Supplementary Table S1

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Table S1 Entry Entry name Status Protein names Gene names Organism Length Q969Z0 TBRG4_HUMAN reviewed Protein TBRG4 (Cell cycle progression restoration protein 2) (Cell cycle progression protein 2) (FAST kinase domain-containing protein 4) (Transforming growth factor beta regulator 4)TBRG4 CPR2 FASTKD4 KIAA0948 Homo sapiens (Human) 631 Q15397 PUM3_HUMAN reviewed Pumilio homolog 3 (HBV X-transactivated gene 5 protein) (HBV XAg-transactivated protein 5) (Minor histocompatibility antigen HA-8) (HLA-HA8)PUM3 cPERP-C KIAA0020 PUF-A XTP5 Homo sapiens (Human) 648 Q9H4M9 EHD1_HUMAN reviewed EH domain-containing protein 1 (PAST homolog 1) (hPAST1) (Testilin) EHD1 PAST PAST1 CDABP0131 Homo sapiens (Human) 534 Q52LR7 EPC2_HUMAN reviewed Enhancer of polycomb homolog 2 (EPC-like) EPC2 Homo sapiens (Human) 807 Q01831 XPC_HUMAN reviewed DNA repair protein complementing XP-C cells (Xeroderma pigmentosum group C-complementing protein) (p125) XPC XPCC Homo sapiens (Human) 940 Q8NDF8 PAPD5_HUMAN reviewed Non-canonical poly(A) RNA polymerase PAPD5 (EC 2.7.7.19) (PAP-associated domain-containing protein 5) (Terminal uridylyltransferase 3) (TUTase 3) (Topoisomerase-related function protein 4-2) (TRF4-2)PAPD5 Homo sapiens (Human) 572 O75691 UTP20_HUMAN reviewed Small subunit processome component 20 homolog (Down-regulated in metastasis protein) (Novel nucleolar protein 73) (NNP73) (Protein Key-1A6)UTP20 DRIM Homo sapiens (Human) 2785 P49750 YLPM1_HUMAN reviewed YLP motif-containing protein 1 (Nuclear protein ZAP3) (ZAP113) YLPM1 C14orf170 ZAP3 Homo sapiens (Human) 1951 Q6P9B9 INT5_HUMAN reviewed Integrator complex subunit 5 (Int5) INTS5 KIAA1698 Homo sapiens (Human) 1019 O15213 WDR46_HUMAN reviewed WD repeat-containing protein 46 (WD repeat-containing protein BING4) WDR46 BING4 C6orf11 FP221 Homo sapiens (Human) 610 O15047 SET1A_HUMAN reviewed Histone-lysine N-methyltransferase SETD1A (EC 2.1.1.43) (Lysine N-methyltransferase 2F) (SET domain-containing protein 1A) (hSET1A) (Set1/Ash2 histone methyltransferase complex subunit SET1)SETD1A KIAA0339 KMT2F SET1 SET1A Homo sapiens (Human) 1707 Q92925 SMRD2_HUMAN reviewed SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily D member 2 (60 kDa BRG-1/Brm-associated factor subunit B) (BRG1-associated factor 60B) (BAF60B)SMARCD2 BAF60B PRO2451 Homo sapiens (Human) 531 Q9Y6K5 OAS3_HUMAN reviewed 2'-5'-oligoadenylate synthase 3 ((2-5')oligo(A) synthase 3) (2-5A synthase 3) (EC 2.7.7.84) (p100 OAS) (p100OAS) OAS3 P/OKcl.4 Homo sapiens (Human) 1087 Q2KHR3 QSER1_HUMAN reviewed Glutamine and serine-rich protein 1 QSER1 Homo sapiens (Human) 1735 Q9NV31 IMP3_HUMAN reviewed U3 small nucleolar ribonucleoprotein protein IMP3 (U3 snoRNP