1) an Arrayed Pipeline for Genetic Interaction Mapping of HIV Host-Dependency Factors 2) the HIV Ve-MAP Highlights Complexes
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Polyclonal Antibody to APC11 / ANAPC11 - Serum
OriGene Technologies, Inc. OriGene Technologies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] R1503 Polyclonal Antibody to APC11 / ANAPC11 - Serum Alternate names: Anaphase-promoting complex subunit 11, Cyclosome subunit 11, HSPC214, Hepatocellular carcinoma-associated RING finger protein Quantity: 0.1 ml Concentration: 85 mg/ml (by Refractometry) Background: APC11 is also known as Anaphase promoting complex subunit 11, APC11, Cyclosome subunit 11, Hepatocellular carcinoma associated RING finger protein, and HSPC214. APC11 is a component of the anaphase promoting complex/cyclosome (APC/C), a cell cycle-regulated E3 ubiquitin ligase that controls progression through mitosis and the G1 phase of the cell cycle. APC11 may function to recruit the E2 ubiquitin-conjugating enzymes to the complex. APC11 interacts with the cullin domain of ANAPC2 and also interacts with UBE2D2. APC11 shows both a cytoplasmic and nuclear localization. APC11 is expressed at high levels in skeletal muscle and heart; in moderate levels in brain, kidney, and liver; and at low levels in colon, thymus, spleen, small intestine, placenta, lung and peripheral blood leukocyte. APC11 is a member of the RING-type zinc finger family and is auto-ubiquitinylated. Uniprot ID: Q9NYG5 NCBI: NP_001002244.1 GeneID: 51529 Host: Rabbit Immunogen: This APC11 antibody was prepared from whole rabbit serum produced by repeated immunizations with a synthetic peptide corresponding to amino acids 76-84 of Human APC11 (C-terminal) coupled to KLH. -
Ankrd9 Is a Metabolically-Controlled Regulator of Impdh2 Abundance and Macro-Assembly
ANKRD9 IS A METABOLICALLY-CONTROLLED REGULATOR OF IMPDH2 ABUNDANCE AND MACRO-ASSEMBLY by Dawn Hayward A dissertation submitted to The Johns Hopkins University in conformity with the requirements of the degree of Doctor of Philosophy Baltimore, Maryland April 2019 ABSTRACT Members of a large family of Ankyrin Repeat Domains proteins (ANKRD) regulate numerous cellular processes by binding and changing properties of specific protein targets. We show that interactions with a target protein and the functional outcomes can be markedly altered by cells’ metabolic state. ANKRD9 facilitates degradation of inosine monophosphate dehydrogenase 2 (IMPDH2), the rate-limiting enzyme in GTP biosynthesis. Under basal conditions ANKRD9 is largely segregated from the cytosolic IMPDH2 by binding to vesicles. Upon nutrient limitation, ANKRD9 loses association with vesicles and assembles with IMPDH2 into rod-like structures, in which IMPDH2 is stable. Inhibition of IMPDH2 with Ribavirin favors ANKRD9 binding to rods. The IMPDH2/ANKRD9 assembly is reversed by guanosine, which restores association of ANKRD9 with vesicles. The conserved Cys109Cys110 motif in ANKRD9 is required for the vesicles-to-rods transition as well as binding and regulation of IMPDH2. ANKRD9 knockdown increases IMPDH2 levels and prevents formation of IMPDH2 rods upon nutrient limitation. Thus, the status of guanosine pools affects the mode of ANKRD9 action towards IMPDH2. Advisor: Dr. Svetlana Lutsenko, Department of Physiology, Johns Hopkins University School of Medicine Second reader: -
An Amplified Fatty Acid-Binding Protein Gene Cluster In
cancers Review An Amplified Fatty Acid-Binding Protein Gene Cluster in Prostate Cancer: Emerging Roles in Lipid Metabolism and Metastasis Rong-Zong Liu and Roseline Godbout * Department of Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB T6G 1Z2, Canada; [email protected] * Correspondence: [email protected]; Tel.: +1-780-432-8901 Received: 6 November 2020; Accepted: 16 December 2020; Published: 18 December 2020 Simple Summary: Prostate cancer is the second most common cancer in men. In many cases, prostate cancer grows very slowly and remains confined to the prostate. These localized cancers can usually be cured. However, prostate cancer can also metastasize to other organs of the body, which often results in death of the patient. We found that a cluster of genes involved in accumulation and utilization of fats exists in multiple copies and is expressed at much higher levels in metastatic prostate cancer compared to localized