RT² Profiler PCR Array (96-Well Format and 384-Well [4 X 96] Format)
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RT² Profiler PCR Array (96-Well Format and 384-Well [4 X 96] Format)
RT² Profiler PCR Array (96-Well Format and 384-Well [4 x 96] Format) Human Mitochondria Cat. no. 330231 PAHS-087ZA For pathway expression analysis Format For use with the following real-time cyclers RT² Profiler PCR Array, Applied Biosystems® models 5700, 7000, 7300, 7500, Format A 7700, 7900HT, ViiA™ 7 (96-well block); Bio-Rad® models iCycler®, iQ™5, MyiQ™, MyiQ2; Bio-Rad/MJ Research Chromo4™; Eppendorf® Mastercycler® ep realplex models 2, 2s, 4, 4s; Stratagene® models Mx3005P®, Mx3000P®; Takara TP-800 RT² Profiler PCR Array, Applied Biosystems models 7500 (Fast block), 7900HT (Fast Format C block), StepOnePlus™, ViiA 7 (Fast block) RT² Profiler PCR Array, Bio-Rad CFX96™; Bio-Rad/MJ Research models DNA Format D Engine Opticon®, DNA Engine Opticon 2; Stratagene Mx4000® RT² Profiler PCR Array, Applied Biosystems models 7900HT (384-well block), ViiA 7 Format E (384-well block); Bio-Rad CFX384™ RT² Profiler PCR Array, Roche® LightCycler® 480 (96-well block) Format F RT² Profiler PCR Array, Roche LightCycler 480 (384-well block) Format G RT² Profiler PCR Array, Fluidigm® BioMark™ Format H Sample & Assay Technologies Description The Human Mitochondria RT² Profiler PCR Array profiles the expression of 84 genes involved in the biogenesis and function of the cell's powerhouse organelle. The genes monitored by this array include regulators and mediators of mitochondrial molecular transport of not only the metabolites needed for the electron transport chain and oxidative phosphorylation, but also the ions required for maintaining the mitochondrial membrane polarization and potential important for ATP synthesis. Metabolism and energy production are not the only functions of mitochondria. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Mitochondrial Carriers Regulating Insulin Secretion Profiled in Human Islets Upon Metabolic Stress
Jiménez-Sánchez et al. Supplementary files Mitochondrial carriers regulating insulin secretion profiled in human islets upon metabolic stress Supplementary Table S1: Clinical Data of the human donors of pancreatic islets, type of analyses performed and tested conditions. Supplementary Table S2: Quantitative data related to the transcriptomic profiles of mitochondrial solute carriers and associated genes in human islets upon metabolic stress. NA: Not applicable, ND: not detected. Supplementary Table S3: Quantitative data related to the transcriptomic profiles of the electron transport chain machinery and related mitochondrial carriers in human islets upon metabolic stress.NA: Not applicable, ND: not detected. Supplementary Table S4: Quantitative data related to the transcriptomic profiles of the outer and inner mitochondrial membrane translocases TOM/TIM machinery in human islets upon metabolic stress.NA: Not applicable, ND: not detected. Supplementary Table S5: Quantitative data related to the transcriptomic profiles of mitochondrial iron transport genes in human islets under metabolic stress. NA: Not applicable, ND: not detected. Supplementary Table S6: Quantitative data related to the transcriptomic profiles of mitochondrial calcium transport genes in human islets upon metabolic stress. NA: Not applicable, ND: not detected. Supplementary Table S7: Primers used for quantitative RT-PCR analysis Supplementary Figure S1: Functional interaction network of human (a) mitochondrial calcium transport genes; (b) outer and inner mitochondrial membrane translocases TOM/TIM machinery; (c) electron transport chain machinery and related carriers; (d) mitochondrial iron transport genes. Nodes were connected using the STRING interaction knowledgebase with a confidence score >0.4. Supplementary Figure S2: Effects of high 25 mM glucose (G25) and 0.4 mM oleate (Olea) or palmitate (Palm) on the transcriptional regulation of the electron transport chain machinery. -
A Cross-Platform Analysis of 14,177 Expression Quantitative Trait Loci Derived from Lymphoblastoid Cell Lines
Downloaded from genome.cshlp.org on October 5, 2021 - Published by Cold Spring Harbor Laboratory Press Resource A cross-platform analysis of 14,177 expression quantitative trait loci derived from lymphoblastoid cell lines Liming Liang,1 Nilesh Morar,2 Anna L. Dixon,2 G. Mark Lathrop,3 Goncalo R. Abecasis,4 Miriam F. Moffatt,2,5 and William O.C. Cookson2,5,6 1Department of Epidemiology and Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts 02115, USA; 2National Heart and Lung Institute, Imperial College London, London SW3 6LY, United Kingdom; 3Centre National de Genotypage, 91057 Evry Cedex, France; 4Center for Statistical Genetics, School of Public Health, University of Michigan, Ann Arbor, Michigan 48109-2029, USA Gene expression levels can be an important link DNA