protein IMP3) (BRMS2) IMP3 C15orf12 MRPS4 Homo sapiens (Human) 184 Q9Y6J9 TAF6L_HUMAN reviewed TAF6-like RNA polymerase II p300/CBP-associated factor-associated factor 65 kDa subunit 6L (PCAF-associated factor 65-alpha) (PAF65-alpha)TAF6L PAF65A Homo sapiens (Human) 622 Q8N6H7 ARFG2_HUMAN reviewed ADP-ribosylation factor GTPase-activating protein 2 (ARF GAP 2) (GTPase-activating protein ZNF289) (Zinc finger protein 289) ARFGAP2 ZNF289 Nbla10535 Homo sapiens (Human) 521 Q13535 ATR_HUMAN reviewed Serine/threonine-protein kinase ATR (EC 2.7.11.1) (Ataxia telangiectasia and Rad3-related protein) (FRAP-related protein 1) ATR FRP1 Homo sapiens (Human) 2644 P82663 RT25_HUMAN reviewed 28S ribosomal protein S25, mitochondrial (MRP-S25) (S25mt) MRPS25 RPMS25 Homo sapiens (Human) 173 Q8WVB6 CTF18_HUMAN reviewed Chromosome transmission fidelity protein 18 homolog (hCTF18) (CHL12) CHTF18 C16orf41 CTF18 Homo sapiens (Human) 975 Q9H9L3 I20L2_HUMAN reviewed Interferon-stimulated 20 kDa exonuclease-like 2 (EC 3.1.-.-) ISG20L2 HSD-38 HSD38 Homo sapiens (Human) 353 Q96JB5 CK5P3_HUMAN reviewed CDK5 regulatory subunit-associated protein 3 (CDK5 activator-binding protein C53) (LXXLL/leucine-zipper-containing ARF-binding protein) (Protein HSF-27)CDK5RAP3 IC53 LZAP MSTP016 OK/SW-cl.114 PP1553Homo sapiens (Human) 506 Q460N5 PAR14_HUMAN reviewed Poly [ADP-ribose] polymerase 14 (PARP-14) (EC 2.4.2.30) (ADP-ribosyltransferase diphtheria toxin-like 8) (ARTD8) (B aggressive lymphoma protein 2)PARP14 BAL2 KIAA1268 Homo sapiens (Human) 1801 Q9UBL3 ASH2L_HUMAN reviewed Set1/Ash2 histone methyltransferase complex subunit ASH2 (ASH2-like protein) ASH2L ASH2L1 Homo sapiens (Human) 628 Q15291 RBBP5_HUMAN reviewed Retinoblastoma-binding protein 5 (RBBP-5) (Retinoblastoma-binding protein RBQ-3) RBBP5 RBQ3 Homo sapiens (Human) 538 O75448 MED24_HUMAN reviewed Mediator of RNA polymerase II transcription subunit 24 (Activator-recruited cofactor 100 kDa component) (ARC100) (Cofactor required for Sp1 transcriptional activation subunit 4) (CRSP complex subunit 4) (Mediator complex subunit 24) (Thyroid hormone receptor-associated protein 4) (Thyroid hormone receptor-associated protein complex 100 kDa component) (Trap100) (hTRAP100) (Vitamin D3 receptor-interacting protein complex 100 kDa component) (DRIP100)MED24 ARC100 CRSP4 DRIP100 KIAA0130 THRAP4 TRAP100Homo sapiens (Human) 989 Q6RFH5 WDR74_HUMAN reviewed WD repeat-containing protein 74 (NOP seven-associated protein 1) WDR74 NSA1 Homo sapiens (Human) 385 Q8N3Z6 ZCHC7_HUMAN reviewed Zinc finger CCHC domain-containing protein 7 (TRAMP-like complex RNA-binding factor ZCCHC7) ZCCHC7 HSPC086 Homo sapiens (Human) 543 Q9UHR4 BI2L1_HUMAN reviewed Brain-specific angiogenesis inhibitor 1-associated protein 2-like protein 1 (BAI1-associated protein 2-like protein 1) (Insulin receptor tyrosine kinase substrate)BAIAP2L1 IRTKS Homo sapiens (Human) 511 Q9Y3C6 PPIL1_HUMAN reviewed Peptidyl-prolyl cis-trans isomerase-like 1 (PPIase) (EC 5.2.1.8) (Rotamase PPIL1) PPIL1 CYPL1 CGI-124 UNQ2425/PRO4984 Homo sapiens (Human) 166 P54198 HIRA_HUMAN reviewed Protein HIRA (TUP1-like enhancer of split protein 1) HIRA DGCR1 HIR TUPLE1 Homo sapiens (Human) 1017 Q8IVW6 ARI3B_HUMAN reviewed AT-rich interactive domain-containing protein 3B (ARID domain-containing protein 3B) (Bright and dead ringer protein) (Bright-like protein)ARID3B BDP DRIL2 Homo sapiens (Human) 561 Q96PZ2 F111A_HUMAN reviewed Protein FAM111A FAM111A KIAA1895 Homo sapiens (Human) 611 Q15554 TERF2_HUMAN reviewed Telomeric repeat-binding factor 2 (TTAGGG repeat-binding factor 2) (Telomeric DNA-binding protein) TERF2 TRBF2 TRF2 Homo sapiens (Human) 542 Q9UH17 ABC3B_HUMAN reviewed DNA dC->dU-editing enzyme APOBEC-3B (A3B) (EC 3.5.4.-) (Phorbolin-1-related protein) (Phorbolin-2/3) APOBEC3B Homo sapiens (Human) 382 P78345 RPP38_HUMAN reviewed Ribonuclease P protein subunit p38 (RNaseP protein p38) (EC 3.1.26.5) RPP38 Homo sapiens (Human) 283 Q9NV06 DCA13_HUMAN reviewed DDB1- and CUL4-associated factor 13 (WD repeat and SOF domain-containing protein 1) DCAF13 WDSOF1 HSPC064 Homo sapiens (Human) 445 Q9NPI1 BRD7_HUMAN reviewed Bromodomain-containing protein 7 (75 kDa bromodomain protein) (Protein CELTIX-1) BRD7 BP75 CELTIX1 Homo sapiens (Human) 651 Q86Y91 KI18B_HUMAN reviewed Kinesin-like protein KIF18B KIF18B Homo sapiens (Human) 864 Q9HAN9 NMNA1_HUMAN reviewed Nicotinamide/nicotinic acid mononucleotide adenylyltransferase 1 (NMN/NaMN adenylyltransferase 1) (EC 2.7.7.1) (EC 2.7.7.18) (Nicotinamide-nucleotide adenylyltransferase 1) (NMN adenylyltransferase 1) (Nicotinate-nucleotide adenylyltransferase 1) (NaMN adenylyltransferase 1)NMNAT1 NMNAT Homo sapiens (Human) 279 Q9P0U4 CXXC1_HUMAN reviewed CXXC-type zinc finger protein 1 (CpG-binding protein) (PHD finger and CXXC domain-containing protein 1) CXXC1 CFP1 CGBP PCCX1 PHF18 Homo sapiens (Human) 656 Q9UIV1 CNOT7_HUMAN reviewed CCR4-NOT transcription complex subunit 7 (EC 3.1.13.4) (BTG1-binding factor 1) (CCR4-associated factor 1) (CAF-1) (Caf1a) CNOT7 CAF1 Homo sapiens (Human) 285 Q9H9A7 RMI1_HUMAN reviewed RecQ-mediated genome instability protein 1 (BLM-associated protein of 75 kDa) (BLAP75) (FAAP75) RMI1 C9orf76 Homo sapiens (Human) 625 Q86XZ4 SPAS2_HUMAN reviewed Spermatogenesis-associated serine-rich protein 2 (Serine-rich spermatocytes and round spermatid 59 kDa protein) (p59scr) SPATS2 SCR59 SPATA10 Nbla00526 Homo sapiens (Human) 545 Q13492 PICAL_HUMAN reviewed Phosphatidylinositol-binding clathrin assembly protein (Clathrin assembly lymphoid myeloid