Full Text Journal Articles by
Author Kim A Caldwell

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Enhanced pentylenetetrazole sensitivity in a C. elegans mutant associated with DNM1 encephalopathy.

Madeline A Vaji, Guy A Caldwell, Kim A Caldwell,

(microPublication biology)
[2020, 2020:]

Cited: 0 times

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Phenotypic modulation of pentylenetetrazole-induced convulsive behaviors in C. elegans carrying a mutation associated with Alzheimer's disease.

Madeline A Vaji, Guy A Caldwell, Kim A Caldwell,

(microPublication biology)
[2020, 2020:]

Cited: 0 times

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Modeling neurodegeneration in Caenorhabditis elegans.

Kim A Caldwell, Corey W Willicott, Guy A Caldwell,

The global burden of neurodegenerative diseases underscores the urgent need for innovative strategies to define new drug targets and disease-modifying factors. The nematode Caenorhabditis elegans has served as the experimental subject for multiple transformative discoveries that have redefined our understanding of biology for ∼60 years. More recently, the considerable attributes of ... Read more >>

Dis Model Mech (Disease models & mechanisms)
[2020, 13(10):]

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Moving Pharmacy Benefits from Nice to Have to Essential Benefits.

Kim A Caldwell, Babette Edgar,

DISCLOSURES:No funding supported the writing of this commentary. The authors have nothing to disclose. ... Read more >>

J Manag Care Spec Pharm (Journal of managed care & specialty pharmacy)
[2020, 26(8):943-944]

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Genetic Defects in Mitochondrial Dynamics in Caenorhabditis elegans Impact Ultraviolet C Radiation- and 6-hydroxydopamine-Induced Neurodegeneration.

Jessica H Hartman, Claudia Gonzalez-Hunt, Samantha M Hall, Ian T Ryde, Kim A Caldwell, Guy A Caldwell, Joel N Meyer,

BACKGROUND:Parkinson's disease (PD) is one of the most common neurodegenerative disorders involving devastating loss of dopaminergic neurons in the substantia nigra. Early steps in PD pathogenesis include mitochondrial dysfunction, and mutations in mitochondrial genes have been linked to familial forms of the disease. However, low penetrance of mutations indicates a ... Read more >>

Int J Mol Sci (International journal of molecular sciences)
[2019, 20(13):]

Cited: 1 time

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Vacuolar protein sorting protein 41 (VPS41) at an intersection of endosomal traffic in neurodegenerative disease.

Edward F Griffin, Kim A Caldwell, Guy A Caldwell,

(Neural regeneration research)
[2019, 14(7):1210-1212]

Cited: 0 times

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Found in Translation: The Utility of C. elegans Alpha-Synuclein Models of Parkinson's Disease.

Anthony L Gaeta, Kim A Caldwell, Guy A Caldwell,

Parkinson's Disease (PD) is the second-most common neurodegenerative disease in the world, yet the fundamental and underlying causes of the disease are largely unknown, and treatments remain sparse and impotent. Several biological systems have been employed to model the disease but the nematode roundworm Caenorhabditis elegans (C. elegans) shows unique ... Read more >>

Brain Sci (Brain sciences)
[2019, 9(4):]

Cited: 3 times

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ApoE-associated modulation of neuroprotection from Aβ-mediated neurodegeneration in transgenic Caenorhabditis elegans.

Edward F Griffin, Samuel E Scopel, Cayman A Stephen, Adam C Holzhauer, Madeline A Vaji, Ryan A Tuckey, Laura A Berkowitz, Kim A Caldwell, Guy A Caldwell,

Allele-specific distinctions in the human apolipoprotein E (APOE) locus represent the best-characterized genetic predictor of Alzheimer's disease (AD) risk. Expression of isoform APOEε2 is associated with reduced risk, while APOEε3 is neutral and APOEε4 carriers exhibit increased susceptibility. Using Caenorhabditis elegans, we generated a novel suite of humanized transgenic nematodes ... Read more >>

Dis Model Mech (Disease models & mechanisms)
[2019, 12(2):]

Cited: 1 time

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No Country for Old Worms: A Systematic Review of the Application of C. elegans to Investigate a Bacterial Source of Environmental Neurotoxicity in Parkinson's Disease.

