Norma Andrews

About

Norma Andrews is a Professor in the Department of Cell Biology & Molecular Genetics at the University of Maryland. Her research focuses on the molecular strategies utilized by intracellular pathogens to interact with their host cells and on fundamental cell biological processes subverted by pathogens during infection. She has uncovered mechanisms by which the protozoan Trypanosoma cruzi invades host cells, notably a Ca2+-dependent mobilization and fusion of lysosomes with the plasma membrane, a process exploited by the parasite to form a membrane-bounded vacuole for entry. Her work has also demonstrated that Ca2+-triggered lysosomal exocytosis plays a central role in mammalian cell membrane resealing after wounding. Currently, her research investigates the role of the lysosomal enzyme acid sphingomyelinase in triggering endocytic processes responsible for removing toxin pores and lesions from the plasma membrane. Additionally, she studies the molecular mechanisms of intracellular survival of Leishmania, a parasite causing serious human disease worldwide. Norma Andrews earned her Ph.D. from the University of Sao Paulo, Brazil, in 1983.

Research topics

• Biochemistry
• Cell biology
• Biology
• Immunology
• Microbiology

Selected publications

• Plasma membrane repair

  Current Biology · 2018-04-01 · 175 citations

  reviewOpen access1st authorCorresponding
  PublisherOA PDFDOI

• PLEKHM1/DEF8/RAB7 complex regulates lysosome positioning and bone homeostasis

  JCI Insight · 2016-10-19 · 97 citations

  articleOpen access

  Mutations of the Plekhm1 gene in humans and rats cause osteopetrosis, an inherited bone disease characterized by diminished bone resorption by osteoclasts. PLEKHM1 binds to RAB7 and is critical for lysosome trafficking. However, the molecular mechanisms by which PLEKHM1 regulates lysosomal pathways remain unknown. Here, we generated germline and conditional Plekhm1 -deficient mice. These mice displayed no overt abnormalities in major organs, except for an increase in trabecular bone mass. Furthe…

  PublisherOA PDFDOI

• The iron-dependent mitochondrial superoxide dismutase SODA promotes Leishmania virulence

  Journal of Biological Chemistry · 2017-05-27 · 71 citations

  articleOpen accessSenior authorCorresponding

  virulence by protecting the parasites against mitochondrion-generated oxidative stress and by initiating ROS-mediated signaling mechanisms required for the differentiation of infective forms.

  PublisherOA PDFDOI

• Gaucher disease iPSC-derived osteoblasts have developmental and lysosomal defects that impair bone matrix deposition

  Human Molecular Genetics · 2017-12-29 · 49 citations

  articleOpen access

  Gaucher disease (GD) is caused by bi-allelic mutations in GBA1, the gene that encodes acid β-glucocerebrosidase (GCase). Individuals affected by GD have hematologic, visceral and bone abnormalities, and in severe cases there is also neurodegeneration. To shed light on the mechanisms by which mutant GBA1 causes bone disease, we examined the ability of human induced pluripotent stem cells (iPSC) derived from patients with Types 1, 2 and 3 GD, to differentiate to osteoblasts and carry out bone depo…

  PublisherOA PDFDOI

• Detection of Lysosomal Exocytosis by Surface Exposure of Lamp1 Luminal Epitopes

  Methods in molecular biology · 2017-01-01 · 45 citations

  article1st authorCorresponding
  PublisherDOI

Recent grants

• Molecular Determinants of Intracellular Survival and Replication in Leishmania

  NIH · $3.8M · 2007–2021

• NIH Grant R37AI034867

  NIH · $4.5M · 2014

• NIH Grant R01AI034867

  NIH · $2.2M · 2005

Frequent coauthors

• Victor Nussenzweig

  New York University

  24 shared

• Vincent Idone

  Regeneron (United States)

  22 shared

• Sabyasachi Chakrabarti

  Yale University

  22 shared

• Chau Huynh

  22 shared

• E. Robbins

  22 shared

• Christina Tam

  Alcohol Research Group

  21 shared

• Bidyottam Mittra

  University of Maryland, College Park

  19 shared

• Andrew R. Flannery

  Smiths Detection (United States)

  19 shared

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