The Klase Lab is interested in the overlapping problems of HIV-1 transcription, HIV-1 neuropathogenesis and substance use disorders.
We are working on:
- Understanding how prescription benzodiazepines (such as Valium and Xanax) alter chromatin and affect viral gene expression.
- Studying the role of the HIV-1 Tat protein in neuropathogenesis.
- Determining how alteration of miRNA expression by the virus may drive neuropathogenesis.
- Describing the mechanism whereby substances of abuse (such as opioids and benzodiazepines) exacerbate HIV-1 associated neurodegenerative disorders.
- Studying the immune mechanisms that allow a small fraction of HIV-1 infected individuals to control the virus in the absence of therapy.
- Developing technologies to improve our understanding of epigenetics and chromatin dynamics in the nucleus.
Prescription benzodiazepines activate the latent HIV-1 LTR
The Tat protein and morphine show combined affect in suppressing β-catenin, a key neuroprotective factor
High-resolution imaging of chromatin in three dimensions: green – histone H3 methylated at lysine 27, red – the methyltransferase SUV39H1
A model for alprazolam alters the chromatin at the integrated HIV-1 LTR through inhibition of RUNX1 and activation of STAT5.
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