CCDC47 Antibody

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Efficient Professional Protein and Antibody Platforms CCDC47 Antibody Basic information: Catalog No.: UMA60617 Source: Mouse Size: 50ul/100ul Clonality: Monoclonal Concentration: 1mg/ml Isotype: Mouse IgG1 Purification: -- Useful Information: WB:1:500-1:1000 ICC:1:50-1:200 Applications: IHC:1:50-1:200 Reactivity: Human, Mouse Specificity: This antibody recognizes CCDC47 protein. Immunogen: Recombinant protein Coiled-coil domain 47 (CCDC47) is a gene located on human chromosome 17, specifically locus 17q23.3 which encodes for the protein CCDC47. The gene has several aliases including GK001 and MSTP041. The protein itself contains coiled-coil domains, the SEEEED superfamily, a domain of unknown function (DUF1682) and a transmembrane domain. The function of the protein is unknown, but it has been proposed that CCDC47 is involved in Description: calcium ion homeostasis and the endoplasmic reticulum overload response. In addition to the high levels of phosphorylation seen in CCDC47, three sul- fination sites are predicted and conserved in mammals, reptiles and birds but not in fish, amphibians or invertebrates. Five potential sumoylation sites are also seen and conserved back to the bony fish. There is no glycosylation of the protein as it is not predicted to extend into the extracellular portion of the cell. Uniprot: Q96A33 (human) BiowMW: 56 kDa Buffer: 1*TBS (pH7.4), 1%BSA, 40%Glycerol. Preservative: 0.05% Sodium Azide. Storage: Store at 4°C short term and -20°C long term. Avoid freeze-thaw cycles. Note: For research use only, not for use in diagnostic procedure. Data: Gene Universal Technology Co. Ltd www.universalbiol.com Tel: 0550-3121009 E-mail: [email protected] Efficient Professional Protein and Antibody Platforms Western blot analysis of CCDC47 on recombinant protein using anti-CCDC47 antibody at 1/1,000 dilution. ICC staining CCDC47 in F9 cells (red). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS. ICC staining CCDC47 in MCF-7 cells (red). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS. Immunohistochemical analysis of paraf- fin-embedded human lung tissue using anti-CCDC47 antibody. Counter stained with hema- toxylin. Gene Universal Technology Co. Ltd www.universalbiol.com Tel: 0550-3121009 E-mail: [email protected] .

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bioRxiv preprint doi: https://doi.org/10.1101/850776; this version posted January 19, 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. Intramembrane protease RHBDL4 cleaves oligosaccharyltransferase subunits to target them for ER-associated degradation Julia D. Knopf1, Nina Landscheidt1, Cassandra L. Pegg2, Benjamin L. Schulz2, Nathalie Kühnle1, Chao-Wei Chao1, Simon Huck1 and Marius K. Lemberg1, # 1Centre for Molecular Biology of Heidelberg University (ZMBH), DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany. 2School of Chemistry and Molecular Biosciences, ARC Training Centre for Biopharmaceutical Innovation, The University of Queensland, St Lucia QLD 4072, Australia. #Corresponding author: [email protected] Running title: RHBDL4 triggers ERAD of OST subunits Key words: Rhomboid serine protease, Rhbdd1, ubiquitin-dependent proteolysis, post- translational protein abundance control, N-linked glycosylation. Abbreviations ERAD, ER-associated degradation; OST, oligosacharyltransferase; TM, transmembrane; UIM, ubiquitin-interacting motif. Abstract The Endoplasmic Reticulum (ER)-resident intramembrane rhomboid protease RHBDL4 generates metastable protein fragments and together with the ER-associated degradation (ERAD) machinery provides a clearance mechanism for aberrant and surplus proteins. However, the endogenous substrate spectrum and with that the role of RHBDL4 in physiological ERAD is mainly unknown. Here, we use a substrate trapping approach in combination with quantitative proteomics to identify physiological RHBDL4 substrates. This revealed oligosacharyltransferase (OST) complex subunits such as the catalytic active subunit STT3A as substrates for the RHBDL4-dependent ERAD pathway. RHBDL4-catalyzed cleavage inactivates OST subunits by triggering dislocation into the cytoplasm and subsequent proteasomal degradation.