between variation and phenotypic manifestations. Our previous map of global gene expression, based on ~400K single nucleotide polymorphisms (SNPs) and 50K transcripts in 400 sib pairs from the MRCA family panel, has been widely used to interpret the results of genome-wide association studies (GWASs). Here, we more than double the size of our initial data set with expression data on 550 additional individuals from the MRCE family panel using the Illumina whole-genome expression array. We have used new statistical methods for dimension reduction to account for nongenetic effects in estimates of expression levels, and we have also included SNPs imputed from the 1000 Genomes Project. Our methods reduced false-discovery rates and increased the number of ex- pression quantitative trait loci (eQTLs) mapped either locally or at a distance (i.e., in cis or trans) from 1534 in the MRCA data set to 4452 (with <5% FDR). -
Human CLPB) Is a Potent Mitochondrial Protein Disaggregase That Is Inactivated By
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.17.911016; this version posted January 18, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Skd3 (human CLPB) is a potent mitochondrial protein disaggregase that is inactivated by 3-methylglutaconic aciduria-linked mutations Ryan R. Cupo1,2 and James Shorter1,2* 1Department of Biochemistry and Biophysics, 2Pharmacology Graduate Group, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, U.S.A. *Correspondence: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.01.17.911016; this version posted January 18, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. ABSTRACT Cells have evolved specialized protein disaggregases to reverse toxic protein aggregation and restore protein functionality. In nonmetazoan eukaryotes, the AAA+ disaggregase Hsp78 resolubilizes and reactivates proteins in mitochondria. Curiously, metazoa lack Hsp78. Hence, whether metazoan mitochondria reactivate aggregated proteins is unknown. Here, we establish that a mitochondrial AAA+ protein, Skd3 (human CLPB), couples ATP hydrolysis to protein disaggregation and reactivation. The Skd3 ankyrin-repeat domain combines with conserved AAA+ elements to enable stand-alone disaggregase activity. A mitochondrial inner-membrane protease, PARL, removes an autoinhibitory peptide from Skd3 to greatly enhance disaggregase activity. Indeed, PARL-activated Skd3 dissolves α-synuclein fibrils connected to Parkinson’s disease. Human cells lacking Skd3 exhibit reduced solubility of various mitochondrial proteins, including anti-apoptotic Hax1. -
Role and Regulation of the P53-Homolog P73 in the Transformation of Normal Human Fibroblasts
Role and regulation of the p53-homolog p73 in the transformation of normal human fibroblasts Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Bayerischen Julius-Maximilians-Universität Würzburg vorgelegt von Lars Hofmann aus Aschaffenburg Würzburg 2007 Eingereicht am Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Dr. Martin J. Müller Gutachter: Prof. Dr. Michael P. Schön Gutachter : Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am Erklärung Hiermit erkläre ich, dass ich die vorliegende Arbeit selbständig angefertigt und keine anderen als die angegebenen Hilfsmittel und Quellen verwendet habe. Diese Arbeit wurde weder in gleicher noch in ähnlicher Form in einem anderen Prüfungsverfahren vorgelegt. Ich habe früher, außer den mit dem Zulassungsgesuch urkundlichen Graden, keine weiteren akademischen Grade erworben und zu erwerben gesucht. Würzburg, Lars Hofmann Content SUMMARY ................................................................................................................ IV ZUSAMMENFASSUNG ............................................................................................. V 1. INTRODUCTION ................................................................................................. 1 1.1. Molecular basics of cancer .......................................................................................... 1 1.2. Early research on tumorigenesis ................................................................................. 3 1.3. Developing -
Skd3 (Human CLPB) Is a Potent Mitochondrial Protein Disaggregase That Is Inactivated By