leukemia protein) PICALM CALM Homo sapiens (Human) 652 Q8IVF7 FMNL3_HUMAN reviewed Formin-like protein 3 (Formin homology 2 domain-containing protein 3) (WW domain-binding protein 3) (WBP-3) FMNL3 FHOD3 FRL2 KIAA2014 WBP3 Homo sapiens (Human) 1028 Q9NP72 RAB18_HUMAN reviewed Ras-related protein Rab-18 RAB18 Homo sapiens (Human) 206 Q9H4H8 FA83D_HUMAN reviewed Protein FAM83D (Spindle protein CHICA) FAM83D C20orf129 Homo sapiens (Human) 585 P49454 CENPF_HUMAN reviewed Centromere protein F (CENP-F) (AH antigen) (Kinetochore protein CENPF) (Mitosin) CENPF Homo sapiens (Human) 3210 Q15022 SUZ12_HUMAN reviewed Polycomb protein SUZ12 (Chromatin precipitated E2F target 9 protein) (ChET 9 protein) (Joined to JAZF1 protein) (Suppressor of zeste 12 protein homolog)SUZ12 CHET9 JJAZ1 KIAA0160 Homo sapiens (Human) 739 Q96JP5 ZFP91_HUMAN reviewed E3 ubiquitin-protein ligase ZFP91 (EC 6.3.2.-) (Zinc finger protein 757) (Zinc finger protein 91 homolog) (Zfp-91) ZFP91 ZNF757 FKSG11 Homo sapiens (Human) 570 O75529 TAF5L_HUMAN reviewed TAF5-like RNA polymerase II p300/CBP-associated factor-associated factor 65 kDa subunit 5L (PCAF-associated factor 65 beta) (PAF65-beta)TAF5L PAF65B Homo sapiens (Human) 589 A1A4S6 RHG10_HUMAN reviewed Rho GTPase-activating protein 10 (GTPase regulator associated with focal adhesion kinase 2) (Graf-related protein
Recommended publications
  • The Rise and Fall of the Bovine Corpus Luteum
    University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Spring 5-6-2017 The Rise and Fall of the Bovine Corpus Luteum Heather Talbott University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Biochemistry Commons, Molecular Biology Commons, and the Obstetrics and Gynecology Commons Recommended Citation Talbott, Heather, "The Rise and Fall of the Bovine Corpus Luteum" (2017). Theses & Dissertations. 207. https://digitalcommons.unmc.edu/etd/207 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. THE RISE AND FALL OF THE BOVINE CORPUS LUTEUM by Heather Talbott A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor John S. Davis University of Nebraska Medical Center Omaha, Nebraska May, 2017 Supervisory Committee: Carol A. Casey, Ph.D. Andrea S. Cupp, Ph.D. Parmender P. Mehta, Ph.D. Justin L. Mott, Ph.D. i ACKNOWLEDGEMENTS This dissertation was supported by the Agriculture and Food Research Initiative from the USDA National Institute of Food and Agriculture (NIFA) Pre-doctoral award; University of Nebraska Medical Center Graduate Student Assistantship; University of Nebraska Medical Center Exceptional Incoming Graduate Student Award; the VA Nebraska-Western Iowa Health Care System Department of Veterans Affairs; and The Olson Center for Women’s Health, Department of Obstetrics and Gynecology, Nebraska Medical Center.