Kim A Caldwell, Jennifer L Thies, Guy A Caldwell,

While progress has been made in discerning genetic associations with Parkinson's disease (PD), identifying elusive environmental contributors necessitates the application of unconventional hypotheses and experimental strategies. Here, we provide an overview of studies that we conducted on a neurotoxic metabolite produced by a species of common soil bacteria, Streptomyces venezuelae ... Read more >>

(Metabolites)
[2018, 8(4):]

Cited: 1 time

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Correction to: The Small GTPase RAC1/CED-10 Is Essential in Maintaining Dopaminergic Neuron Function and Survival Against α-Synuclein-Induced Toxicity.

Hanna Kim, Carles Calatayud, Sanjib Guha, Irene Fernández-Carasa, Laura Berkowitz, Iria Carballo-Carbajal, Mario Ezquerra, Rubén Fernández-Santiago, Pankaj Kapahi, Ángel Raya, Antonio Miranda-Vizuete, Jose Miguel Lizcano, Miquel Vila, Kim A Caldwell, Guy A Caldwell, Antonella Consiglio, Esther Dalfo,

With the author(s)' decision to opt for Open Choice the copyright of the article changed on March 2018 to ... Read more >>

Mol. Neurobiol. (Molecular neurobiology)
[2018, 55(9):7553-7554]

Cited: 0 times

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Alpha-synuclein inhibits Snx3-retromer-mediated retrograde recycling of iron transporters in S. cerevisiae and C. elegans models of Parkinson's disease.

Dhaval Patel, Chuan Xu, Sureshbabu Nagarajan, Zhengchang Liu, Wayne O Hemphill, Runhua Shi, Vladimir N Uversky, Guy A Caldwell, Kim A Caldwell, Stephan N Witt,

We probed the role of alpha-synuclein (α-syn) in modulating sorting nexin 3 (Snx3)-retromer-mediated recycling of iron transporters in Saccharomyces cerevisiae and Caenorhabditis elegans. In yeast, the membrane-bound heterodimer Fet3/Ftr1 is the high affinity iron importer. Fet3 is a membrane-bound multicopper ferroxidase, whose ferroxidase domain is orthologous to human ceruloplasmin (Cp), ... Read more >>

Hum. Mol. Genet. (Human molecular genetics)
[2018, 27(9):1514-1532]

Cited: 5 times

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Genetic and Pharmacological Discovery for Alzheimer's Disease Using Caenorhabditis elegans.

Edward F Griffin, Kim A Caldwell, Guy A Caldwell,

The societal burden presented by Alzheimer's disease warrants both innovative and expedient means by which its underlying molecular causes can be both identified and mechanistically exploited to discern novel therapeutic targets and strategies. The conserved characteristics, defined neuroanatomy, and advanced technological application of Caenorhabditis elegans render this metazoan an unmatched ... Read more >>

ACS Chem Neurosci (ACS chemical neuroscience)
[2017, 8(12):2596-2606]

Cited: 9 times

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Dysregulation of the Mitochondrial Unfolded Protein Response Induces Non-Apoptotic Dopaminergic Neurodegeneration in C. elegans Models of Parkinson's Disease.

Bryan A Martinez, Daniel A Petersen, Anthony L Gaeta, Samuel P Stanley, Guy A Caldwell, Kim A Caldwell,

Due to environmental insult or innate genetic deficiency, protein folding environments of the mitochondrial matrix are prone to dysregulation, prompting the activation of a specific organellar stress-response mechanism, the mitochondrial unfolded protein response (UPRMT). In Caenorhabditis elegans, mitochondrial damage leads to nuclear translocation of the ATFS-1 transcription factor to activate ... Read more >>

J. Neurosci. (The Journal of neuroscience : the official journal of the Society for Neuroscience)
[2017, 37(46):11085-11100]

Cited: 16 times

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NCEH-1 modulates cholesterol metabolism and protects against α-synuclein toxicity in a C. elegans model of Parkinson's disease.

