Supplementary Figure 1. Network Map Associated with Upregulated Canonical Pathways Shows Interferon Alpha As a Key Regulator
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Genetic Associations Between Voltage-Gated Calcium Channels (Vgccs) and Autism Spectrum Disorder (ASD)
Liao and Li Molecular Brain (2020) 13:96 https://doi.org/10.1186/s13041-020-00634-0 REVIEW Open Access Genetic associations between voltage- gated calcium channels and autism spectrum disorder: a systematic review Xiaoli Liao1,2 and Yamin Li2* Abstract Objectives: The present review systematically summarized existing publications regarding the genetic associations between voltage-gated calcium channels (VGCCs) and autism spectrum disorder (ASD). Methods: A comprehensive literature search was conducted to gather pertinent studies in three online databases. Two authors independently screened the included records based on the selection criteria. Discrepancies in each step were settled through discussions. Results: From 1163 resulting searched articles, 28 were identified for inclusion. The most prominent among the VGCCs variants found in ASD were those falling within loci encoding the α subunits, CACNA1A, CACNA1B, CACN A1C, CACNA1D, CACNA1E, CACNA1F, CACNA1G, CACNA1H, and CACNA1I as well as those of their accessory subunits CACNB2, CACNA2D3, and CACNA2D4. Two signaling pathways, the IP3-Ca2+ pathway and the MAPK pathway, were identified as scaffolds that united genetic lesions into a consensus etiology of ASD. Conclusions: Evidence generated from this review supports the role of VGCC genetic variants in the pathogenesis of ASD, making it a promising therapeutic target. Future research should focus on the specific mechanism that connects VGCC genetic variants to the complex ASD phenotype. Keywords: Autism spectrum disorder, Voltage-gated calcium -
Michael Antoni
Stress Management Effects on Biological and Molecular Pathways in Women Treated for Breast Cancer APS/NCI Conference on “Toward Precision Cancer Care: Biobehavioral Contributions to the Exposome” Chicago IL Michael H. Antoni, Ph.D. Department of Psychology Div of Health Psychology Director, Center for Psycho- Oncology Director, Cancer Prevention and Control Research, Sylvester Cancer Center University of Miami E.g., Stress Management for Women with Breast Cancer • Rationale – Breast Cancer (BCa) is a stressor – Challenges of surgery and adjuvant tx – Patient assets can facilitate adjustment – Cognitive Behavioral Stress Management (CBSM) can fortify these assets in women with BCa – Improving Psychosocial Adaptation may Affect Physiological Adaptation Theoretical Model for CBSM during CA Tx Negative Adapt Positive Adapt Physical Funct Awareness C ∆ Cog Appraisals B Physical Emot Processing + Health Beh. S Health M Relaxation QOL Social Support Normalize endocrine and immune regulation Antoni (2003). Stress Management for Women with Breast Cancer. American Psychological Association. Assessment Time Points T1 T2 T3 T4 B SMART-10 wks. 2-8 wks post 3 months post 6 months post surgery One year post surgery Topics of CBSM Week Relaxation Stress Management 1 PMR 7 Stress & Awareness 2 PMR 4/D.B. Stress & Awareness/Stress Appraisals 3 D.B./PMR Disease-Specific, Automatic Thoughts 4 Autogenics Auto. Thghts, Distortions, Thght Rep. 5 D.B./Visualiz. Cognitive Restructuring 6 Sunlight Med. Effective Coping I 7 Color Meditation Effective Coping -
Protein Interaction Network of Alternatively Spliced Isoforms from Brain Links Genetic Risk Factors for Autism
