of gene expression in FACs-sorted pre-B cells derived from Fnip1-null and normal wildtype littermate mice. 3 arrays from 3 different mice per genotype were utilized to generate the expression data (mouse WG-6 v.2.0 beadchip (Illumina Inc, San Diego CA)) and statistics. P-values are shown. Total RNAs were isolated from sorted B220+CD43+ cell from Fnip1-/- and WT mice (n=3)

2012-05-01 | E-GEOD-37687 | biostudies-arrayexpress

RNAseq analysis of skeletal muscle transcriptomes from wild-type, FNIP1-knockout (FNIP1-KO) mice, and mice expressing FNIP1 only in skeletal muscle (FNIP1-TgKO).

Project description:This experiment was conducted to identify FNIP1-dependent mRNA transcripts alteration in skeletal muscle. Mouse FNIP1 was specifically overexpressed in skeletal muscle in FNIP1-transgenic (FNIP1-Tg) mice. FNIP1-Tg mice were crossed with FNIP1-knockout (FNIP1-KO) mice to generate FNIP1-TgKO mice expressing FNIP1 only in skeletal muscle but not in other tissues. The muscle glycolytic-to-oxidative transformation is determined, largely in part, at the level of gene expression. To gain insight into the FNIP1-dependent regulation of skeletal muscle energy metabolism, transcriptome analysis was performed by whole-genome gene expression profiling experiments in gastrocnemius (GC) muscle from both FNIP1-KO and FNIP1-TGKO mice. We were particularly interested in the subset of genes that were regulated only in the FNIP1-KO mice but not in FNIP1-TGKO mice. Gene ontology (GO) analysis revealed that the primary FNIP1-regulated genes were mitochondrial metabolic genes. A broad array of genes involved in mitochondria was regulated FNIP1-KO muscle in a FNIP1-dependent manner. Together, the transcriptional profiling results indicate that a significant subset of FNIP1 target genes, were those involved in mitochondrial function.

2021-03-17 | GSE150193 | GEO

Fnip1 null kidney versus wildtype kidney RNAseq data

Project description:This RNAseq data was generated by comparing kidney tissue from Fnip1 null mice versus Wildtype Mice

2018-05-15 | GSE103303 | GEO

RNAseq analysis of adipose tissue transcriptomes from wild-type and FNIP1 adipocyte specific knockout (FNIP1-AKO) mice

Project description:Activation of thermogenesis in brown and beige adipocytes upon activation by external stimuli burns fuel energy as heat. Owing to its remarkable benefits on metabolic health and its demonstrated presence in adult humans, beige adipocytes holds great promise to combat obesity and metabolic diseases. Folliculin interacting protein 1 (FNIP1) is an adaptor protein originally identified through its interaction with folliculin (FLCN) and AMPK. To investigate the physiological role of FNIP1 in adipose tissue in vivo, we generated adipocyte-specific FNIP1 deficient mice (referred to as FNIP1-AKO) by crossing mice bearing a conditional Fnip1 allele with introns 5 and 6 floxed (Fnip1 lox/lox) with the adiponectin promoter–driven Cre mice. We performed transcriptome analysis by whole-genome gene expression profiling experiments in inguinal white adipose tissue (iWAT) from both wild-type (WT) and FNIP1-AKO mice. We were particularly interested in the subset of genes that were up-regulated in the FNIP1-AKO mice. Gene ontology (GO) analysis revealed that the primary up-regulated genes were mitochondrial and lipid metabolism-related genes. Gene expression validation studies demonstrated that a broad array of genes involved in thermogenic and mitochondrial oxidative program was induced in FNIP1-AKO iWAT. Together, the transcriptional profiling results indicate that loss of FNIP1 activate thermogenic program in white adipocytes.

2022-02-26 | GSE185067 | GEO

RNAseq analysis of skeletal muscle transcriptomes from wild-type, FNIP1-knockout (FNIP1-KO) mice, and mice expressing FNIP1 only in skeletal muscle (FNIP1-TgKO).