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Plenary and Platform Abstracts
American Society of Human Genetics 68th Annual Meeting PLENARY AND PLATFORM ABSTRACTS Abstract #'s Tuesday, October 16, 5:30-6:50 pm: 4. Featured Plenary Abstract Session I Hall C #1-#4 Wednesday, October 17, 9:00-10:00 am, Concurrent Platform Session A: 6. Variant Insights from Large Population Datasets Ballroom 20A #5-#8 7. GWAS in Combined Cancer Phenotypes Ballroom 20BC #9-#12 8. Genome-wide Epigenomics and Non-coding Variants Ballroom 20D #13-#16 9. Clonal Mosaicism in Cancer, Alzheimer's Disease, and Healthy Room 6A #17-#20 Tissue 10. Genetics of Behavioral Traits and Diseases Room 6B #21-#24 11. New Frontiers in Computational Genomics Room 6C #25-#28 12. Bone and Muscle: Identifying Causal Genes Room 6D #29-#32 13. Precision Medicine Initiatives: Outcomes and Lessons Learned Room 6E #33-#36 14. Environmental Exposures in Human Traits Room 6F #37-#40 Wednesday, October 17, 4:15-5:45 pm, Concurrent Platform Session B: 24. Variant Interpretation Practices and Resources Ballroom 20A #41-#46 25. Integrated Variant Analysis in Cancer Genomics Ballroom 20BC #47-#52 26. Gene Discovery and Functional Models of Neurological Disorders Ballroom 20D #53-#58 27. Whole Exome and Whole Genome Associations Room 6A #59-#64 28. Sequencing-based Diagnostics for Newborns and Infants Room 6B #65-#70 29. Omics Studies in Alzheimer's Disease Room 6C #71-#76 30. Cardiac, Valvular, and Vascular Disorders Room 6D #77-#82 31. Natural Selection and Human Phenotypes Room 6E #83-#88 32. Genetics of Cardiometabolic Traits Room 6F #89-#94 Wednesday, October 17, 6:00-7:00 pm, Concurrent Platform Session C: 33.
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Investigating Developmental and Functional Deficits in Neurodegenerative
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3D Interactions with the Growth Hormone Locus in Cellular Signalling and Cancer-Related Pathways
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Epigenetic Regulators in Neuroblastoma: Brg1, a Future Therapeutic Target
ADVERTIMENT. Lʼaccés als continguts dʼaquesta tesi queda condicionat a lʼacceptació de les condicions dʼús establertes per la següent llicència Creative Commons: http://cat.creativecommons.org/?page_id=184 ADVERTENCIA. El acceso a los contenidos de esta tesis queda condicionado a la aceptación de las condiciones de uso establecidas por la siguiente licencia Creative Commons: http://es.creativecommons.org/blog/licencias/ WARNING. The access to the contents of this doctoral thesis it is limited to the acceptance of the use conditions set by the following Creative Commons license: https://creativecommons.org/licenses/?lang=en EPIGENETIC REGULATORS IN NEUROBLASTOMA: BRG1, A FUTURE THERAPEUTIC TARGET PhD thesis presented by Luz Jubierre Zapater To obtain the degree of PhD for the Universitat Autónoma de Barcelona (UAB) PhD thesis carried out at the Translational Research in Child and Adolescent Cancer Laboratory, at Vall d’Hebron Research Institute (VHIR), under the supervision of Dr. Miguel F. Segura and Dr. Soledad Gallego Thesis affiliated to the Department of Biochemistry and Molecular Biology from the UAB, in the PhD program of Biochemistry, Molecular Biology and Biomedicine, under the tutoring of Dr. José Miguel Lizcano Universidad Autónoma de Barcelona, Septiembre 5th 2017 Dr. Miguel F. Segura Dr. Soledad Gallego (Director) (Director) Luz Jubierre Zapater (Student) 2017 Is this the real life? Is this just fantasy? Caught in a landslide No escape from reality; Open your eyes Look up to the skies and see Bohemian Rhapsody, Queen To my Mom To my Dad To Adri ACKNOWLEDGEMENTS ACKNOWLEDGEMENTS ACKNOWLEDGEMENTS Acknowledgement Desde que escribí la primera palabra en el libro de mi vida mucha gente se ha cruzado en mi camino para dejar su huella en él.