ARTICLE Received 24 Aug 2013 | Accepted 14 Mar 2014 | Published 11 Apr 2014 DOI: 10.1038/ncomms4650 OPEN Protein interaction network of alternatively spliced isoforms from brain links genetic risk factors for autism Roser Corominas1,*, Xinping Yang2,3,*, Guan Ning Lin1,*, Shuli Kang1,*, Yun Shen2,3, Lila Ghamsari2,3,w, Martin Broly2,3, Maria Rodriguez2,3, Stanley Tam2,3, Shelly A. Trigg2,3,w, Changyu Fan2,3, Song Yi2,3, Murat Tasan4, Irma Lemmens5, Xingyan Kuang6, Nan Zhao6, Dheeraj Malhotra7, Jacob J. Michaelson7,w, Vladimir Vacic8, Michael A. Calderwood2,3, Frederick P. Roth2,3,4, Jan Tavernier5, Steve Horvath9, Kourosh Salehi-Ashtiani2,3,w, Dmitry Korkin6, Jonathan Sebat7, David E. Hill2,3, Tong Hao2,3, Marc Vidal2,3 & Lilia M. Iakoucheva1 Increased risk for autism spectrum disorders (ASD) is attributed to hundreds of genetic loci. The convergence of ASD variants have been investigated using various approaches, including protein interactions extracted from the published literature. However, these datasets are frequently incomplete, carry biases and are limited to interactions of a single splicing isoform, which may not be expressed in the disease-relevant tissue. Here we introduce a new interactome mapping approach by experimentally identifying interactions between brain-expressed alternatively spliced variants of ASD risk factors. The Autism Spliceform Interaction Network reveals that almost half of the detected interactions and about 30% of the newly identified interacting partners represent contribution from splicing variants, emphasizing the importance of isoform networks. Isoform interactions greatly contribute to establishing direct physical connections between proteins from the de novo autism CNVs. Our findings demonstrate the critical role of spliceform networks for translating genetic knowledge into a better understanding of human diseases. -
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. -
Function of Deptor and Its Roles in Hematological Malignancies
www.aging-us.com AGING 2021, Vol. 13, No. 1 Review Function of Deptor and its roles in hematological malignancies Mario Morales-Martinez1, Alan Lichtenstein2, Mario I. Vega1,2 1Molecular Signal Pathway in Cancer Laboratory, UIMEO, Oncology Hospital, Siglo XXI National Medical Center, IMSS, México, México 2Department of Medicine, Hematology-Oncology Division, Greater Los Angeles VA Healthcare Center, UCLA Medical Center, Jonsson Comprehensive Cancer Center, Los Angeles, CA 90024, USA Correspondence to: Mario I. Vega; email: [email protected] Keywords: Deptor, Multiple Myeloma, leukemia, Non-Hodgkin Lymphoma, hematological malignances Received: November 6, 2020 Accepted: December 10, 2020 Published: January 7, 2020 Copyright: © 2020 Morales-Martinez et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Deptor is a protein that interacts with mTOR and that belongs to the mTORC1 and mTORC2 complexes. Deptor is capable of inhibiting the kinase activity of mTOR. It is well known that the mTOR pathway is involved in various signaling pathways that are involved with various biological processes such as cell growth, apoptosis, autophagy, and the ER stress response. Therefore, Deptor, being a natural inhibitor of mTOR, has become very important in its study. Because of this, it is important to research its role regarding the development and progression of human malignancies, especially in hematologic malignancies. Due to its variation in expression in cancer, it has been suggested that Deptor can act as an oncogene or tumor suppressor depending on the cellular or tissue context. -
Properties of Human Genes Guided by Their Enrichment in Rare and Common Variants
Properties of human genes guided by their enrichment in rare and common variants Authors: Eman Alhuzimi, Luis G. Leal, Michael J.E. Sternberg, Alessia David Affiliation: Structural Bioinformatics Group, Department of Life Sciences, Imperial College London, London, SW7 2AZ, UK SUPPLEMENTARY MATERIAL Construction of the dataset Genetic variants occurring in protein coding genes were extracted from ExAC (version 0.3, Release: 13-Jan-2015), UniProt (humsavar.txt, release: 04-Feb-2015) and ClinVar (release:7-Jan-2015). Variants were classified as ‘disease-causing’ if a disease association was reported in humsavar.txt or ClinVar. For variants