Project description:RNAseq analysis of skeletal muscle transcriptomes from wild-type, FNIP1-knockout (FNIP1-KO) mice, and mice expressing FNIP1 only in skeletal muscle (FNIP1-TgKO).

| PRJNA631493 | ENA

Genomic profiling of chondrosarcoma: chromosomal patterns in central and peripheral tumors (Illumina)

Project description:Gene expression profiling of 17 fresh frozen chondrosarcoma biopsies using the Human-6 v2 Expression BeadChip (Illumina Inc., San Diego, CA, USA). DNA copy number analyses was also performed in these tumors. Keywords: chondrosarcoma, gene expression profiling, Illumina

2009-04-01 | GSE12475 | GEO

CoIP-MS based method to identify FNIP1 binding proteins in exercising muscle

Project description:Using muscle-specific FNIP1 (WT) and FNIP1 (S220A Tg) muscle tissues, we identified approximately 600 potential FNIP1 (WT) or FNIP1 (S220A) binding proteins in exercising muscle tissue of the corresponding mice by the CoIP-MS method, proteomic analysis showed that both FNIP1 (WT) and FNIP1 (S220A) interacted with major mitochondrial proteins, such as the respiratory complex subunits. Notably, FNIP1 (S220A) specifically interacted with additional mitochondrial subunits that were not observed for FNIP1 (WT), including protein involved in NADH metabolism and sulfur cluster binding. These data suggested that non-phosphorylated FNIP1 (S220A) could enhance its interaction with mitochondria.

2023-11-17 | PXD046977 | Pride

Circulating Extracellular Vesicular MicroRNA Signatures in Early Gestation Show an Association with Subsequent Clinical Features of Pre-Eclampsia

Project description:We report the differential abundance of cell free miRNAs extracted from extracellular vesicles (EV) in the peripheral blood of pregnant women with or without preeclampsia by Next Generation Sequencing. Maternal blood samples were collected form pregnant women enrolled in the study during first to very early second trimester (11–14 weeks ), mid- to late second trimester (19–22 weeks), third trimester (36 weeks) and at delivery. Extracellular vesicles were isolated from peripheral blood and total RNA was extracted using the miRNeasy Mini Kit (Qiagen, Valencia, CA) following manufacturer’s instruction. miRNA libraries were prepared utilizing NEB Next Multiplex small RNA Library prep kit (NEB E7300S; New England Biolabs, Inc, Ipswich, MA, USA) and libraries were subsequently sequenced using the HiSeq-2500 platform with single-end 50bp reads (Illumina Inc.; San Diego, CA, USA).

2024-08-01 | GSE247251 | GEO

Mitochondrial energetic stress triggers AMPK/FNIP1-dependent TFEB nuclear translocation, inducing transcriptional waves of lysosomal and mitochondrial biogenesis.

Project description:Cells respond to mitochondrial energetic stress with rapid activation of the AMP-activated protein kinase (AMPK), which acutely inhibits anabolism and stimulates catabolism. AMPK also induces sustained transcriptional reprogramming of metabolism. The TFEB transcription factor is a major effector of AMPK signals, inducing lysosome genes following energetic stress. Yet the molecular mechanism underlying how AMPK activates TFEB remains unresolved. We demonstrate here that AMPK directly phosphorylates five conserved serine residues in FNIP1, which suppresses the function of the FLCN/FNIP1 RagC GAP complex, in turn controlling TFEB lysosomal localization. We demonstrate that FNIP1 phosphorylation is required for AMPK to induce nuclear translocation of TFEB, which is fully separable from AMPK control of canonical mTORC1 signaling. Using a non-phosphorylatable allele of FNIP1, we show that in parallel to lysosomal biogenesis, AMPK induces mitochondrial biogenesis via TFEB-dependent induction of PGC1a mRNA. This signaling from mitochondrial stress is also independent of amino-acid control of the Rags and TFEB, which still proceed normally in cells bearing the AMPK-non phosphorylatable allele of FNIP1. Taken together, mitochondrial energetic stress triggers AMPK/FNIP1-dependent TFEB nuclear translocation, inducing transcriptional waves of lysosomal and mitochondrial biogenesis.

2023-05-08 | GSE218827 | GEO

Genome-wide methylation profiles of post-mortem tissue samples (human) 3

Project description:In this study, 60 post-mortem tissue samples comprising four tissue types (dermis, epidermis, and muscle) were collected from autopsies of 20 Koreans aged 18 to 78. 250 ng of genomic DNA (gDNA) was employed to generate DNA methylation profiles utilizing the Illumina Infinium MethylationEPIC BeadChip array (Illumina, San Diego, CA, USA) at Macrogen Inc. (Macrogen, Seoul, Korea).

2023-10-22 | GSE244995 | GEO

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