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Max Delbrück Center (MDC) for Molecula... Publications | LitMetric

29 results match your criteria: "Max Delbrück Center (MDC) for Molecular Medicine in the Helmholtz Association[Affiliation]"

Dominance is common in mammals and is associated with trans-acting gene expression and alternative splicing.

Genome Biol

September 2023

National Key Laboratory for Pig Genetic Improvement and Production Technology, Jiangxi Agricultural University, Nanchang, 330045, People's Republic of China.

Background: Dominance and other non-additive genetic effects arise from the interaction between alleles, and historically these phenomena play a major role in quantitative genetics. However, most genome-wide association studies (GWAS) assume alleles act additively.

Results: We systematically investigate both dominance-here representing any non-additive within-locus interaction-and additivity across 574 physiological and gene expression traits in three mammalian stocks: F2 intercross pigs, rat heterogeneous stock, and mice heterogeneous stock.

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Article Synopsis
  • * There is still limited understanding of the pathogenesis of VHD, but metabolomics can help in understanding its development, diagnosis, and prognosis.
  • * The study reviews key metabolic biomarkers for different types of VHD, discusses their potential for patient outcome predictions, and addresses challenges in conducting metabolomics research in a clinical setting.
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SPSB1-mediated inhibition of TGF-β receptor-II impairs myogenesis in inflammation.

J Cachexia Sarcopenia Muscle

August 2023

Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin, Max Delbrück Center (MDC) for Molecular Medicine in the Helmholtz Association, Berlin, Germany.

Background: Sepsis-induced intensive care unit-acquired weakness (ICUAW) features profound muscle atrophy and attenuated muscle regeneration related to malfunctioning satellite cells. Transforming growth factor beta (TGF-β) is involved in both processes. We uncovered an increased expression of the TGF-β receptor II (TβRII)-inhibitor SPRY domain-containing and SOCS-box protein 1 (SPSB1) in skeletal muscle of septic mice.

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Defects in blood development frequently occur among syndromic congenital anomalies. Thrombocytopenia-Absent Radius (TAR) syndrome is a rare congenital condition with reduced platelets (hypomegakaryocytic thrombocytopenia) and forelimb anomalies, concurrent with more variable heart and kidney defects. TAR syndrome associates with hypomorphic gene function for that encodes a component of the exon junction complex involved in mRNA splicing, transport, and nonsense-mediated decay.

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Many studies have shown that abdominal adiposity is more strongly related to health risks than peripheral adiposity. However, the underlying pathways are still poorly understood. In this cross-sectional study using data from RNA-sequencing experiments and whole-body MRI scans of 200 participants in the EPIC-Potsdam cohort, our aim was to identify novel genes whose gene expression in subcutaneous adipose tissue has an effect on body fat mass (BFM) and body fat distribution (BFD).

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Muscular myostatin gene expression and plasma concentrations are decreased in critically ill patients.

Crit Care

August 2022

Department of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.

Background: The objective was to investigate the role of gene expression and plasma levels of the muscular protein myostatin in intensive care unit-acquired weakness (ICUAW). This was performed to evaluate a potential clinical and/or pathophysiological rationale of therapeutic myostatin inhibition.

Methods: A retrospective analysis from pooled data of two prospective studies to assess the dynamics of myostatin plasma concentrations (day 4, 8 and 14) and myostatin gene (MSTN) expression levels in skeletal muscle (day 15) was performed.

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The Transcription Factor EB (TFEB) Sensitizes the Heart to Chronic Pressure Overload.

Int J Mol Sci

May 2022

Experimental and Clinical Research Center (ECRC), Max Delbrück Center (MDC) for Molecular Medicine in the Helmholtz Association, Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.

The transcription factor EB (TFEB) promotes protein degradation by the autophagy and lysosomal pathway (ALP) and overexpression of TFEB was suggested for the treatment of ALP-related diseases that often affect the heart. However, TFEB-mediated ALP induction may perturb cardiac stress response. We used adeno-associated viral vectors type 9 (AAV9) to overexpress TFEB (AAV9-Tfeb) or Luciferase-control (AAV9-Luc) in cardiomyocytes of 12-week-old male mice.

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Critically ill patients at the intensive care unit (ICU) often develop a generalized weakness, called ICU-acquired weakness (ICUAW). A major contributor to ICUAW is muscle atrophy, a loss of skeletal muscle mass and function. Skeletal muscle assures almost all of the vital functions of our body.

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Recently, there has been growing interest in short-chain fatty acids (SCFA) and ketone bodies (KB) due to their potential use as biomarkers of health and disease. For instance, these diet-related metabolites can be used to monitor and reduce the risk of immune response, diabetes, or cardiovascular diseases. Given the interest in these metabolites, different targeted metabolomic methods based on UPLC-MS/MS have been developed in recent years to detect and quantify SCFA and KB.

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Background: There are no systematic reviews of cerebrospinal fluid and blood biomarkers for sporadic Creutzfeldt-Jakob disease (sCJD) in specialized care settings that compare diagnostic accuracies in a network meta-analysis (NMA).

Methods: We searched Medline, Embase, and Cochrane Library for diagnostic studies of sCJD biomarkers. Studies had to use established diagnostic criteria for sCJD and for diseases in the non-CJD groups, which had to represent a consecutive population of patients suspected as a CJD case, as reference standard.

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Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling.

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Sepsis induces interleukin 6, gp130/JAK2/STAT3, and muscle wasting.

J Cachexia Sarcopenia Muscle

February 2022

Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany.

Background: Sepsis and inflammation can cause intensive care unit-acquired weakness (ICUAW). Increased interleukin-6 (IL-6) plasma levels are a risk factor for ICUAW. IL-6 signalling involves the glycoprotein 130 (gp130) receptor and the JAK/STAT-pathway, but its role in sepsis-induced muscle wasting is uncertain.

