Daniel Goldberg
Washington University in St Louis, MO·Microbiology & Immunology
Malaria, caused by the parasite Plasmodium falciparum, kills by infecting red blood cells and can leave patients vulnerable to other infections. Drug resistance creates an ongoing need for new drug targets.
- Fields
Microbiology & Immunology
Biochemistry
Pharmacology
- Topics
malaria
Plasmodium falciparum
PfNCR1
- Grants
- 2 known grants, through Jun 2030
What they work on
- Define how two new putative allosteric inhibitors of PfNCR1, a malaria parasite cholesterol pump, block its function, combining cryo-EM structures with physiological, genetic and cell biological approaches.
- Identify the proteins in the contact zone between the parasite plasma membrane and the surrounding vacuolar membrane by studying transporters found near PfNCR1 through proximity biotinylation, using protein biochemistry and structural studies.
- Test which known signaling pathways let heme-loaded HRPII, a secreted parasite protein, suppress the oxidative burst of neutrophil-like dHL60 cells, using targeted molecular blockade of each pathway.
- Find genes essential for HRPII's effects on neutrophil-like cells using RNA-seq profiling and a genome-wide CRISPR/Cas9 knockout screen.
More about the research
Two projects study parasite proteins from different angles. One examines a cholesterol pump that the parasite needs to survive and that drugs might block. The other asks how a protein the parasite releases into the blood weakens the immune system's defenses against bacteria.
Why it matters
Antimalarial drug resistance demands new drug targets. Understanding how PfNCR1 inhibitors block cholesterol transport could guide development of new malaria drugs. Separately, finding the pathways by which the parasite protein HRPII disables neutrophils could point to therapies that restore immune function and prevent dangerous bacterial infections in people, especially children, recovering from malaria.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Elizabeth Egan
Stanford University, CA·Microbiology & Immunology
Determine which precise steps of Plasmodium falciparum invasion of human red blood cells require the surface proteins CD44 and CD55, using live-cell imaging and advanced microscopy of CRISPR-edited cultured red blood cells.
Jennifer Small-Saunders
Columbia University, NY·Microbiology & Immunology·Early-career
Identify long noncoding RNAs and tRNA-derived fragments that change in artemisinin-resistant versus sensitive Plasmodium falciparum after drug exposure or isoleucine starvation, using transcriptomics.
James Chen
University of California-San Francisco, CA·Biophysics·Early-career
Purify the cell-wall proteins PonA1 and CrgA and their partner complexes directly from Mycobacterium tuberculosis and M. smegmatis, and determine their 3D structures by single-particle cryo-EM.
The school
Washington University in St Louis: 97 labs on PI Pages, $1.2B a year on research, 365 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.