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IMP2 increases mouse skeletal muscle mass and voluntary activity by enhancing autocrine IGF2 production and optimizing muscle metabolism

ABSTRACT: IMP2 increases mouse skeletal muscle mass and voluntary activity by enhancing autocrine IGF2 production and optimizing muscle metabolism

PROVIDER: PRJNA490347 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7819350.fastq.gz	Fastqsanger.gz
	SRR7819351.fastq.gz	Fastqsanger.gz
	SRR7819352.fastq.gz	Fastqsanger.gz
	SRR7819353.fastq.gz	Fastqsanger.gz
	SRR7819354.fastq.gz	Fastqsanger.gz

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Similar Datasets

IMP2 increases mouse skeletal muscle mass and voluntary activity by enhancing autocrine IGF2 production and optimizing muscle metabolism

Project description:The Igf2 mRNA binding protein2/Imp2 was selectively deleted from adult mouse muscle; two phenotypes were observed: modestly decreased accrual of skeletal muscle mass after weaning and reduced wheel running activity but normal forced treadmill performance. Reduced voluntary activity occurs when fed a high fat diet but is normalized when consuming standard chow. The reduced muscle mass is due to diminished autocrine Igf2 production, reduced Akt1 activation, disinhibition of Gsk3α and reduced protein synthesis, without altered mTOR complex1 activity. The diet-dependent reduction in spontaneous exercise is accompanied by suboptimal muscle fatty acid oxidation, caused by reduced PPARα mRNA and protein, the former an Imp2 client. Nevertheless, in contrast to global Imp2 deficiency, muscle specific Imp2 inactivation does not alter glucose tolerance or the hypoglycemic effect of insulin. Imp2 deficiency in skeletal muscle reduces autocrine production of Igf2 and fiber growth and disorders nutrient metabolism so as to reduce voluntary physical activity.

2018-12-31 | GSE119801 | GEO

IGF2 mRNA Binding Protein-2 is a tumor promoter that drives cancer proliferation through its client mRNAs IGF2 and HMGA1

Project description:The gene encoding the IGF2 mRNA binding protein-2/IMP2 is amplified and overexpressed in many cancers, accompanied by a poorer prognosis. Mice deficient in IMP2 exhibit a longer lifespan and a reduced tumor burden at old age. Herein we show in a diverse array of cancer cells that IMP2 overexpression stimulates and IMP2 elimination diminishes proliferation by 50-80%. In addition to its known ability to promote IGF2 abundance, we find that IMP2 strongly promotes IGF action, by binding and stabilizing HMGA1 mRNA. The HMGA1 DNA binding protein, a known oncogene, suppresses the abundance of IGFBP2 and Grb14, inhibitors of IGF action. IMP2 stabilization of HMGA1 mRNA plus IMP2 stimulated IGF2 production synergistically drive cancer cell proliferation and account for IMP2’s tumor promoting action. IMP2’s ability to promote proliferation and IGF action requires mTOR-catalyzed IMP2 phosphorylation.

2017-09-14 | GSE101311 | GEO

IMP2 Increases Mouse Skeletal Muscle Mass and Voluntary Activity by Enhancing Autocrine Insulin-Like Growth Factor 2 Production and Optimizing Muscle Metabolism.

Project description:Insulin-like growth factor 2 (IGF2) mRNA binding protein 2 (IMP2) was selectively deleted from adult mouse muscle; two phenotypes were observed: decreased accrual of skeletal muscle mass after weaning and reduced wheel-running activity but normal forced treadmill performance. Reduced wheel running occurs when mice are fed a high-fat diet but is normalized when mice consume standard chow. The two phenotypes are due to altered output from different IMP2 client mRNAs. The reduced fiber size of IMP2-deficient muscle is attributable, in part, to diminished autocrine Igf2 production; basal tyrosine phosphorylation of the insulin and IGF1 receptors is diminished, and Akt1 activation is selectively reduced. Gsk3α is disinhibited, and S536-phosphorylated ε subunit of eukaryotic initiation factor 2B [eIF2Bε(S536)] is hyperphosphorylated. Protein synthesis is reduced despite unaltered mTOR complex 1 activity. The diet-dependent reduction in voluntary exercise is likely due to altered muscle metabolism, as contractile function is normal. IMP2-deficient muscle exhibits reduced fatty acid oxidation, due to a reduced abundance of mRNA of peroxisome proliferator-activated receptor α (PPARα), an IMP2 client, and PPARα protein. IMP2-deficient muscle fibers treated with a mitochondrial uncoupler to increase electron flux, as occurs with exercise, exhibit reduced oxygen consumption from fatty acids, with higher oxygen consumption from glucose. The greater dependence on muscle glucose metabolism during increased oxygen demand may promote central fatigue and thereby diminish voluntary activity.

