Brandon Downing

ORCID: 0000-0001-8666-9263
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About
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Research Areas
  • Neurofibromatosis and Schwannoma Cases
  • DNA Repair Mechanisms
  • Peptidase Inhibition and Analysis
  • Fungal and yeast genetics research
  • Connective tissue disorders research
  • Aortic aneurysm repair treatments
  • Genomics and Chromatin Dynamics
  • Cardiac tumors and thrombi
  • CRISPR and Genetic Engineering
  • Neuropeptides and Animal Physiology
  • Neuroblastoma Research and Treatments
  • Signaling Pathways in Disease
  • Carcinogens and Genotoxicity Assessment
  • Plant Genetic and Mutation Studies
  • Phagocytosis and Immune Regulation
  • Aortic Disease and Treatment Approaches
  • Macrophage Migration Inhibitory Factor
  • Chromosomal and Genetic Variations
  • Cardiovascular Issues in Pregnancy
  • Nerve injury and regeneration
  • Genetic Neurodegenerative Diseases

Washington University in St. Louis
2018-2020

Indiana University – Purdue University Indianapolis
2008-2018

University of Indianapolis
2018

Indiana University School of Medicine
2013-2016

Indiana University
2013

Duke University
2007

Inverted DNA repeats are known to cause genomic instabilities.Here we demonstrate that double-strand breaks (DSBs) introduced a large distance from inverted in the yeast (Saccharomyces cerevisiae) chromosome lead burst of instability.Inverted located as far 21 kb each other caused rearrangements response single DSB.We DSB initiates pairing interaction between repeats, resulting formation dicentric dimers.Furthermore, observed propagation cells containing dimers led gross chromosomal...

10.1128/mcb.01740-06 article EN Molecular and Cellular Biology 2007-01-23

Abstract Break-induced replication (BIR) is an important process of DNA metabolism that has been implicated in the restart collapsed forks, as well various chromosomal instabilities, including loss heterozygosity, translocations, and alternative telomere lengthening. Therefore, knowledge how BIR carried out regulated for better understanding maintenance genomic stability eukaryotes. Here we present a new yeast experimental system enables genetic control to be investigated. Analysis mutations...

10.1534/genetics.108.087940 article EN Genetics 2008-08-01

Background— Neurofibromatosis type 1 (NF1) is a genetic disorder resulting from mutations in the NF1 tumor suppressor gene. Neurofibromin, protein product of , functions as negative regulator Ras activity circulating hematopoietic and vascular wall cells, which are critical for maintaining vessel homeostasis. patients have evidence chronic inflammation development premature cardiovascular disease, including arterial aneurysms, may manifest sudden death. However, molecular pathogenesis...

10.1161/circulationaha.113.006320 article EN Circulation 2013-12-27

Neurofibromatosis type 1 (NF1) results from mutations in the NF1 tumor-suppressor gene, which encodes neurofibromin, a negative regulator of diverse Ras signaling cascades. Arterial stenosis is nonneoplastic manifestation that predisposes some patients to debilitating morbidity and sudden death. Recent murine studies demonstrate Nf1 heterozygosity (Nf1(+/-)) monocytes/macrophages significantly enhances intimal proliferation after arterial injury. However, downstream effector pathway...

10.1016/j.ajpath.2013.09.022 article EN cc-by-nc-nd American Journal Of Pathology 2013-11-07

Double strand DNA breaks (DSBs) are dangerous events that can result from various causes including environmental assaults or the collapse of replication. While efficient and precise repair DSBs is essential for cell survival, faulty lead to genetic instability, making choice DSB an important step. Here we report inverted repeats (IRs) placed near a channel its accurate pathway leads gene conversion instead break-induced replication (BIR) instabilities. The effect IRs explained by their...

10.1371/journal.pgen.1007543 article EN cc-by PLoS Genetics 2018-08-09

Objectives Marfan syndrome and Ehlers-Danlos represent two connective tissue vascular diseases requiring unique consideration in their surgical care. A comprehensive national review encompassing all hospitalizations for the Syndrome patient population is lacking. Methods The National (Nationwide) Inpatient Sample from 2010 to 2014 was reviewed inpatient surgery procedures including those with a diagnosis of syndrome. estimates rates were generated provided weights. Patient demographics,...

10.1177/1708538120925597 article EN Vascular 2020-05-19
Kevin A. Roth Audra Cox Martha Furie Reviews Steven L. Gonias W. Marie Campana and 95 more Huang‐Ge Zhang William E. Grizzle Dominic De Nardo Christine De Nardo Eicke Latz Radha Gopal Javier Rangel‐Moreno Beth Fallert Junecko Daniel Mallon Kong Chen Derek Pociask John W. Connell Todd A. Reinhart John F. Alcorn Ted M. Ross Jay K. Kolls Shabaana A. Khader Zuzana Krejciova Paul A. De Sousa Jean Manson James W. Ironside Mark Head Allison R. Larson Chung‐Wei Lee Cecilia Lezcano Qian Zhan John Huang Andrew Fischer Gëorge F. Murphy Ras-Mek-Erk Signaling Regulates Nf Heterozygous Neointima Brian K. Stansfield Waylan Bessler Raghuveer Singh Mali Julie A. Mund Brandon Downing Reuben Kapur David R. Ingram Victoria Marsh Durban Marnix Jansen Emma Jane Davies Folkert H.M. Morsink Johan Offerhaus Alan Clarke Chinmay Mantri Jyoti Velamarti Mantri Jui Pandhare Chandravanu Dash Tanuja L. Gutti Jaclyn Knibbe Edward Makarov Jinjin Zhang Govardhana Rao Yannam Santhi Gorantla Yimin Sun D. Evan Mercer Hiroshi Suemizu James L. Wisecarver Natalia A. Osna Tatiana K. Bronich Larisa Y. Poluektova Tatyana V. Masyuk Seungok Lee Brynn N. Radtke Angela J. Stroope Bing Huang Jesús M. Bañales Anatoliy I. Masyuk Patrick L. Splinter Sergio A. Gradilone Gabriella B. Gajdos Nicholas F. LaRusso Zan Huang Hai‐Bin Ruan Zeng-Di Zhang Weiqian Chen Zhaoyu Lin Hu Zeng Xiang Gao Min Gao Ren‐Chin Wu Alice Herlinger Kai Lee Yap Jung-Won Kim Tian‐Li Wang Ie‐Ming Shih Xin Cheng Ping He Taehee Lee Hailan Yao Rena Li Yong Shen Abhijit Ghosh Guanyi Lu

10.1016/s0002-9440(13)00749-9 article EN publisher-specific-oa American Journal Of Pathology 2013-12-11
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