    [Show full text]
  • Autophagy: from Basic Science to Clinical Application
    nature publishing group REVIEW See COMMENTARY page XX Autophagy: from basic science to clinical application J Va n L i m b e r g e n 1 , 2 , 3 , C S t e v e n s 4 , E R N i m m o 1 , D C W i l s o n 2 , 3 a n d J S a t s a n g i 1 Autophagy is a cellular pathway involved in protein and organelle degradation, which is likely to represent an innate adaptation to starvation. In times of nutrient deficiency, the cell can self-digest and recycle some nonessential components through nonselective autophagy, thus sustaining minimal growth requirements until a food source becomes available. Over recent years, autophagy has been implicated in an increasing number of clinical scenarios, notably infectious diseases, cancer, neurodegenerative diseases, and autoimmunity. The recent identification of the importance of autophagy genes in the genetic susceptibility to Crohn ’ s disease suggests that a selective autophagic response may play a crucial role in the pathogenesis of common complex immune-mediated diseases. In this review, we discuss the autophagic mechanisms, their molecular regulation, and summarize their clinical relevance. This progress has led to great interest in the therapeutic potential of manipulation of both selective and nonselective autophagy in established disease. INTRODUCTION The ability to adapt to environmental change is essential for sur- Autophagy encompasses several distinct processes involving vival. This is true for the organism as a whole and for individual the delivery of portions of the cytoplasm to the lysosome for cells alike.
    [Show full text]
  • XPB Induces C1D Expression to Counteract UV-Induced Apoptosis
    Published OnlineFirst June 8, 2010; DOI: 10.1158/1541-7786.MCR-09-0467 Molecular DNA Damage and Cellular Stress Responses Cancer Research XPB Induces C1D Expression to Counteract UV-Induced Apoptosis Guang Li1, Juhong Liu2, Mones Abu-Asab1, Shibuya Masabumi3, and Yoshiro Maru4 Abstract Although C1D has been shown to be involved in DNA double-strand break repair, how C1D expression was induced and the mechanism(s) by which C1D facilitates DNA repair in mammalian cells remain poorly understood. We and others have previously shown that expression of xeroderma pigmentosum B (XPB) pro- tein efficiently compensated the UV irradiation–sensitive phenotype of 27-1 cells, which lack functional XPB. To further explore XPB-regulated genes that could be involved in UV-induced DNA repair, differential dis- play analysis of mRNA levels from CHO-9, 27-1, and 27-1 complemented with wild-type XPB was done and C1D gene was identified as one of the major genes whose expression was significantly upregulated by restoring XPB function. We found that XPB is essential to induce C1D transcription after UV irradiation. The increase in C1D expression effectively compensates for the UV-induced proteolysis of C1D and thus maintains cellular C1D level to cope with DNA damage inflicted by UV irradiation. We further showed that although insufficient to rescue 27-1 cells from UV-induced apoptosis by itself, C1D facilitates XPB DNA repair through direct interaction with XPB. Our findings provided direct evidence that C1D is associated with DNA repair complex and may promote repair of UV-induced DNA damage. Mol Cancer Res; 8(6); 885–95.
    [Show full text]
  • In Vivo Studies Using the Classical Mouse Diversity Panel
    The Mouse Diversity Panel Predicts Clinical Drug Toxicity Risk Where Classical Models Fail Alison Harrill, Ph.D The Hamner-UNC Institute for Drug Safety Sciences 0 The Importance of Predicting Clinical Adverse Drug Reactions (ADR) Figure: Cath O’Driscoll Nature Publishing 2004 Risk ID PGx Testing 1 People Respond Differently to Drugs Pharmacogenetic Markers Identified by Genome-Wide Association Drug Adverse Drug Risk Allele Reaction (ADR) Abacavir Hypersensitivity HLA-B*5701 Flucloxacillin Hepatotoxicity Allopurinol Cutaneous ADR HLA-B*5801 Carbamazepine Stevens-Johnson HLA-B*1502 Syndrome Augmentin Hepatotoxicity DRB1*1501 Ximelagatran Hepatotoxicity DRB1*0701 Ticlopidine Hepatotoxicity HLA-A*3303 Average preclinical populations and human hepatocytes lack the diversity to detect incidence of adverse events that occur only in 1/10,000 people. Current Rodent Models of Risk Assessment The Challenge “At a time of extraordinary scientific progress, methods have hardly changed in several decades ([FDA] 2004)… Toxicologists face a major challenge in the twenty-first century. They need to embrace the new “omics” techniques and ensure that they are using the most appropriate animals if their discipline is to become a more effective tool in drug development.” -Dr. Michael Festing Quantitative geneticist Toxicol Pathol. 2010;38(5):681-90 Rodent Models as a Strategy for Hazard Characterization and Pharmacogenetics Genetically defined rodent models may provide ability to: 1. Improve preclinical prediction of drugs that carry a human safety risk 2.
