Publications by authors named "T M F Buck"

After decades of inactivity throughout the Americas, western equine encephalitis virus (WEEV) recently re-emerged in South America, causing a large-scale outbreak in humans and horses. WEEV binds protocadherin 10 (PCDH10) as a receptor; however, nonpathogenic strains no longer bind human or equine PCDH10 but retain the ability to bind avian receptors. Highly virulent WEEV strains can also bind the very low-density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2) as alternative receptors.

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Background: The incidence of syphilis among cisgender women and heterosexual men in the U.S. has risen sharply.

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The maintenance of fluid and electrolyte homeostasis by the kidney requires proper folding and trafficking of ion channels and transporters in kidney epithelia. Each of these processes requires a specific subset of a diverse class of proteins termed molecular chaperones. One such chaperone is GRP170, which is an Hsp70-like, endoplasmic reticulum (ER)-localized chaperone that plays roles in protein quality control and protein folding in the ER.

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Article Synopsis
  • Western equine encephalitis virus (WEEV) used to cause significant outbreaks in humans and horses but has become less virulent over time, raising questions about the reasons for this change and the potential for re-emergence of deadly strains.
  • Researchers identified protocadherin 10 (PCDH10) as a key receptor for WEEV, which ancient strains could bind to, while contemporary strains show reduced binding abilities indicating a shift in the virus’s host adaptation.
  • The study suggests that PCDH10 not only facilitates infection in neurons but also that a soluble form can protect against WEEV, offering insights for future medical treatments and risk assessments of the virus.
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Prenatal stress increases the risk of neurodevelopmental disorders. NMDA-type glutamate receptor (NMDAR) activity plays an important pathophysiological role in the cortico-hippocampal circuit in these disorders. We tested the hypothesis that transcription of NMDAR subunits is modified in the frontal cortex (FCx) and hippocampus after exposure to prenatal restraint stress (PRS) in mice.

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