| S-EPMC6425142 | biostudies-literature

A Long Non-coding RNA, LncMyoD, Regulates Skeletal Muscle Differentiation by Blocking IMP2-mediated mRNA Translation

Project description:Increasing evidence suggests that Long non-coding RNAs (LncRNAs) represent a new class of regulators of stem cells. However, the roles of LncRNAs in stem cell maintenance and myogenesis remain largely unexamined. For this study, hundreds of novel intergenic LncRNAs were identified that are expressed in myoblasts and regulated during differentiation. One of these LncRNAs, termed LncMyoD, is encoded next to the Myod gene and is directly activated by MyoD during myoblast differentiation. Knockdown of LncMyoD strongly inhibits terminal muscle differentiation largely due to a failure to exit the cell cycle. LncMyoD directly binds to IGF2-mRNA-binding-protein 2 (IMP2) and negatively regulates IMP2-mediated translation of proliferation genes such as N-Ras and c-Myc. While the RNA sequence of LncMyoD is not well-conserved between human and mouse, its locus, gene structure and function is preserved. The MyoD-LncMyoD-IMP2 pathway elucidates a mechanism as to how MyoD blocks proliferation to create a permissive state for differentiation. In order to perform an unbiased search for downstream signaling pathways perturbed by LncMyodD downregulation, microarrays were performed on myoblasts treated with control vs LncMyoD shRNAs. Total RNA was extracted using the TRIzol reagent (Invitrogen) and purified with Qiagen RNeasy separation columns (Qiagen) from myoblasts treated with control vs. LncMyoD shRNA. First-strand cDNA was synthesized and hybridized to GeneChip Mouse Genome 430 2.0 Array (Affymetrix).

2015-08-11 | E-GEOD-68842 | biostudies-arrayexpress

A Long Non-coding RNA, LncMyoD, Regulates Skeletal Muscle Differentiation by Blocking IMP2-mediated mRNA Translation

2015-08-11 | GSE68842 | GEO

Next Generation Sequencing (NGS) analysis of mice pancreatic islets from control and IMP2 islet specific knockout (Rip2;IMP2).

Project description:The goal of this study is to understand how IMP2 contributes to T2D traits by regulating pancreatic beta cell growth and function. Islets from control and Rip2;IMP2 mice were generated by deep sequencing. In additon, we also perfomred IMP2 RIP-Seq to identify IMP2 targets.

2023-06-11 | GSE152424 | GEO

IMP2-TRIBE

Project description:Detection of IMP2 binding sites

| PRJEB71750 | ENA

Quantitative proteomes of Imp2 KO mouse 2-cell-stage embryos

Project description:Data showing the late 2-cell-stage, control embryos (Imp2♀+/♂+) and Imp2-knockout embryos (Imp2♀−/♂+) for HPLC MS/MS analysis. 3 replicates were performed using 330 embryos per group.

2019-11-12 | PXD010397 | Pride

IMP2/IGF2BP2 HITS-CLIP from E13.5 mouse brain

Project description:HITS-CLIP is performed for the RNA-binding protein, IMP2/IGF2BP2, from E13.5 mouse brain.

2016-06-06 | E-MTAB-3636 | biostudies-arrayexpress

IMP2 axonal localization, RNA interactome, and function in development of axon trajectories

Project description:RNA-based regulatory mechanisms play important roles in the development and plasticity of neural circuits and neurologic disease. Developing axons provide a well suited model to study RNA-based regulation, and contain specific subsets of mRNAs that are locally translated and have roles in axon pathfinding. However, the RNA-binding proteins involved in axon pathfinding, and their corresponding mRNA targets, are still largely unknown. Here we find that the RNA-binding protein IMP2 (Igf2bp2) is strikingly enriched in developing axon tracts, including in spinal commissural axons. We used the HITS-CLIP approach to perform a genome-wide identification of RNAs that interact directly with IMP2 in the native context of developing brain. This IMP2 interactome was highly enriched for mRNA targets related to axon guidance. Accordingly, IMP2 knockdown in the developing spinal cord led to strong defects in commissural axon trajectories at the midline intermediate target. These results reveal a highly distinctive axonal enrichment of IMP2, show that it interacts with a network of axon guidance-related mRNAs, and reveal its requirement for normal axon pathfinding during vertebrate development. CLIP-seq

2016-08-02 | E-GEOD-83822 | biostudies-arrayexpress

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