bioRxiv preprint first posted online Jan. 18, 2020; doi: http://dx.doi.org/10.1101/2020.01.17.911016. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Skd3 (human CLPB) is a potent mitochondrial protein disaggregase that is inactivated by 3-methylglutaconic aciduria-linked mutations Ryan R. Cupo1,2 and James Shorter1,2* 1Department of Biochemistry and Biophysics, 2Pharmacology Graduate Group, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, U.S.A. *Correspondence: [email protected] 1 bioRxiv preprint first posted online Jan. 18, 2020; doi: http://dx.doi.org/10.1101/2020.01.17.911016. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. ABSTRACT Cells have evolved specialized protein disaggregases to reverse toxic protein aggregation and restore protein functionality. In nonmetazoan eukaryotes, the AAA+ disaggregase Hsp78 resolubilizes and reactivates proteins in mitochondria. Curiously, metazoa lack Hsp78. Hence, whether metazoan mitochondria reactivate aggregated proteins is unknown. Here, we establish that a mitochondrial AAA+ protein, Skd3 (human CLPB), couples ATP hydrolysis to protein disaggregation and reactivation. The Skd3 ankyrin-repeat domain combines with conserved AAA+ elements to enable stand-alone disaggregase activity. A mitochondrial inner-membrane protease, PARL, removes an autoinhibitory peptide from Skd3 to greatly enhance disaggregase activity. Indeed, PARL-activated Skd3 dissolves α-synuclein fibrils connected to Parkinson’s disease. -
Protein Tyrosine Phosphorylation in Haematopoietic Cancers and the Functional Significance of Phospho- Lyn SH2 Domain
Protein Tyrosine Phosphorylation in Haematopoietic Cancers and the Functional Significance of Phospho- Lyn SH2 Domain By Lily Li Jin A thesis submitted in conformity with the requirements for the degree of Ph.D. in Molecular Genetics, Graduate Department of Molecular Genetics, in the University of Toronto © Copyright by Lily Li Jin (2015) Protein Tyrosine Phosphorylation in Haematopoietic Cancers and the Functional Significance of Phospho-Lyn SH2 Domain Lily Li Jin 2015 Ph.D. in Molecular Genetics Graduate Department of Molecular Genetics University of Toronto Abstract Protein-tyrosine phosphorylation (pY) is a minor but important protein post-translational modification that modulates a wide range of cellular functions and is involved in cancer. Dysregulation of tyrosine kinases (TKs) and protein-tyrosine phosphatases (PTPs) have been observed in multiple myeloma (MM) and acute myeloid leukemia (AML) and is a subject of study. Using recently developed mass spectrometry-based proteomics techniques, quantitative PTP expression and cellular pY profiles were generated for MM cell lines and mouse xenograft tumors, as well as primary AML samples. Integrated comprehensive analyses on these data implicated a subset of TKs and PTPs in MM and AML, with valuable insights gained on the dynamic regulation of pY in biological systems. In particular, I propose a model that describes the cellular pY state as a functional output of the total activated TKs and PTPs in the cell. My results show that the global pY profile in the cancer models is quantitatively related to the cellular levels of activated TKs and PTPs. Furthermore, the identity of the implicated TK/PTPs is system- ii dependent, demonstrating context-dependent regulation of pY. -
Spatial Sorting Enables Comprehensive Characterization of Liver Zonation
ARTICLES https://doi.org/10.1038/s42255-019-0109-9 Spatial sorting enables comprehensive characterization of liver zonation Shani Ben-Moshe1,3, Yonatan Shapira1,3, Andreas E. Moor 1,2, Rita Manco1, Tamar Veg1, Keren Bahar Halpern1 and Shalev Itzkovitz 1* The mammalian liver is composed of repeating hexagonal units termed lobules. Spatially resolved single-cell transcriptomics has revealed that about half of hepatocyte genes are differentially expressed across the lobule, yet technical limitations have impeded reconstructing similar global spatial maps of other hepatocyte features. Here, we show how zonated surface markers can be used to sort hepatocytes from defined lobule zones with high spatial resolution. We apply transcriptomics, microRNA (miRNA) array measurements and mass spectrometry proteomics to reconstruct spatial atlases of multiple zon- ated features. We demonstrate that protein zonation largely overlaps with messenger RNA zonation, with the periportal HNF4α as an exception. We identify zonation of miRNAs, such as miR-122, and inverse zonation of miRNAs and their hepa- tocyte target genes, highlighting potential regulation of gene expression levels through zonated mRNA degradation. Among the targets, we find the pericentral Wingless-related integration site (Wnt) receptors Fzd7 and Fzd8 and the periportal Wnt inhibitors Tcf7l1 and Ctnnbip1. Our approach facilitates reconstructing spatial atlases of multiple cellular features in the liver and other structured tissues. he mammalian liver is a structured organ, consisting of measurements would broaden our understanding of the regulation repeating hexagonally shaped units termed ‘lobules’ (Fig. 1a). of liver zonation and could be used to model liver metabolic func- In mice, each lobule consists of around 9–12 concentric lay- tion more precisely. -
Characterization of Mitochondrial DNA Quantity and Quality in the Human Aged and Alzheimer’S Disease Brain