Siyuan Zhang, Samantha A Glukhova, Kim A Caldwell, Guy A Caldwell,

Parkinson's disease (PD) is an aging-associated neurodegenerative disease affecting millions worldwide. Misfolding, oligomerization and accumulation of the human α-synuclein protein is a key pathological hallmark of PD and is associated with the progressive loss of dopaminergic neurons over the course of aging. Lifespan extension via the suppression of IGF-1/insulin-like signaling ... Read more >>

Hum. Mol. Genet. (Human molecular genetics)
[2017, 26(19):3823-3836]

Cited: 6 times

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Dihydropyrimidine-Thiones and Clioquinol Synergize To Target β-Amyloid Cellular Pathologies through a Metal-Dependent Mechanism.

Daniel F Tardiff, Lauren E Brown, Xiaohui Yan, Richard Trilles, Nathan T Jui, M Inmaculada Barrasa, Kim A Caldwell, Guy A Caldwell, Scott E Schaus, Susan Lindquist,

The lack of therapies for neurodegenerative diseases arises from our incomplete understanding of their underlying cellular toxicities and the limited number of predictive model systems. It is critical that we develop approaches to identify novel targets and lead compounds. Here, a phenotypic screen of yeast proteinopathy models identified dihydropyrimidine-thiones (DHPM-thiones) ... Read more >>

ACS Chem Neurosci (ACS chemical neuroscience)
[2017, 8(9):2039-2055]

Cited: 3 times

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C. elegans as a model system to accelerate discovery for Parkinson disease.

Bryan A Martinez, Kim A Caldwell, Guy A Caldwell,

The nematode Caenorhabditis elegans possesses a wealth of opportunities to explore mechanisms which regulate metazoan complexity, basic cellular biology, and neuronal system attributes. Together, these provide a basis for tenable understanding of neurodegenerative disorders such as Parkinson disease (PD) through functional genomic analysis and pharmacological manipulation for the discovery of ... Read more >>

Curr. Opin. Genet. Dev. (Current opinion in genetics & development)
[2017, 44:102-109]

Cited: 16 times

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Chemical Compensation of Mitochondrial Phospholipid Depletion in Yeast and Animal Models of Parkinson's Disease.

Shaoxiao Wang, Siyuan Zhang, Chuan Xu, Addie Barron, Floyd Galiano, Dhaval Patel, Yong Joo Lee, Guy A Caldwell, Kim A Caldwell, Stephan N Witt,

We have been investigating the role that phosphatidylethanolamine (PE) and phosphatidylcholine (PC) content plays in modulating the solubility of the Parkinson's disease protein alpha-synuclein (α-syn) using Saccharomyces cerevisiae and Caenorhabditis elegans. One enzyme that synthesizes PE is the conserved enzyme phosphatidylserine decarboxylase (Psd1/yeast; PSD-1/worms), which is lodged in the inner ... Read more >>

PLoS One (PloS one)
[2016, 11(10):e0164465]

Cited: 4 times

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Phosphatidylethanolamine deficiency disrupts α-synuclein homeostasis in yeast and worm models of Parkinson disease.

Shaoxiao Wang, Siyuan Zhang, Liang-Chun Liou, Qun Ren, Zhaojie Zhang, Guy A Caldwell, Kim A Caldwell, Stephan N Witt,

Phosphatidylserine decarboxylase, which is embedded in the inner mitochondrial membrane, synthesizes phosphatidylethanolamine (PE) and, in some cells, synthesizes the majority of this important phospholipid. Normal levels of PE can decline with age in the brain. Here we used yeast and worms to test the hypothesis that low levels of PE ... Read more >>

Proc. Natl. Acad. Sci. U.S.A. (Proceedings of the National Academy of Sciences of the United States of America)
[2014, 111(38):E3976-85]

Cited: 25 times

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RTCB-1 mediates neuroprotection via XBP-1 mRNA splicing in the unfolded protein response pathway.

Arpita Ray, Siyuan Zhang, Courtney Rentas, Kim A Caldwell, Guy A Caldwell,

Parkinson's disease (PD), the second most prevalent neurodegenerative disorder, is characterized by the degeneration of dopamine (DA) neurons and age-dependent formation of protein inclusions that contain the α-synuclein (α-syn) protein. RNA interference (RNAi) screening using Caenorhabditis elegans identified RTCB-1, an uncharacterized gene product, as one of several significant modifiers of ... Read more >>

J. Neurosci. (The Journal of neuroscience : the official journal of the Society for Neuroscience)
[2014, 34(48):16076-16085]

Cited: 18 times

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Phenazine derivatives cause proteotoxicity and stress in C. elegans.