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Inhibition of the NLRP3/IL-1β axis protects against sepsis-induced cardiomyopathy.

J Cachexia Sarcopenia Muscle

December 2021

Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin, Max Delbrück Center (MDC) for Molecular Medicine in the Helmholtz Association, Berlin, Germany.

Background: Septic cardiomyopathy worsens the prognosis of critically ill patients. Clinical data suggest that interleukin-1β (IL-1β), activated by the NLRP3 inflammasome, compromises cardiac function. Whether or not deleting Nlrp3 would prevent cardiac atrophy and improve diastolic cardiac function in sepsis was unclear.

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Rationale: The ubiquitin-proteasome system (UPS) is responsible for skeletal muscle atrophy. We showed earlier that the transcription factor EB (TFEB) plays a role by increasing E3 ubiquitin ligase muscle really interesting new gene-finger 1(MuRF1)/ () expression. MuRF 1 ubiquitinates structural proteins and mediates their UPS-dependent degradation.

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In genetic association studies of rare variants, the low power of association tests is one of the main challenges. In this study, we propose a new single-marker association test called C-JAMP (Copula-based Joint Analysis of Multiple Phenotypes), which is based on a joint model of multiple phenotypes given genetic markers and other covariates. We evaluated its performance and compared its empirical type I error and power with existing univariate and multivariate single-marker and multi-marker rare-variant tests in extensive simulation studies.

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Background: Adipokines are hormones secreted from adipose tissue (AT), and a number of them have been established as risk factors for chronic diseases. However, it is not clear whether and to what extent adiposity, gene expression, and other factors determine their circulating levels.

Objectives: To assess to what extent adiposity, as measured by the amount of subcutaneous AT (SAT) and visceral AT (VAT) using magnetic resonance imaging, and gene expression levels in SAT determine plasma concentrations of the adipokines adiponectin, leptin, soluble leptin receptor, resistin, interleukin 6, and fatty acid-binding protein 4 (FABP4).

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deletion causes extensive vacuolation that consumes the insulin content of pancreatic β cells.

Proc Natl Acad Sci U S A

October 2019

Molecular Diabetology, Paul Langerhans Institute Dresden (PLID) of the Helmholtz German Center for Diabetes Research (DZD e.V.) Munich, University Hospital Carl Gustav Carus and Faculty of Medicine, TU Dresden, 01307 Dresden, Germany.

Article Synopsis
  • Pancreatic β cells store insulin in granules, which release insulin when blood glucose rises, while damaged granules are degraded through processes like crinophagy and autophagy.* -
  • A study showed that deleting a specific component essential for lysosomal function in mouse β cells led to the buildup of large vacuoles, reduced insulin levels, and poor regulation of glucose.* -
  • The findings highlight that the regulation of insulin granule turnover is crucial for β cell health, suggesting that maintaining this balance is important for preventing diabetes.*
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The muscle-specific RING-finger protein MuRF1 (also known as TRIM63) constitutes a bona fide ubiquitin ligase that routes proteins like several different myosin heavy chain proteins (MyHC) to proteasomal degradation during muscle atrophy. In two unbiased screens, we identified DCAF8 as a new MuRF1-binding partner. MuRF1 physically interacts with DCAF8 and both proteins localize to overlapping structures in muscle cells.

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Maximal exercise and plasma cytochrome P450 and lipoxygenase mediators: a lipidomics study.

Physiol Rep

July 2019

Experimental and Clinical Research Center (ECRC), a Joint Institution between the Charité University Medicine, Max Delbrück Center (MDC) for Molecular Medicine, Berlin-Buch, Germany.

Epoxides derived from arachidonic acid (AA) are released during exercise and may contribute to vasodilation. However, exercise may also affect circulating levels of other epoxides derived from cytochromes P450 (CYP) monooxygenase and lipoxygenase (LOX) pathways, many of whose exhibit cardiovascular activity in vitro. The effects of exercise on their levels have not been documented.

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Author Correction: Excitotoxic inactivation of constitutive oxidative stress detoxification pathway in neurons can be rescued by PKD1.

Nat Commun

January 2018

Instituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), C/ Arturo Duperier 4, 28029, Madrid, Spain.

The original version of this Article contained an error in the spelling of the author Álvaro Sebastián-Serrano, which was incorrectly given as Álvaro Sebastián Serrano. This has now been corrected in both the PDF and HTML versions of the Article.

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Individual mRNA molecules can be imaged in fixed cells by hybridization with multiple, singly labeled oligonucleotide probes, followed by computational identification of fluorescent signals. This approach, called single-molecule RNA fluorescence in situ hybridization (smRNA FISH), allows subcellular localization and absolute quantification of RNA molecules in individual cells. Here, we describe a simple smRNA FISH protocol for two-color imaging of a circular RNA, CDR1as, simultaneously with an unrelated messenger RNA.

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Excitotoxic inactivation of constitutive oxidative stress detoxification pathway in neurons can be rescued by PKD1.

Nat Commun

December 2017

Instituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), C/ Arturo Duperier 4, 28029, Madrid, Spain.

Excitotoxicity, a critical process in neurodegeneration, induces oxidative stress and neuronal death through mechanisms largely unknown. Since oxidative stress activates protein kinase D1 (PKD1) in tumor cells, we investigated the effect of excitotoxicity on neuronal PKD1 activity. Unexpectedly, we find that excitotoxicity provokes an early inactivation of PKD1 through a dephosphorylation-dependent mechanism mediated by protein phosphatase-1 (PP1) and dual specificity phosphatase-1 (DUSP1).

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