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Content Based Search in Gene Expression Databases and a Meta-analysis of Host Responses to Infection A Thesis Submitted to the Faculty of Drexel University by Francis X. Bell in partial fulﬁllment of the requirements for the degree of Doctor of Philosophy November 2015 c Copyright 2015 Francis X. Bell. All Rights Reserved. ii Acknowledgments I would like to acknowledge and thank my advisor, Dr. Ahmet Sacan. Without his advice, support, and patience I would not have been able to accomplish all that I have. I would also like to thank my committee members and the Biomed Faculty that have guided me. I would like to give a special thanks for the members of the bioinformatics lab, in particular the members of the Sacan lab: Rehman Qureshi, Daisy Heng Yang, April Chunyu Zhao, and Yiqian Zhou. Thank you for creating a pleasant and friendly environment in the lab. I give the members of my family my sincerest gratitude for all that they have done for me. I cannot begin to repay my parents for their sacriﬁces. I am eternally grateful for everything they have done. The support of my sisters and their encouragement gave me the strength to persevere to the end. iii Table of Contents LIST OF TABLES.......................................................................... vii LIST OF FIGURES ........................................................................ xiv ABSTRACT ................................................................................ xvii 1. A BRIEF INTRODUCTION TO GENE EXPRESSION............................. 1 1.1 Central Dogma of Molecular Biology........................................... 1 1.1.1 Basic Transfers .......................................................... 1 1.1.2 Uncommon Transfers ................................................... 3 1.2 Gene Expression ................................................................. 4 1.2.1 Estimating Gene Expression ............................................ 4 1.2.2 DNA Microarrays ......................................................
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bioRxiv preprint doi: https://doi.org/10.1101/2021.03.25.436925; this version posted March 25, 2021. 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. The endosome is a master regulator of plasma membrane collagen fibril assembly 1Joan Chang*, 1Adam Pickard, 1Richa Garva, 1Yinhui Lu, 2Donald Gullberg and 1Karl E. Kadler* 1Wellcome Centre for Cell-Matrix Research, Faculty of Biology, Medical and Health, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT UK, 2Department of Biomedicine and Center for Cancer Biomarkers, Norwegian Center of Excellence, University of Bergen, Norway. * Co-corresponding authors: JC email: [email protected] (orcid.org/0000-0002-7283- 9759); KEK email: [email protected] (orcid.org/0000-0003-4977-4683) Keywords: collagen-I, endocytosis, extracellular matrix, fibril, fibrillogenesis, integrin-a11, trafficking, VPS33b, [abstract] [149 word max] Collagen fibrils are the principal supporting elements in vertebrate tissues. They account for 25% of total protein mass, exhibit a broad range of size and organisation depending on tissue and stage of development, and can be under circadian clock control. Here we show that the remarkable dynamic pleomorphism of collagen fibrils is underpinned by a mechanism that distinguishes between collagen secretion and initiation of fibril assembly, at the plasma membrane. Collagen fibrillogenesis occurring at the plasma membrane requires vacuolar protein sorting (VPS) 33b (which is under circadian clock control), collagen-binding integrin-a11 subunit, and is reduced when endocytosis is inhibited. Fibroblasts lacking VPS33b secrete soluble collagen without assembling fibrils, whereas constitutive over-expression of VPS33b increases fibril number with loss of fibril rhythmicity.
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Us 2018 / 0305689 A1
US 20180305689A1 ( 19 ) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2018 /0305689 A1 Sætrom et al. ( 43 ) Pub . Date: Oct. 25 , 2018 ( 54 ) SARNA COMPOSITIONS AND METHODS OF plication No . 62 /150 , 895 , filed on Apr. 22 , 2015 , USE provisional application No . 62/ 150 ,904 , filed on Apr. 22 , 2015 , provisional application No. 62 / 150 , 908 , (71 ) Applicant: MINA THERAPEUTICS LIMITED , filed on Apr. 22 , 2015 , provisional application No. LONDON (GB ) 62 / 150 , 900 , filed on Apr. 22 , 2015 . (72 ) Inventors : Pål Sætrom , Trondheim (NO ) ; Endre Publication Classification Bakken Stovner , Trondheim (NO ) (51 ) Int . CI. C12N 15 / 113 (2006 .01 ) (21 ) Appl. No. : 15 /568 , 046 (52 ) U . S . CI. (22 ) PCT Filed : Apr. 21 , 2016 CPC .. .. .. C12N 15 / 113 ( 2013 .01 ) ; C12N 2310 / 34 ( 2013. 01 ) ; C12N 2310 /14 (2013 . 01 ) ; C12N ( 86 ) PCT No .: PCT/ GB2016 /051116 2310 / 11 (2013 .01 ) $ 371 ( c ) ( 1 ) , ( 2 ) Date : Oct . 20 , 2017 (57 ) ABSTRACT The invention relates to oligonucleotides , e . g . , saRNAS Related U . S . Application Data useful in upregulating the expression of a target gene and (60 ) Provisional application No . 62 / 150 ,892 , filed on Apr. therapeutic compositions comprising such oligonucleotides . 22 , 2015 , provisional application No . 62 / 150 ,893 , Methods of using the oligonucleotides and the therapeutic filed on Apr. 22 , 2015 , provisional application No . compositions are also provided . 62 / 150 ,897 , filed on Apr. 22 , 2015 , provisional ap Specification includes a Sequence Listing . SARNA sense strand (Fessenger 3 ' SARNA antisense strand (Guide ) Mathew, Si Target antisense RNA transcript, e . g . NAT Target Coding strand Gene Transcription start site ( T55 ) TY{ { ? ? Targeted Target transcript , e .
