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Full-Text Articles in Cell Biology

#7 - The Role Of Rnf216/Triad3 In Neuroinflammation Through Interactions With Toll-Like-Receptors, Dustin Grossman Nov 2019

#7 - The Role Of Rnf216/Triad3 In Neuroinflammation Through Interactions With Toll-Like-Receptors, Dustin Grossman

Georgia Undergraduate Research Conference (GURC)

Ubiquitin E3 ligases are enzymes that mark certain substrates with ubiquitin proteins which leads to different cellular fates. Ring finger protein 216 (RNF216) is a ubiquitin E3 ligase that is involved in synaptic plasticity, inhibiting cellular autophagy, and the immune response in the peripheral nervous system. Previous literature has demonstrated that RNF216 participates in various aspects of inflammation by regulating ubiquitination and proteasomal degradation of receptor-interacting serine-threonine kinase 1 (RIPK1), toll-interleukin 1 receptor domain containing adaptor protein (TIRAP), and TIR-domain-containing adapter-inducing interferon-β (TRIF), targeting TNF receptor associated factor 3 (TRAF3) for degradation. TLRs initiate signal transduction pathways which can lead ...


Targeting Pro-Inflammatory Function Of Microglia Using Small Molecules To Combat Neurodegeneration, Gabrielle C. Williams, Priya Prakash, Gaurav Chopra Aug 2018

Targeting Pro-Inflammatory Function Of Microglia Using Small Molecules To Combat Neurodegeneration, Gabrielle C. Williams, Priya Prakash, Gaurav Chopra

The Summer Undergraduate Research Fellowship (SURF) Symposium

Microglia are the brain’s resident immune cells that are responsible for maintaining homeostasis in healthy conditions. During injury or infection, resting microglia get activated and produce pro-inflammatory cytokines such as IL-1b, IL-1a, IL-6, etc. along with reactive oxygen species like nitric oxide (NO) to combat neuroinflammatory diseases such as Alzheimer’s disease (AD). Inflammation is characterized by the activation of resident-immune cells in the brain called microglia that respond to the eat-me signals released by the toxic amyloid beta peptides as well as the dying neurons in the microenvironment. Recent studies have shown that activated microglia induce neuronal death ...


P32. Altered Sensory Processing In Response To Novel Dreadd-Induced Inactivation Of Gaba In Pedunculopontine Tegmental Nucleus, Niveen Fulcher Mar 2017

P32. Altered Sensory Processing In Response To Novel Dreadd-Induced Inactivation Of Gaba In Pedunculopontine Tegmental Nucleus, Niveen Fulcher

Western Research Forum

Niveen Fulcher1, Cleusa De Oliveira2, & Susanne Schmid1,2

1Schulich School of Medicine & Dentistry, University of Western Ontario

2Anatomy and Cell Biology, University of Western Ontario

Altered sensory processing in response to novel DREADD-induced inactivation of GABA in pedunculopontine tegmental nucleus

Background: Sensory processing deficits are associated with certain psychiatric illnesses, such as schizophrenia and autism spectrum disorder (ASD). Sensory filtering and sensorimotor gating are evolutionarily conserved preattentive responses that filter and block redundant sensory stimuli that would otherwise overwhelm our brains. To date, underlying mechanisms of these deficits are undefined. Prepulse inhibition (PPI) of the ...


Analysis Of Mitochondrial Turnover In Neuromuscular Junctions Of Parkin Mutants, Kenny Nguyen, Hyun Sung, Peter J. Hollenbeck Aug 2015

Analysis Of Mitochondrial Turnover In Neuromuscular Junctions Of Parkin Mutants, Kenny Nguyen, Hyun Sung, Peter J. Hollenbeck

The Summer Undergraduate Research Fellowship (SURF) Symposium

The accumulation of dysfunctional or damaged mitochondria in neurons has been linked to the pathogenesis of many neurodegenerative diseases, such as Parkinson’s disease. It has been proposed that proteins PINK1 and Parkin regulate mitochondrial quality control by selectively targeting depolarized mitochondria for autophagic degradation, a process known as mitophagy. Though previously analyzed in the cell bodies and axons of neurons, the role of the PINK1/Parkin pathway in the synapse is unclear, and it is not known whether mitochondrial turnover occurs in the neuromuscular junctions (NMJs). To study this, intact Drosophila nervous systems were analyzed in vivo by performing ...