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Marnie Williams on Muck Rack

Marnie Williams

As seen in: Scripps News, BioRxiv, WFLD-TV (Chicago, IL), WTVT-TV (Tampa, FL), KTBC-TV (Austin, TX), KCOP-TV (Los Angeles, CA), WRBW-TV (Orlando, FL), KTVU-TV (Oakland, CA), KTXH-TV (Houston, TX), O'Dwyer's PR News, The Journal of Biological Chemistry and
Tweeting my favorite stories in news, entertainment, sports & weather daily! #USF #HornsUp #GoBolts #Bucs RT are my own opinions.
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Articles

A GluN2B disease-associated variant promotes the degradation of NMDA receptors via autophagy

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By Taylor M Benske, Marnie Williams, Pei-Pei Zhang, Adrian J Palumbo
| The Journal of Biological Chemistry Verified
Keywords ER-phagy LC3-interacting region (LIR) NMDAR proteostasis CCPG1 Introduction N-methyl-D-aspartate receptors (NMDARs) are ionotropic glutamate receptors that mediate excitatory neurotransmission, support synaptic development and plasticity, and maintain the excitation-inhibition balance in the central nervous system (1). These heterotetrameric receptors assemble from two obligatory, glycine-binding, GluN1 subunits and two GluN2(A-D) or GluN3(A-B) subunits, encoded by seven GRIN genes (2).
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A GluN2B disease-associated variant promotes degradation of NMDA receptors via autophagy

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By Taylor M Benske, Marnie Williams, Pei-Pei Zhang, Adrian J Palumbo
| BioRxiv
Abstract N-methyl-D-aspartate receptors (NMDARs) are essential for excitatory neurotransmission and their pathogenic variants can lead to proteostasis defects and thus neurological diseases. However, how the proteostasis network degrades pathogenic variants is not well understood.
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GABRA1 frameshift variants impair GABAA receptor proteostasis

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By Marnie Williams, Ya-Juan Wang, Jing-Qiong Kang, Tingwei Mu
| BioRxiv
Abstract The gamma-aminobutyric acid type A receptor (GABAAR) is the most common inhibitory neurotransmitter-gated ion channel in the central nervous system. Pathogenic variants in genes encoding GABAAR subunits can cause receptor dysfunction and lead to genetic epilepsy. Frameshift variants in these genes can result in a premature termination codon, producing truncated receptor subunit variants.
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