reported in ClinVar, we defined the variant as disease-causing only if it was annotated as “pathogenic”. In order to avoid a potential bias, variants annotated as “likely pathogenic” were not included in the analysis. Variants were classified as ‘neutral’ when no association with disease was present (variants reported as “polymorphisms” in humsavar.txt and variants from ExAC, not reported as disease-causing in other databases). Non-disease variants were divided according to their global minor allele frequencies (MAF) into: ‘rare variants’ (MAF < 0.01) and ‘common variants’ (MAF ≥ 0.01). Global MAF data were extracted from Ensembl using the BioMart data-mining tool. We used the global MAF calculated in the ExAC project. For variants not reported in ExAC database we used the global MAF reported in dbSNP (which is calculated from the 1000Genomes project), when available. Variants with no MAF information or reported as “unclassified” in humsavar.txt, were not included in the analysis. When the gene enrichment analysis (described below) was performed, one gene overlapped between the disease- and rare- EVsets and three genes between the disease- and common- EVsets. -
Noninvasive Sleep Monitoring in Large-Scale Screening of Knock-Out Mice
bioRxiv preprint doi: https://doi.org/10.1101/517680; this version posted January 11, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. Noninvasive sleep monitoring in large-scale screening of knock-out mice reveals novel sleep-related genes Shreyas S. Joshi1*, Mansi Sethi1*, Martin Striz1, Neil Cole2, James M. Denegre2, Jennifer Ryan2, Michael E. Lhamon3, Anuj Agarwal3, Steve Murray2, Robert E. Braun2, David W. Fardo4, Vivek Kumar2, Kevin D. Donohue3,5, Sridhar Sunderam6, Elissa J. Chesler2, Karen L. Svenson2, Bruce F. O'Hara1,3 1Dept. of Biology, University of Kentucky, Lexington, KY 40506, USA, 2The Jackson Laboratory, Bar Harbor, ME 04609, USA, 3Signal solutions, LLC, Lexington, KY 40503, USA, 4Dept. of Biostatistics, University of Kentucky, Lexington, KY 40536, USA, 5Dept. of Electrical and Computer Engineering, University of Kentucky, Lexington, KY 40506, USA. 6Dept. of Biomedical Engineering, University of Kentucky, Lexington, KY 40506, USA. *These authors contributed equally Address for correspondence and proofs: Shreyas S. Joshi, Ph.D. Dept. of Biology University of Kentucky 675 Rose Street 101 Morgan Building Lexington, KY 40506 U.S.A. Phone: (859) 257-2805 FAX: (859) 257-1717 Email: [email protected] Running title: Sleep changes in knockout mice bioRxiv preprint doi: https://doi.org/10.1101/517680; this version posted January 11, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. -
Interactions Between the Parasite Philasterides Dicentrarchi and the Immune System of the Turbot Scophthalmus Maximus.A Transcriptomic Analysis
biology Article Interactions between the Parasite Philasterides dicentrarchi and the Immune System of the Turbot Scophthalmus maximus.A Transcriptomic Analysis Alejandra Valle 1 , José Manuel Leiro 2 , Patricia Pereiro 3 , Antonio Figueras 3 , Beatriz Novoa 3, Ron P. H. Dirks 4 and Jesús Lamas 1,* 1 Department of Fundamental Biology, Institute of Aquaculture, Campus Vida, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain; [email protected] 2 Department of Microbiology and Parasitology, Laboratory of Parasitology, Institute of Research on Chemical and Biological Analysis, Campus Vida, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain; [email protected] 3 Institute of Marine Research, Consejo Superior de Investigaciones Científicas-CSIC, 36208 Vigo, Spain; [email protected] (P.P.); antoniofi[email protected] (A.F.); [email protected] (B.N.) 4 Future Genomics Technologies, Leiden BioScience Park, 2333 BE Leiden, The Netherlands; [email protected] * Correspondence: [email protected]; Tel.: +34-88-181-6951; Fax: +34-88-159-6904 Received: 4 September 2020; Accepted: 14 October 2020; Published: 