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Christopher B. Eckman

Christopher B. Eckman

D-Index & Metrics

Biology and Biochemistry

D-Index
67
Citations
33829
World Ranking
8034
National Ranking
3642

Overview

Christopher B. Eckman is affiliated with the Mayo Clinic in the United States and has contributed to several research studies primarily in the fields of Biochemistry, Genetics and Molecular Biology, and Medicine. Their work spans multiple subfields including Cell Biology, Molecular Biology, Surgery, Oncology, and Pulmonary and Respiratory Medicine.

The scientist's research covers key topics such as Ubiquitin and proteasome pathways, Cancer-related molecular pathways, Microtubule and mitosis dynamics, Endoplasmic Reticulum stress and disease, Heat shock proteins research, Calpain protease function and regulation, and Gallbladder and bile duct disorders.

Christopher B. Eckman has published several research papers, notably:

  • Deletion of the Ubiquitin Ligase CHIP Leads to the Accumulation, But Not the Aggregation, of Both Endogenous Phospho- and Caspase-3-Cleaved Tau Species (2021, UNC Libraries)
  • The high-affinity HSP90-CHIP complex recognizes and selectively degrades phosphorylated tau client proteins (2020, UNC Libraries)
  • S4300 Seronegative Pernicious Anemia from Chronic Atrophic Gastritis Mimicking Thrombotic Thrombocytopenic Purpura (2023, The American Journal of Gastroenterology)
  • Subcapsular Splenic Hematoma After Diagnostic Colonoscopy: A Case Report (2024, Cureus)

The frequent coauthors collaborating with Eckman include:

  • Chad A. Dickey
  • Dennis W. Dickson
  • Judith Dunmore
  • Cam Patterson
  • Michael Hutton

Research publications by Eckman have appeared in a variety of venues, including:

  • UNC Libraries
  • The American Journal of Gastroenterology
  • Cureus

Best Publications

  • Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease.

    D. Scheuner;C. Eckman;C. Eckman;M. Jensen;X. Song

  • An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants

    Nobuhiro Suzuki;Tobun T. Cheung;Xiao Dan Cai;Asano Odaka

  • Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo

    David R. Borchelt;Gopal Thinakaran;Christopher B. Eckman;Christopher B. Eckman;Michael K. Lee

  • Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1

    Karen Duff;Karen Duff;Chris Eckman;Cindy Zehr;Cindy Zehr;Xin Yu

  • Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP.

    Jada Lewis;Dennis W. Dickson;Wen-Lang Lin;Louise Chisholm

  • Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo

    Wesley Farris;Stefan Mansourian;Yang Chang;Loren Lindsley

  • Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes

    Leigh Holcomb;Marcia N. Gordon;Eileen Mcgowan;Xin Yu

  • The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Abeta protofibril formation.

    Camilla Nilsberth;Anita Westlind-Danielsson;Anita Westlind-Danielsson;Christopher B. Eckman;Margaret M. Condron

  • Amyloid β Protein (Aβ) in Alzheimeri's Disease Brain BIOCHEMICAL AND IMMUNOCYTOCHEMICAL ANALYSIS WITH ANTIBODIES SPECIFIC FOR FORMS ENDING AT Aβ40 OR Aβ42(43)

    Stephen A. Gravina;Libin Ho;Christopher B. Eckman;Kristin E. Long

  • The high-affinity HSP90-CHIP complex recognizes and selectively degrades phosphorylated tau client proteins

    Chad A. Dickey;Chad A. Dickey;Adeela Kamal;Karen Lundgren;Natalia Klosak

  • Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice

    Eileen McGowan;Fiona Pickford;Jungsu Kim;Luisa Onstead

  • Age-Related CNS Disorder and Early Death in Transgenic FVB/N Mice Overexpressing Alzheimer Amyloid Precursor Proteins

    Karen K. Hsiao;David R. Borchelt;Kristine Olson;Rosa Johannsdottir

  • The Secreted -Amyloid Precursor Protein Ectodomain APPs Is Sufficient to Rescue the Anatomical, Behavioral, and Electrophysiological Abnormalities of APP-Deficient Mice

    Sabine Ring;Sascha W. Weyer;Susanne B. Kilian;Elaine Waldron

  • Linkage of Plasma Aβ42 to a Quantitative Locus on Chromosome 10 in Late-Onset Alzheimer's Disease Pedigrees

    Nilufer Ertekin-Taner;Neill Graff-Radford;Linda H. Younkin;Christopher Eckman

  • SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein.

    Costantino Iadecola;Fangyi Zhang;Kiyoshi Niwa;Chris Eckman

  • Biochemical detection of Aβ isoforms: implications for pathogenesis, diagnosis, and treatment of Alzheimer’s disease

    Todd E Golde;Christopher B Eckman;Steven G Younkin

  • Degradation of the Alzheimer's Amyloid β Peptide by Endothelin-converting Enzyme

    Elizabeth A. Eckman;Dana Kim Reed;Christopher B. Eckman

  • Amyloid-β peptide levels in brain are inversely correlated with insulysin activity levels in vivo

    Bonnie C. Miller;Elizabeth A. Eckman;Kumar Sambamurti;Kumar Sambamurti;Nicole Dobbs

  • Substrate-targeting γ-secretase modulators

    Thomas L. Kukar;Thomas B. Ladd;Maralyssa A. Bann;Patrick C. Fraering;Patrick C. Fraering

  • Cellular prion protein regulates beta-secretase cleavage of the Alzheimer's amyloid precursor protein

    Edward T Parkin;Nicole T Watt;Ishrut Hussain;Elizabeth A Eckman

Frequent Co-Authors

Mike Hutton
Mike Hutton Eli Lilly (United States)
Todd E. Golde
Todd E. Golde Emory University
Chad A. Dickey
Chad A. Dickey University of South Florida
Rudolph E. Tanzi
Rudolph E. Tanzi Harvard University
Kumar Sambamurti
Kumar Sambamurti Medical University of South Carolina
Dennis J. Selkoe
Dennis J. Selkoe Brigham and Women's Hospital
John Hardy
John Hardy University College London
Nobuhiro Suzuki
Nobuhiro Suzuki Sophia University

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