disease. These genes, called fatty acid-binding protein (or FABP) genes, individually and collectively, promote properties associated with prostate cancer metastasis. We propose that levels of these FABP genes may serve as an indicator of prostate cancer aggressiveness, and that inhibiting the action of FABP genes may provide a new approach to prevent and/or treat metastatic prostate cancer. Abstract: Treatment for early stage and localized prostate cancer (PCa) is highly effective. Patient survival, however, drops dramatically upon metastasis due to drug resistance and cancer recurrence. The molecular mechanisms underlying PCa metastasis are complex and remain unclear. It is therefore crucial to decipher the key genetic alterations and relevant molecular pathways driving PCa metastatic progression so that predictive biomarkers and precise therapeutic targets can be developed. -
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. -
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Supplementary Figure S1. Results of flow cytometry analysis, performed to estimate CD34 positivity, after immunomagnetic separation in two different experiments. As monoclonal antibody for labeling the sample, the fluorescein isothiocyanate (FITC)- conjugated mouse anti-human CD34 MoAb (Mylteni) was used. Briefly, cell samples were incubated in the presence of the indicated MoAbs, at the proper dilution, in PBS containing 5% FCS and 1% Fc receptor (FcR) blocking reagent (Miltenyi) for 30 min at 4 C. Cells were then washed twice, resuspended with PBS and analyzed by a Coulter Epics XL (Coulter Electronics Inc., Hialeah, FL, USA) flow cytometer. only use Non-commercial 1 Supplementary Table S1. Complete list of the datasets used in this study and their sources. GEO Total samples Geo selected GEO accession of used Platform Reference series in series samples samples GSM142565 GSM142566 GSM142567 GSM142568 GSE6146 HG-U133A 14 8 - GSM142569 GSM142571 GSM142572 GSM142574 GSM51391 GSM51392 GSE2666 HG-U133A 36 4 1 GSM51393 GSM51394 only GSM321583 GSE12803 HG-U133A 20 3 GSM321584 2 GSM321585 use Promyelocytes_1 Promyelocytes_2 Promyelocytes_3 Promyelocytes_4 HG-U133A 8 8 3 GSE64282 Promyelocytes_5 Promyelocytes_6 Promyelocytes_7 Promyelocytes_8 Non-commercial 2 Supplementary Table S2. Chromosomal regions up-regulated in CD34+ samples as identified by the LAP procedure with the two-class statistics coded in the PREDA R package and an FDR threshold of 0.5. Functional enrichment analysis has been performed using DAVID (http://david.abcc.ncifcrf.gov/) -
APC/C Is Essential for Hematopoiesis and Impaired in Aplastic Anemia
www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 38), pp: 63360-63369 Research Paper APC/C is essential for hematopoiesis and impaired in aplastic anemia Jia Wang1,*, Min-Zhi Yin2,*, Ke-Wen Zhao1,*, Fang Ke1,*, Wen-Jie Jin3, Xiao-Lin Guo1, Tian-Hui Liu1, Xiao-Ye Liu1, Hao Gu1, Xiao-Min Yu1, Zhen Li1, Li-Li Mu1, Deng-Li Hong1, Jing Chen4 and Guo-Qiang Chen1 1Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, 200025, China 2Department of Pathology, Shanghai Children’s Medical Center, SJTU-SM, Shanghai, 200025, China 3Department of Orthopaedics, Shanghai Ninth People's Hospital, SJTU-SM, Shanghai, 200025, China 4Key Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology and Oncology, Shanghai Children’s Medical Center, SJTU-SM, Shanghai, 200127, China *These authors have contributed equally to this work Correspondence to: Guo-Qiang Chen, email: [email protected] Jing Chen, email: [email protected] Deng-Li Hong, email: [email protected] Keywords: anaphase promoting complex/cyclosome (APC/C), Anapc2, hematopoietic stem and progenitor cells (HSPCs), dormant HPSCs, aplastic anemia Received: November 22, 2016 Accepted: June 02, 2017 Published: June 28, 2017 Copyright: Wang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Anaphase promoting complex/cyclosome (APC/C) is essential for cell cycle progression. -
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine -
Hsa-Mir-21-5P