15 October 2020 Simple Summary: Philasterides dicentrarchi is a free-living ciliate that causes high mortality in marine cultured fish, particularly flatfish, and in fish kept in aquaria. At present, there is still no clear picture of what makes this ciliate a fish pathogen and what makes fish resistant to this ciliate. In the present study, we used transcriptomic techniques to evaluate the interactions between P. dicentrarchi and turbot leucocytes during the early stages of infection. The findings enabled us to identify some parasite genes/proteins that may be involved in virulence and host resistance, some of which may be good candidates for inclusion in fish vaccines. -
The Effect of Galactose on the Expression of Genes Regulated by Rrp6p
The Review: A Journal of Undergraduate Student Research Volume 18 Article 1 2017 The Effect of Galactose on the Expression of Genes Regulated by Rrp6p Mary Megan Pelkowski Saint John Fisher College, [email protected] Kevin Callahan Saint John Fisher College, [email protected] Follow this and additional works at: https://fisherpub.sjfc.edu/ur Part of the Biochemistry Commons, and the Molecular Genetics Commons How has open access to Fisher Digital Publications benefited ou?y Recommended Citation Pelkowski, Mary Megan and Callahan, Kevin. "The Effect of Galactose on the Expression of Genes Regulated by Rrp6p." The Review: A Journal of Undergraduate Student Research 18 (2017): -. Web. [date of access]. <https://fisherpub.sjfc.edu/ur/vol18/iss1/1>. This document is posted at https://fisherpub.sjfc.edu/ur/vol18/iss1/1 and is brought to you for free and open access by Fisher Digital Publications at St. John Fisher College. For more information, please contact [email protected]. The Effect of Galactose on the Expression of Genes Regulated by Rrp6p Abstract Gene expression is a multi-faceted phenomenon, governed not only by the sequence of nucleotides, but also by the extent to which a particular gene gets transcribed, how the transcript is processed, and whether or not the transcript ever makes it out of the nucleus. Rrp6p is a 5’-3’ exonuclease that can function independently and as part of the nuclear exosome in Saccharomyces cerevisiae (Portin, 2014). It degrades various types of aberrant RNA species including small nuclear RNAs, small nucleolar RNAs, telomerase RNA, unspliced RNAs, and RNAs that have not been properly packaged for export (Butler & Mitchell, 2010). -
IER3 Is a Crucial Mediator of Tap73b-Induced Apoptosis In
OPEN IER3 is a crucial mediator of SUBJECT AREAS: TAp73b-induced apoptosis in cervical CELL DEATH TUMOUR SUPPRESSORS cancer and confers etoposide sensitivity Hanyong Jin1*, Dae-Shik Suh2*, Tae-Hyoung Kim3, Ji-Hyun Yeom4, Kangseok Lee4 & Jeehyeon Bae5 Received 14 September 2014 1Department of Pharmacy, CHA University, Seongnam, 463-836, Korea, 2Department of Obstetrics and Gynecology, Asan Accepted Medical Center, University of Ulsan College of Medicine, 3Department of Biochemistry, Chosun University School of Medicine, 4 5 9 January 2015 Gwangju 501-759, Korea, Department of Life Science, Chung-Ang University, Seoul, 156-756, Korea, School of Pharmacy, Chung-Ang University, Seoul, 156-756, Korea. Published 10 February 2015 Infection with high-risk human papillomaviruses (HPVs) causes cervical cancer. E6 oncoprotein, an HPV gene product, inactivates the major gatekeeper p53. In contrast, its isoform, TAp73b, has become increasingly important, as it is resistant to E6. However, the intracellular signaling mechanisms that account Correspondence and for TAp73b tumor suppressor activity in cervix are poorly understood. Here, we identified that IER3 is a requests for materials novel target gene of TAp73b. In particular, TAp73b exclusively transactivated IER3 in cervical cancer cells, should be addressed to whereas p53 and TAp63 failed to do. IER3 efficiently induced apoptosis, and its knockdown promoted K.L. (kangseok@cau. survival of HeLa cells. In addition, TAp73b-induced cell death, but not p53-induced cell death, was inhibited ac.kr) or J.B. upon IER3 silencing. Moreover, etoposide, a DNA-damaging chemotherapeutics, upregulated TAp73b and IER3 in a c-Abl tyrosine kinase-dependent manner, and the etoposide chemosensitivity of HeLa cells was ([email protected]) largely determined by TAp73b-induced IER3. -