medRxiv preprint doi: https://doi.org/10.1101/2021.05.20.21257456; this version posted May 25, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Characterization of mitochondrial DNA quantity and quality in the human aged and Alzheimer’s disease brain Hans-Ulrich Klein1,2,*, Caroline Trumpff3, Hyun-Sik Yang4, Annie J. Lee2, Martin Picard3,5, David A. Bennett6, Philip L. De Jager1,2,* 1Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA 2Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY 10032, USA 3Division of Behavioral Medicine, Department of Psychiatry, Columbia University Irving Medical Center, New York, NY 10032, USA 4Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA 5Merritt Center and Columbia Translational Neuroscience Initiative, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA 6Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA *Correspondance: [email protected] (HUK), [email protected] (PLD) Summary Mitochondrial dysfunction is a feature of neurodegenerative diseases, including Alzheimer’s disease (AD). Using whole-genome sequencing, we assessed mitochondrial DNA (mtDNA) heteroplasmy levels and mtDNA copy number (mtDNAcn) in 1,361 human brain samples of five brain regions from three studies. Multivariable analysis of ten common brain pathologies identified tau pathology in the dorsolateral prefrontal cortex and TDP-43 pathology in the posterior cingulate cortex as primary drivers of reduced mtDNAcn in the aged human brain. -
Prognostic Value of TIMM50 Expression in Colorectal Cancer
Clinical research Prognostic value of TIMM50 expression in colorectal cancer Bo Sun1, Jun Wang2, Yan-Feng Zhu3, Zhen-Yang Li2, Jian-Bin Xiang2, Zong-You Chen2, Zhi-Gang He4, Xiao-Dong Gu2 1Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, Corresponding authors: China 200032 Zhi-Gang He 2Department of General Surgery, Huashan Hospital, Fudan University, Shanghai, Department of General China 200040 Surgery 3Department of Nursing, Huashan Hospital, Fudan University, Shanghai, China 200040 Shanghai Songjiang District 4Department of General Surgery, Shanghai Songjiang District Central Hospital, Central Hospital Shanghai, China 201600 746 Zhongshan Middle Road Shanghai, China 201600 Submitted: 8 April 2019 Phone: +86-21-67720001 Accepted: 12 September 2019 E-mail: [email protected] Arch Med Sci Xiao-Dong Gu DOI: https://doi.org/10.5114/aoms.2020.94487 Department of General Surgery Copyright © 2020 Termedia & Banach Huashan Hospital Fudan University 12 Wulumuqi Middle Road Abstract Shanghai, China 200040 Phone: +86-21-52887333 Translocase of the inner mitochondrial membrane 50 (TIMM50) Introduction: E-mail: [email protected] is universally considered to play a key role in several malignancies. Howev- er, its role in predicting colorectal cancer (CRC) patient prognosis remains unclear. Material and methods: A total of 192 CRC patients (123 men and 69 women) who underwent radical resection participated in this study. The patients were followed up every three months after surgery for five years. TIMM50 expression in tumour tissues was measured by quantitative real-time PCR, Western blotting and immunohistochemistry. TIMM50 expression was stud- ied to assess correlations with clinicopathological factors and survival time. Results: TIMM50 expression increased significantly in CRC tumour tis- sues. -
Understanding Regulatory Mechanisms Underlying Stem Cells Helps to Identify Cancer Biomarkers
Understanding Regulatory Mechanisms Underlying Stem Cells Helps to Identify Cancer Biomarkers A dissertation submitted towards the degree Doctor of Engineering (Dr.-Ing) of the Faculty of Mathematics and Computer Science of Saarland University by Maryam Nazarieh Saarbrücken, June 2018 i iii Day of Colloquium Jun 28, 2018 Dean of the Faculty Prof. Dr. Sebastian Hack Chair of the Committee Prof. Dr. Hans-Peter Lenhof Reporters First reviewer Prof. Dr. Volkhard Helms Second reviewer Prof. Dr. Dr. Thomas Lengauer Academic Assistant Dr. Christina Backes Acknowledgements Firstly, I would like to thank Prof. Volkhard Helms for offering me a position at his group and for his supervision and support on the SFB 1027 project. I am grateful to Prof. Thomas Lengauer for his helpful comments. I am thankful to Prof. Andreas Wiese for his contribution and discussion. I would like to thank Prof. Jan Baumbach that allowed me to spend a training phase in his group during my PhD preparatory phase and the collaborative work which I performed with his PhD student Rashid Ibragimov where I proposed a heuristic algorithm based on the characteristics of protein-protein interaction networks for solving the graph edit dis- tance problem. I would like to thank Graduate School of Computer Science and Center for Bioinformatics at Saarland University, especially Prof. Raimund Seidel and Dr. Michelle Carnell for giving me an opportunity to carry out my PhD studies. Furthermore, I would like to thank to Prof. Helms for enhancing my experience by intro- ducing master students and working as their advisor for successfully accomplishing their master projects.