Supporting Information An exosomal urinary miRNA signature for early diagnosis of renal fibrosis in Lupus Nephritis 1 2 2 1 1 Cristina Solé , Teresa Moliné , Marta Vidal , Josep Ordi-Ros , Josefina Cortés-Hernández 1Hospital Universitari Vall d’Hebron, Vall d’Hebron Research Institute (VHIR), Lupus Unit, Barcelona, Spain; [email protected] (C.S); [email protected] (J.O-R.); [email protected] (J.C-H.) 2 Hospital Universitari Vall d’Hebron, Department of Renal Pathology, Barcelona, Spain; [email protected] (T.M); [email protected] (M.V). INDEX 1. SI Materials and Methods......................................................................................3 2. SI References…………………………………………………………………………….7 2. SI Figures................................................................................................................8 4. SI Tables................................................................................................................21 2 SI Materials and Methods Patients and samples Patients with biopsy-proven active LN were recruited from the Lupus Unit at Vall d’Hebron Hospital (N=45). All patients fulfilled at least 4 of the American College of rheumatology (ACR) revised classification criteria for SLE [1]. Healthy donors were used as controls (N=20). Urine samples were collected from each patient 1 day before renal biopsy and processed immediately to be stored at -80ºC. Patients with urinary tract infection, diabetes mellitus, pregnancy, malignancy and non-lupus-related renal failure were excluded. In addition, key laboratory measurements were obtained including complement levels (C3 and C4), anti-double-stranded DNA (anti-dsDNA), 24-h proteinuria, blood urea nitrogen (BUN), serum creatinine and the estimated glomerular filtration ratio (eGFR) using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula [2]. SLE disease activity was assessed by the SLE Disease Activity Index 2000 update (SLEDAI-2Ks; range 0–105) [3]. -
Table S2.Up Or Down Regulated Genes in Tcof1 Knockdown Neuroblastoma N1E-115 Cells Involved in Differentbiological Process Anal
Table S2.Up or down regulated genes in Tcof1 knockdown neuroblastoma N1E-115 cells involved in differentbiological process analysed by DAVID database Pop Pop Fold Term PValue Genes Bonferroni Benjamini FDR Hits Total Enrichment GO:0044257~cellular protein catabolic 2.77E-10 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 537 13588 1.944851 8.64E-07 8.64E-07 5.02E-07 process ISG15, ATG7, PSENEN, LOC100046898, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, ASB8, DCUN1D1, PSMA6, SIAH1A, TRIM32, RNF138, GM12396, RNF20, USP17L5, FBXO11, RAD23B, NEDD8, UBE2V2, RFFL, CDC GO:0051603~proteolysis involved in 4.52E-10 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 534 13588 1.93519 1.41E-06 7.04E-07 8.18E-07 cellular protein catabolic process ISG15, ATG7, PSENEN, LOC100046898, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, ASB8, DCUN1D1, PSMA6, SIAH1A, TRIM32, RNF138, GM12396, RNF20, USP17L5, FBXO11, RAD23B, NEDD8, UBE2V2, RFFL, CDC GO:0044265~cellular macromolecule 6.09E-10 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 609 13588 1.859332 1.90E-06 6.32E-07 1.10E-06 catabolic process ISG15, RBM8A, ATG7, LOC100046898, PSENEN, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, ASB8, DCUN1D1, PSMA6, SIAH1A, TRIM32, RNF138, GM12396, RNF20, XRN2, USP17L5, FBXO11, RAD23B, UBE2V2, NED GO:0030163~protein catabolic process 1.81E-09 MKRN1, PPP2R5C, VPRBP, MYLIP, CDC16, ERLEC1, MKRN2, CUL3, 556 13588 1.87839 5.64E-06 1.41E-06 3.27E-06 ISG15, ATG7, PSENEN, LOC100046898, CDCA3, ANAPC1, ANAPC2, ANAPC5, SOCS3, ENC1, SOCS4, -
Chapter 4.1 a 400 Kb Duplication, 2.4 Mb Triplication and 130 Kb
High-resolution karyotyping by oligonucleotide microarrays : the next revolution in cytogenetics Gijsbers, A.C.J. Citation Gijsbers, A. C. J. (2010, November 30). High-resolution karyotyping by oligonucleotide microarrays : the next revolution in cytogenetics. Retrieved from https://hdl.handle.net/1887/16187 Version: Corrected Publisher’s Version Licence agreement concerning inclusion of doctoral thesis in the License: Institutional Repository of the University of Leiden Downloaded from: https://hdl.handle.net/1887/16187 Note: To cite this publication please use the final published version (if applicable). Chapter 4.1 A 400 kb duplication, 2.4 Mb triplication and 130 kb duplication of 9q34.3 in a patient with severe mental retardation Antoinet CJ Gijsbers, Emilia K Bijlsma, Marjan M Weiss, Egbert Bakker, Martijn H Breuning, Mariëtte JV Hoffer and Claudia AL Ruivenkamp Center for Human and Clinical Genetics; Leiden University Medical Center (LUMC), Leiden, The Netherlands Eur J Med Genet 2008;51:479-487 Chapter 4 Abstract The