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Role of MicroRNA in Early Life Placental Programming of Insulin Resistance and Metabolic Health Himawan Harryanto, BSc (Biotechnology), BHSc (Hons) Discipline of Obstetrics and Gynaecology School of Paediatrics and Reproductive Health Faculty of Health Sciences The University of Adelaide South Australia Australia Thesis submitted for the fulfilment for the degree of Doctor of Philosophy (PhD) February 2014 ‘I love fools’ experiment, I am always making them’ – Charles Darwin Table of Contents TABLE OF CONTENTS LIST OF TABLES AND FIGURES ............................................................................. vi ACKNOWLEDGEMENTS ........................................................................................... x STATEMENT OF ORIGINALITY AND AUTHETICITY ...............................................xii TABLE OF ABBREVIATIONS AND BIOCHEMICAL NAMES ................................... xiii CONFERENCE PRESENTATIONS ARISING FROM THIS THESIS ........................xvi ABSTRACT……. ..................................................................................................... xviii Chapter 1 Introduction ................................................................................................. 1 1.1 Overview of the thesis .................................................................................... 3 1.2 IUGR and subsequent metabolic disease ...................................................... 6 1.2.1 Consequences of IUGR ........................................................................... 6 1.2.2 Type
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MECHANISMS OF CIRCADIAN RHYTHM PROTEIN PERIOD2 IN CARDIOPROTECTION by COLLEEN MARIE BARTMAN B.A., College of Wooster, 2012 A dissertation submitted to the Faculty of the Graduate School of the University of Colorado in partial fulfillment of the requirements for the degree of Doctor of Philosophy Cell Biology, Stem Cells, and Development Program 2018 This dissertation for the Doctor of Philosophy degree by Colleen Marie Bartman has been approved for the Cell Biology, Stem Cells, and Development Program by Julie Siegenthaler, Chair Peter Buttrick Lori Walker Bruce Appel Amanda Law Tânia Reis Tobias Eckle, Advisor Date: August 17th, 2018 ii Bartman, Colleen Marie, Ph.D., Cell Biology, Stem Cells, and Development Program Mechanisms of Circadian Rhythm Protein Period2 in Cardioprotection Dissertation directed by Professor Tobias Eckle ABSTRACT Throughout evolutionary time, all organisms and species on Earth evolved with an adaptation to consistent oscillations of sunlight and darkness, now recognized as ‘circadian rhythm.’ Single-cellular to multi-system organisms use circadian biology to synchronize to the external environment and provide predictive adaptation to changes in cellular homeostasis. Dysregulation of circadian biology has been implicated in numerous prevalent human diseases and therefore targeting the circadian machinery may provide innovative preventative or therapeutic treatment strategies. Previous studies from our lab included a wide search for ischemic preconditioning mechanisms of cardioprotection and identified the light-elicited circadian rhythm protein Period2 (PER2) to be cardioprotective from conditions of low oxygen availability, like myocardial ischemia. However, underlying mechanisms of PER2 dependent cardioprotection remained widely unknown. Our goal moving forward was to decipher the molecular nature of PER2 mediated cardioprotection and use these mechanisms to target PER2 to reduce cellular or tissue damage from hypoxia or ischemia, respectively.
