Fluorescent retroviral envelope (Env) proteins were developed for direct visualization of viral particles. By fusing the enhanced green fluorescent protein (eGFP) to the N terminus of the amphotropic 4070A envelope protein, extracellular presentation of eGFP was achieved. Viruses incorporated the modified Env protein and efficiently infected cells. We used the GFP-tagged viruses for staining retrovirus receptor-positive cells, thereby circumventing indirect labeling techniques. By generating cells which conditionally expressed the GFP-tagged Env protein, we could confirm an inverse correlation between retroviral Env expression and infectivity (superinfection). eGFP-tagged virus particles are suitable for monitoring the dynamics of virus-cell interactions.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC154001 | PMC |
| http://dx.doi.org/10.1128/jvi.77.10.6070-6075.2003 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: A case study on a PSEN1 (E280A) carrier with APOECh (R136S) mutation revealed changes in APOE protein function led to a protective effect on AD outcomes. Notably, there is an intriguing disparity between the two hallmark pathologies: a reduction in tauopathy but no change in plaque burden. Given that the APOE protein is predominantly produced by astrocytes and activated microglia, and the APOE gene is among the disease-associated microglia (DAM) genes, it is conceivable that the variance in pathological outcomes may be rooted in the glial response.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
VA Puget Sound GRECC, Seattle, WA, USA.
Background: Alzheimer's disease (AD) is the leading cause of dementia and one of the most devastating neurodegenerative diseases. In the last decades, a large proportion of AD patients have been described as having aberrant accumulation of TDP-43 protein, a well-established driver of neurodegeneration. This TDP-43 proteinopathy in AD can co-occur in neurons with the main hallmarks of the disease, toxic amyloid oligomers and neurofibrillary tangles containing hyperphosphorylated Tau, and correlates with rapid progression and worse prognosis.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Texas Medical Branch, Galveston, TX, USA.
Background: Alzheimer's disease (AD) is the memory-related neurodegenerative disorder, contributing to 70% of the cases globally. Synaptic dysfunction is a well-known early event that causes progressive cognitive decline in AD. The latest AD therapeutics on the forefront only offer a moderate symptomatic relief with significant off-target effects.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Institute for Memory Impairments and Neurological Disorders (MIND), Irvine, CA, USA.
Background: Alzheimer's Disease (AD) presents a significant challenge in understanding its complex pathophysiology, owing to its multifaceted genetic and environmental factors. Despite extensive research, the translatability of findings from animal models to human conditions remains a critical hurdle. This study addresses the need to uncover shared molecular changes in AD by comparing human and mouse models, thereby enhancing our understanding of the disease's underlying mechanisms and improving the prospects for effective treatments.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Michigan State University, Grand Rapids, MI, USA.
Background: A recent study of familial Alzheimer's disease identified a mutation in the RELN gene that appeared to delay the onset of dementia. It was hypothesized that this RELN-COLBOS variant protected against dementia by enhanced signaling at reelin receptors. We previously developed a secreted, bio-active reelin fragment (R36) and packaged it into AAV.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!