    [Show full text]
  • Allele-Specific Expression of Ribosomal Protein Genes in Interspecific Hybrid Catfish
    Allele-specific Expression of Ribosomal Protein Genes in Interspecific Hybrid Catfish by Ailu Chen A dissertation submitted to the Graduate Faculty of Auburn University in partial fulfillment of the requirements for the Degree of Doctor of Philosophy Auburn, Alabama August 1, 2015 Keywords: catfish, interspecific hybrids, allele-specific expression, ribosomal protein Copyright 2015 by Ailu Chen Approved by Zhanjiang Liu, Chair, Professor, School of Fisheries, Aquaculture and Aquatic Sciences Nannan Liu, Professor, Entomology and Plant Pathology Eric Peatman, Associate Professor, School of Fisheries, Aquaculture and Aquatic Sciences Aaron M. Rashotte, Associate Professor, Biological Sciences Abstract Interspecific hybridization results in a vast reservoir of allelic variations, which may potentially contribute to phenotypical enhancement in the hybrids. Whether the allelic variations are related to the downstream phenotypic differences of interspecific hybrid is still an open question. The recently developed genome-wide allele-specific approaches that harness high- throughput sequencing technology allow direct quantification of allelic variations and gene expression patterns. In this work, I investigated allele-specific expression (ASE) pattern using RNA-Seq datasets generated from interspecific catfish hybrids. The objective of the study is to determine the ASE genes and pathways in which they are involved. Specifically, my study investigated ASE-SNPs, ASE-genes, parent-of-origins of ASE allele and how ASE would possibly contribute to heterosis. My data showed that ASE was operating in the interspecific catfish system. Of the 66,251 and 177,841 SNPs identified from the datasets of the liver and gill, 5,420 (8.2%) and 13,390 (7.5%) SNPs were identified as significant ASE-SNPs, respectively.
    [Show full text]
  • Oncogenic H-Ras Up-Regulates Expression of ERCC1 to Protect Cells from Platinum-Based Anticancer Agents
    [CANCER RESEARCH 64, 4849–4857, July 15, 2004] Oncogenic H-Ras Up-Regulates Expression of ERCC1 to Protect Cells from Platinum-Based Anticancer Agents Cha-Kyung Youn,1 Mi-Hwa Kim,1 Hyun-Ju Cho,1 Hong-Beum Kim,1 In-Youb Chang,1 Myung-Hee Chung,3 and Ho Jin You1,2 1Research Center for Proteineous Materials and 2Department of Pharmacology, School of Medicine, Chosun University, Gwangju, and 3Department of Pharmacology, School of Medicine, Seoul National University, Seoul, Korea ABSTRACT elucidated, evidence suggests that the activated Ras may contribute to cisplatin resistance by stimulating the DNA repair activity (9, 12, 13). Tumors frequently contain mutations in the ras genes, resulting in the Hence, there has been considerable interest in determining which constitutive activation of the Ras-activated signaling pathway. The acti- vation of Ras is involved not only in tumor progression but also in the proteins mediate the altered DNA repair capacity in activated Ras- development of resistance of the tumor cells to platinum-based chemo- containing cells. However, the downstream target genes of the onco- therapeutic agents. To investigate the potential mechanisms underlying genic Ras, which are involved in the enhancement of the DNA repair this resistance, we analyzed the effect of activated H-Ras on the expression activity, are unclear. of the nucleotide excision repair genes. Here we identified ERCC1, which Cisplatin is one of the most effective and widely used anticancer is one of the key enzymes involved in nucleotide excision repair, as being drugs for treating human solid tumors (14). However, its therapeutic markedly up-regulated by the activated H-Ras.