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Table 1 the Statistical Metrics for Key Differentially Expressed Genes (Degs)
Table 1 The statistical metrics for key differentially expressed genes (DEGs) Agiliant Id Gene Symbol logFC pValue FDR tvalue Regulation Gene Name PREDICTED: Homo sapiens similar to Filamin-C (Gamma- filamin) (Filamin-2) (Protein FLNc) (Actin-binding-like protein) (ABP-L) (ABP-280-like protein) (LOC649056), mRNA A_24_P237896 LOC649056 0.509843 9.18E-14 4.54E-11 12.07302 Up [XR_018580] Homo sapiens programmed cell death 10 (PDCD10), transcript A_23_P18325 PDCD10 0.243111 2.8E-12 9.24E-10 10.62808 Up variant 1, mRNA [NM_007217] Homo sapiens Rho GTPase activating protein 27 (ARHGAP27), A_23_P141335 ARHGAP27 0.492709 3.97E-12 1.22E-09 10.48571 Up mRNA [NM_199282] Homo sapiens tubby homolog (mouse) (TUB), transcript variant A_23_P53110 TUB 0.528219 1.77E-11 4.56E-09 9.891033 Up 1, mRNA [NM_003320] Homo sapiens MyoD family inhibitor (MDFI), mRNA A_23_P42168 MDFI 0.314474 1.81E-10 3.74E-08 8.998697 Up [NM_005586] PREDICTED: Homo sapiens hypothetical LOC644701 A_32_P56890 LOC644701 0.444703 3.6E-10 7.09E-08 8.743973 Up (LOC644701), mRNA [XM_932316] A_32_P167111 A_32_P167111 0.873588 7.41E-10 1.4E-07 8.47781 Up Unknown Homo sapiens zinc finger protein 784 (ZNF784), mRNA A_24_P221424 ZNF784 0.686781 9.18E-10 1.68E-07 8.399687 Up [NM_203374] Homo sapiens lin-28 homolog (C. elegans) (LIN28), mRNA A_23_P74895 LIN28 0.218876 1.27E-09 2.24E-07 8.282224 Up [NM_024674] Homo sapiens ribosomal protein L5 (RPL5), mRNA A_23_P12140 RPL5 0.247598 1.81E-09 3.11E-07 8.154317 Up [NM_000969] Homo sapiens cDNA FLJ43841 fis, clone TESTI4006137.
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Supplementary Table 1 - Transcriptomics Analysis
Supplementary Table 1 - Transcriptomics analysis Gene mean lower CI upper CI mean lower CI upper CI pval regulation Control Control Control CKD5 CKD5 CKD5 TAX1BP3 166 145 188 127 110 145 0.000025249 DOWN LOC10012869 1147 878 1416 1585 1331 1838 0.000055095 UP LOC728711 219 169 268 295 244 347 0.000147349 UP CHRM2 456 281 631 752 539 965 0.000160221 UP TUFM 249 202 296 186 144 229 0.000275465 DOWN LOC10013356 1757 1336 2178 2381 1908 2853 0.000317399 UP GART 252 197 307 369 268 470 0.000337589 UP ACTG1 3496 2862 4129 2553 1821 3286 0.000358633 DOWN C19ORF12 756 482 1031 1169 846 1492 0.000364414 UP EPHA3 198 153 243 319 206 432 0.000424626 UP CALU 368 251 485 236 149 322 0.000453493 DOWN ZMAT5 304 188 420 505 330 681 0.000486754 UP CALM2 1675 1414 1935 1251 880 1622 0.000565783 DOWN CUEDC2 267 195 339 195 156 235 0.000566311 DOWN MGP 1963 1433 2493 1213 589 1837 0.000596141 DOWN CCNB1IP1 1056 818 1293 1561 1083 2038 0.000602318 UP EIF3I 457 386 527 328 210 446 0.000626151 DOWN GNPTAB 749 412 1086 1177 833 1522 0.000690099 UP RPL10A 1221 772 1669 722 355 1089 0.000773455 DOWN DOPEY2 250 151 349 394 267 522 0.000774827 UP AP3M1 773 506 1040 1163 816 1510 0.00078137 UP LOC439953 1357 1133 1580 979 624 1334 0.000806034 DOWN LOC728624 1153 694 1613 1753 1245 2262 0.000817567 UP STAP2 726 429 1023 1092 792 1392 0.000827991 UP RPLP1 1581 1414 1748 1234 888 1579 0.000853525 DOWN LOC654096 273 168 379 174 117 232 0.000855063 DOWN LOC10013377 1250 720 1780 1794 1419 2170 0.000862097 UP RARRES3 497 378 617 341 203 480 0.00102823 DOWN SLC44A4 586 302
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