P1382-Human Cellexp FLT-3 Ligand, Recombinant Mouse
FOR RESEARCH ONLY! Human CellExp™ FLT-3 Ligand, Mouse Recombinant CATALOG #: P1382-50 P1382-10 AMOUNT: 50 µg 10 µg FLT3LG, FL, FLT3L, Flt3 ligand ALTERNATE NAMES: MOL. WT. The protein has a calculated MW of 20.2 kDa. The protein migrates as 25-33 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation. SOURCE: HEK 293 cells PURITY: >90% as determined by SDS-PAGE. ENDOTOXIN: Less than 1.0 EU per μg by the LAL method FORM: Lyophilized FORMULATION: Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization. Centrifuge the vial prior to opening. Reconstitute in sterile deionized water to a concentration of 100 µg/ml. RECONSTITUTION: Do not vortex. It is recommended to store at -20°C. SPECIFIC ACTIVITY: Immobilized Mouse Flt-3 Ligand, His Tag at 1 μg/mL (100 μL/well) can bind Human Flt-3/Flk-2 Fc Chimera with a linear range of 1-5 ng/mL STORAGE CONDITIONS: Store at -20°C. After reconstitution, aliquot and store at -20°C and use within 3 months. Avoid repeated freezing and thawing cycles. DESCRIPTION: FMS-like tyrosine kinase 3 ligand (Flt-3 Ligand) is also known as FL, Flt3L and FLT3LG, is an α-helical cytokine that promotes the differentiation of multiple hematopoietic cell lineages. FLT3LG is expressed as a noncovalentlylinked dimer by T cells and bone marrow and thymic fibroblasts. Each 36 kDa chain carries approximately 12 kDa of N- and O- linked carbohydrates. FLT3LG is structurally homologous to stem cell factor (SCF) and colony stimulating facor 1 (CSF-1). -
Human Receptor-Interacting Serine/Threonine-Protein Kinase 2 (RIPK2) a Target Enabling Package (TEP)
Human Receptor-Interacting Serine/Threonine-Protein Kinase 2 (RIPK2) A Target Enabling Package (TEP) Gene ID / UniProt ID / EC 8767 / O43353 / - Target Nominator SGC Internal Nomination SGC Authors Peter Canning, Daniel M. Pinkas, Joshua C. Bufton, Sarah Picaud, Jennifer A. Ward, Catherine Rogers, Benedict-Tilman Berger, Stefan Knapp, Susanne Muller-Knapp, Paul E. Brennan, Kilian V. M. Huber, Panagis Filippakopoulos, Alex N. Bullock Collaborating Authors Matous Hrdinka1, Qui Ruan2, Chalada Suebsuwong3, Lisa Schlicher1, Bing Dai2, Jenny L. Maki2, Soumya S. Ray4, Danish Saleh5, Sameer Nikhar6, Tobias Schwerd7, Holm H.Uhlig7, Gregory D. Cuny6, Alexei Degterev2, Mads Gyrd-Hansen1 Target PI Alex N. Bullock (SGC Oxford) Therapeutic Area(s) Inflammatory diseases Disease Relevance Mutations in the NOD2-RIPK2 pathway identify RIPK2 a potential therapeutic target in auto-immune and inflammatory conditions such as Crohn’s disease, Blau syndrome, early-onset osteoarthritis and multiple sclerosis. Date Approved by TEP Evaluation 13th June 2018 Group Document version Version 3 Document version date October 2020 Citation Peter Canning, Daniel M. Pinkas, Joshua C. Bufton, Sarah Picaud, Jennifer A. Ward, Catherine Rogers, … Alex N. Bullock. (2018). Human Receptor- Interacting Serine/Threonine-Protein Kinase 2 (RIPK2); A Target Enabling Package. Zenodo. http://doi.org/10.5281/zenodo.1344501 Affiliations 1. Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford 2. Department of Developmental, Molecular & Chemical Biology, Tufts University School of Medicine 3. Department of Chemistry, Science and Research Building 2, University of Houston 4. Center for Neurologic Diseases, Department of Neurology, Brigham & Women's Hospital and Harvard Medical School 5. Medical Scientist Training Program and Program in Neuroscience, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine 6.