    [Show full text]
  • Characterization of Gf a Drosophila Trimeric G Protein Alpha Subunit
    Characterization of Gf a Drosophila trimeric G protein alpha subunit Naureen Quibria Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2012 © 2012 Naureen Quibria All rights reserved Abstract Characterization of Gf a Drosophila trimeric G-protein alpha subunit Naureen Quibria In the morphogenesis of tissue development, how coordination of patterning and growth achieve the correct organ size and shape is a principal question in biology. Efficient orchestrating mechanisms are required to achieve this and cells have developed sophisticated systems for reception and interpretation of the multitude of extracellular stimuli to which they are exposed. Plasma membrane receptors play a key role in the transmission of such signals. G-protein coupled receptors (GPCRs) are the largest class of cell surface receptors that respond to an enormous diversity of extracellular stimuli, and are critical mediators of cellular signal transduction in eukaryotic organisms. Signaling through GPCRs has been well characterized in many biological contexts. While they are a major class of signal transducers, there are not many defined instances where GPCRs have been implicated in the process of development to date. The Drosophila wing provides an ideal model system to elucidate and address the role of GPCRs in development, as its growth is regulated by a small number of conserved signaling pathways. In my thesis work, I address the role of a trimeric G alpha protein in Drosophila, Gαf, and what part it may play in development. In particular, I explore the role of Gαf as an alpha subunit of a trimeric complex, to determine what heptahelical receptors might act as its cognate receptor.
    [Show full text]
  • Characterization and Stress Response of the Jmjc Domain-Containing Histone Demethylase Gene Family in the Allotetraploid Cotton Species Gossypium Hirsutum
    plants Article Characterization and Stress Response of the JmjC Domain-Containing Histone Demethylase Gene Family in the Allotetraploid Cotton Species Gossypium hirsutum 1, 2, 2, 3 3 3 Jie Zhang y, Junping Feng y, Wei Liu *, Zhongying Ren , Junjie Zhao , Xiaoyu Pei , Yangai Liu 3, Daigang Yang 3 and Xiongfeng Ma 1,3,* 1 Zhengzhou Research Base, State Key Laboratory of Cotton Biology, School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China; [email protected] 2 Collaborative Innovation Center of Henan Grain Crops, Agronomy College, Henan Agricultural University, Zhengzhou 450002, China; [email protected] 3 State Key Laboratory of Cotton Biology, Institute of Cotton Research, Chinese Academy of Agricultural Sciences, Anyang 455000, China; [email protected] (Z.R.); [email protected] (J.Z.); [email protected] (X.P.); [email protected] (Y.L.); [email protected] (D.Y.) * Correspondence: [email protected] (W.L.); [email protected] (X.M.) These authors contributed equally to this work. y Received: 12 October 2020; Accepted: 18 November 2020; Published: 20 November 2020 Abstract: Histone modification is an important epigenetic modification that controls gene transcriptional regulation in eukaryotes. Histone methylation is accomplished by histone methyltransferase and can occur on two amino acid residues, arginine and lysine. JumonjiC (JmjC) domain-containing histone demethylase regulates gene transcription and chromatin structure by changing the methylation state of the lysine residue site and plays an important role in plant growth and development. In this study, we carried out genome-wide identification and comprehensive analysis of JmjC genes in the allotetraploid cotton species Gossypium hirsutum. In total, 50 JmjC genes were identified and in G.