presence of a duplication as well as a triplication in one chromosome is a rare rearrangement and not easy to distinguish with routine chromosomal analysis. Recent developments in array technologies, however, not only allow screening of the whole genome at a higher resolution, but also make it possible to characterize complex chromosomal rearrangements in more detail. Here we report a molecular cytogenetic analysis of a 16-year old female with severe mental retardation and an abnormality on the end of the long arm of chromosome 9. Subtelomeric multiplex ligation-dependent probe amplification (MLPA) analysis revealed that the extra material originated from the telomeric end of chromosome 9q. -
Combinatorial Avidity Selection of Mosaic Landscape Phages Targeted at Breast Cancer Cells—An Alternative Mechanism of Directed Molecular Evolution
viruses Article Combinatorial Avidity Selection of Mosaic Landscape Phages Targeted at Breast Cancer Cells—An Alternative Mechanism of Directed Molecular Evolution Valery A. Petrenko 1,* , James W. Gillespie 1 , Hai Xu 1,2, Tiffany O’Dell 1 and Laura M. De Plano 1,3 1 Department of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849, USA 2 National Veterinary Biological Medicine Engineering Research Center, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, Jiangsu, China 3 Department of Chemical Sciences, Biological, Pharmaceutical and Environmental, University of Messina, Viale F. Stagno d’Alcontres 31, 98166 Messina, Italy * Correspondence: [email protected]; Tel.: +1-334-844-2897 Received: 2 August 2019; Accepted: 22 August 2019; Published: 26 August 2019 Abstract: Low performance of actively targeted nanomedicines required revision of the traditional drug targeting paradigm and stimulated the development of novel phage-programmed, self-navigating drug delivery vehicles. In the proposed smart vehicles, targeting peptides, selected from phage libraries using traditional principles of affinity selection, are substituted for phage proteins discovered through combinatorial avidity selection. Here, we substantiate the potential of combinatorial avidity selection using landscape phage in the discovery of Short Linear Motifs (SLiMs) and their partner domains. We proved an algorithm for analysis of phage populations evolved through multistage screening of landscape phage libraries against the MDA-MB-231 breast cancer cell line. The suggested combinatorial avidity selection model proposes a multistage accumulation of Elementary Binding Units (EBU), or Core Motifs (CorMs), in landscape phage fusion peptides, serving as evolutionary initiators for formation of SLiMs. Combinatorial selection has the potential to harness directed molecular evolution to create novel smart materials with diverse novel, emergent properties. -
2Q13 Microdeletions
2q13 microdeletions rarechromo.org 2q13 microdeletions A 2q13 microdeletion is a rare genetic condition caused by a small piece of missing genetic material from one of the body’s chromosomes - chromosome 2. Deletions can vary in size but those that are too small to be visible under the microscope using standard techniques are called microdeletions. For typical and healthy development, chromosomes should contain the expected amount of genetic material. Like most other chromosome disorders, having a missing piece of chromosome 2 may affect the development and intellectual abilities of a child. The outcome of having a 2q13 microdeletion is very variable and depends on a number of factors including what and how much genetic material is missing. Background on chromosomes Our bodies are made up of different types of cells, almost all of which contain the same chromosomes. Each chromosome consists of DNA that carries the code for hundreds to thousands of genes. Genes can be thought of as individual instruction booklets (or recipes) that contain all the genetic information that tells the body how to develop, grow and function. Chromosomes (and hence genes) usually come in pairs with one member of each chromosome pair being inherited from each parent. Most cells of the human body have a total of 46 (23 pairs of) chromosomes. The egg and the sperm cells, however, have 23 unpaired chromosomes, so that when the egg and sperm join together at conception, the chromosomes pair up to make a total of 46. Of these 46 chromosomes, 44 are grouped in 22 pairs, numbered 1 to 22.