Cagla Eroglu
· Duke Health Distinguished Professor of Cell BiologyDuke University · Genetics and Genomics
Active 1996–2026
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About
Cagla Eroglu is a Duke University faculty member holding the positions of Duke Health Distinguished Professor of Cell Biology, Professor of Cell Biology, and Vice Chair of Research. She is also a Professor in Neurobiology and a Faculty Network Member of the Duke Institute for Brain Sciences. Additionally, she is an Associate of the Duke Initiative for Science & Society and an Affiliate of the Duke Regeneration Center. Her research focuses on cell and molecular biology, with involvement in programs such as Developmental & Stem Cell Biology and the University Program in Genetics and Genomics. She is based at the 333A Nanaline Duke Building in Durham, North Carolina.
Research topics
- Biology
- Neuroscience
- Genetics
- Internal medicine
- Medicine
- Cell biology
- Physiology
- Psychology
- Biochemistry
Selected publications
Chemico-genetic discovery of astrocytic control of inhibition in vivo
Nature · 2020 · 245 citations
Neuron · 2020 · 196 citations
Prenatal environmental stressors impair postnatal microglia function and adult behavior in males
Cell Reports · 2022 · 102 citations
Gestational exposure to environmental toxins and socioeconomic stressors is epidemiologically linked to neurodevelopmental disorders with strong male bias, such as autism. We model these prenatal risk factors in mice by co-exposing pregnant dams to an environmental pollutant and limited-resource stress, which robustly activates the maternal immune system. Only male offspring display long-lasting behavioral abnormalities and alterations in the activity of brain networks encoding social interactio…
Astrocyte-secreted neurocan controls inhibitory synapse formation and function
Neuron · 2024-04-03 · 73 citations
articleOpen accessSenior authorCorrespondingAstrocytes strongly promote the formation and maturation of synapses by secreted proteins. Several astrocyte-secreted synaptogenic proteins controlling excitatory synapse development were identified; however, those that induce inhibitory synaptogenesis remain elusive. Here, we identify neurocan as an astrocyte-secreted inhibitory synaptogenic protein. After secretion from astrocytes, neurocan is cleaved into N- and C-terminal fragments. We found that these fragments have distinct localizations i…
Striatal Projection Neurons Require Huntingtin for Synaptic Connectivity and Survival
Cell Reports · 2020 · 51 citations
Senior authorCorrespondingHuntington's disease (HD) is caused by an autosomal dominant polyglutamine expansion mutation of Huntingtin (HTT). HD patients suffer from progressive motor, cognitive, and psychiatric impairments, along with significant degeneration of the striatal projection neurons (SPNs) of the striatum. HD is widely accepted to be caused by a toxic gain-of-function of mutant HTT. However, whether loss of HTT function, because of dominant-negative effects of the mutant protein, plays a role in HD and whether…
Recent grants
Control of synapse formation and maturation by astrocytes
NIH · $1.7M · 2012–2018
Control of Astrocyte Development and Astrocyte-Synapse Interactions
NIH · $1.9M · 2018–2023
Environmental Toxins and Microglia-Synapse Interactions in Autism
NIH · $2.1M · 2016–2021
Frequent coauthors
- 104 shared
Dhanesh Sivadasan Bindu
Duke University Hospital
- 92 shared
Justin T Savage
Duke University Hospital
- 90 shared
Francesco Paolo Ulloa Severino
Duke University
- 76 shared
Kristina Sakers
Duke University
- 73 shared
Scott H. Soderling
Duke University
- 70 shared
J.J. Ramirez
Duke University
- 67 shared
Christabel Xin Tan
Duke University Hospital
- 66 shared
W. Christopher Risher
Marshall University
Education
- 2008
Postdoctoral Research, Neurobiology
Stanford University
- 2002
Ph.D., Biology
Ruprecht Karls Universitat Heidelberg
- 2002
Predoctoral Student, Structural Biology
European Molecular Biology Laboratory
- 1998
M.Sc., Molecular Biology and Genetics
Bilkent Universitesi
- 1996
B.Sc., Chemical Engineering
Orta Dogu Teknik Universitesi
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