    [Show full text]
  • Modes of Interaction of KMT2 Histone H3 Lysine 4 Methyltransferase/COMPASS Complexes with Chromatin
    cells Review Modes of Interaction of KMT2 Histone H3 Lysine 4 Methyltransferase/COMPASS Complexes with Chromatin Agnieszka Bochy ´nska,Juliane Lüscher-Firzlaff and Bernhard Lüscher * ID Institute of Biochemistry and Molecular Biology, Medical School, RWTH Aachen University, Pauwelsstrasse 30, 52057 Aachen, Germany; [email protected] (A.B.); jluescher-fi[email protected] (J.L.-F.) * Correspondence: [email protected]; Tel.: +49-241-8088850; Fax: +49-241-8082427 Received: 18 January 2018; Accepted: 27 February 2018; Published: 2 March 2018 Abstract: Regulation of gene expression is achieved by sequence-specific transcriptional regulators, which convey the information that is contained in the sequence of DNA into RNA polymerase activity. This is achieved by the recruitment of transcriptional co-factors. One of the consequences of co-factor recruitment is the control of specific properties of nucleosomes, the basic units of chromatin, and their protein components, the core histones. The main principles are to regulate the position and the characteristics of nucleosomes. The latter includes modulating the composition of core histones and their variants that are integrated into nucleosomes, and the post-translational modification of these histones referred to as histone marks. One of these marks is the methylation of lysine 4 of the core histone H3 (H3K4). While mono-methylation of H3K4 (H3K4me1) is located preferentially at active enhancers, tri-methylation (H3K4me3) is a mark found at open and potentially active promoters. Thus, H3K4 methylation is typically associated with gene transcription. The class 2 lysine methyltransferases (KMTs) are the main enzymes that methylate H3K4. KMT2 enzymes function in complexes that contain a necessary core complex composed of WDR5, RBBP5, ASH2L, and DPY30, the so-called WRAD complex.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS
    Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen,
    [Show full text]
  • Utx Is Required for Proper Induction of Ectoderm and Mesoderm During Differentiation of Embryonic Stem Cells
    Utx Is Required for Proper Induction of Ectoderm and Mesoderm during Differentiation of Embryonic Stem Cells Cristina Morales Torres1,2, Anne Laugesen1,2, Kristian Helin1,2,3* 1 Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark, 2 Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark, 3 The Danish Stem Cell Center, University of Copenhagen, Copenhagen, Denmark Abstract Embryonic development requires chromatin remodeling for dynamic regulation of gene expression patterns to ensure silencing of pluripotent transcription factors and activation of developmental regulators. Demethylation of H3K27me3 by the histone demethylases Utx and Jmjd3 is important for the activation of lineage choice genes in response to developmental signals. To further understand the function of Utx in pluripotency and differentiation we generated Utx knockout embryonic stem cells (ESCs). Here we show that Utx is not required for the proliferation of ESCs, however, Utx contributes to the establishment of ectoderm and mesoderm in vitro. Interestingly, this contribution is independent of the catalytic activity of Utx. Furthermore, we provide data showing that the Utx homologue, Uty, which is devoid of detectable demethylase activity, and Jmjd3 partly compensate for the loss of Utx. Taken together our results show that Utx is required for proper formation of ectoderm and mesoderm in vitro, and that Utx, similar to its C.elegans homologue, has demethylase dependent and independent functions. Citation: Morales Torres C, Laugesen A, Helin K (2013) Utx Is Required for Proper Induction of Ectoderm and Mesoderm during Differentiation of Embryonic Stem Cells. PLoS ONE 8(4): e60020. doi:10.1371/journal.pone.0060020 Editor: Qiang Wu, National University of Singapore, Singapore Received December 13, 2012; Accepted February 21, 2013; Published April 3, 2013 Copyright: ß 2013 Morales Torres et al.
    [Show full text]