Arpita Ray, Courtney Rentas, Guy A Caldwell, Kim A Caldwell,

It is widely recognized that bacterial metabolites have toxic effects in animal systems. Phenazines are a common bacterial metabolite within the redox-active exotoxin class. These compounds have been shown to be toxic to the soil invertebrate Caenorhabditis elegans with the capability of causing oxidative stress and lethality. Here we report ... Read more >>

Neurosci Lett (Neuroscience letters)
[2015, 584:23-27]

Cited: 9 times

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Calcineurin determines toxic versus beneficial responses to α-synuclein.

Gabriela Caraveo, Pavan K Auluck, Luke Whitesell, Chee Yeun Chung, Valeriya Baru, Eugene V Mosharov, Xiaohui Yan, Manu Ben-Johny, Martin Soste, Paola Picotti, Hanna Kim, Kim A Caldwell, Guy A Caldwell, David Sulzer, David T Yue, Susan Lindquist,

Calcineurin (CN) is a highly conserved Ca(2+)-calmodulin (CaM)-dependent phosphatase that senses Ca(2+) concentrations and transduces that information into cellular responses. Ca(2+) homeostasis is disrupted by α-synuclein (α-syn), a small lipid binding protein whose misfolding and accumulation is a pathological hallmark of several neurodegenerative diseases. We report that α-syn, from yeast ... Read more >>

Proc. Natl. Acad. Sci. U.S.A. (Proceedings of the National Academy of Sciences of the United States of America)
[2014, 111(34):E3544-52]

Cited: 45 times

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Clioquinol promotes the degradation of metal-dependent amyloid-β (Aβ) oligomers to restore endocytosis and ameliorate Aβ toxicity.

Kent E S Matlack, Daniel F Tardiff, Priyanka Narayan, Shusei Hamamichi, Kim A Caldwell, Guy A Caldwell, Susan Lindquist,

Alzheimer's disease (AD) is a common, progressive neurodegenerative disorder without effective disease-modifying therapies. The accumulation of amyloid-β peptide (Aβ) is associated with AD. However, identifying new compounds that antagonize the underlying cellular pathologies caused by Aβ has been hindered by a lack of cellular models amenable to high-throughput chemical screening. ... Read more >>

Proc. Natl. Acad. Sci. U.S.A. (Proceedings of the National Academy of Sciences of the United States of America)
[2014, 111(11):4013-4018]

Cited: 59 times

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Potentiated Hsp104 variants antagonize diverse proteotoxic misfolding events.

Meredith E Jackrel, Morgan E DeSantis, Bryan A Martinez, Laura M Castellano, Rachel M Stewart, Kim A Caldwell, Guy A Caldwell, James Shorter,

There are no therapies that reverse the proteotoxic misfolding events that underpin fatal neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD). Hsp104, a conserved hexameric AAA+ protein from yeast, solubilizes disordered aggregates and amyloid but has no metazoan homolog and only limited activity against human neurodegenerative disease proteins. ... Read more >>

Cell (Cell)
[2014, 156(1-2):170-182]

Cited: 96 times

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TorsinA rescues ER-associated stress and locomotive defects in C. elegans models of ALS.

Michelle L Thompson, Pan Chen, Xiaohui Yan, Hanna Kim, Akeem R Borom, Nathan B Roberts, Kim A Caldwell, Guy A Caldwell,

Molecular mechanisms underlying neurodegenerative diseases converge at the interface of pathways impacting cellular stress, protein homeostasis and aging. Targeting the intrinsic capacities of neuroprotective proteins to restore neuronal function and/or attenuate degeneration represents a potential means toward therapeutic intervention. The product of the human DYT1 gene, torsinA, is a member ... Read more >>

Dis Model Mech (Disease models & mechanisms)
[2014, 7(2):233-243]

Cited: 11 times

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Yeast reveal a "druggable" Rsp5/Nedd4 network that ameliorates α-synuclein toxicity in neurons.

Daniel F Tardiff, Nathan T Jui, Vikram Khurana, Mitali A Tambe, Michelle L Thompson, Chee Yeun Chung, Hari B Kamadurai, Hari B Kamadurai, Hyoung Tae Kim, Alex K Lancaster, Kim A Caldwell, Guy A Caldwell, Jean-Christophe Rochet, Stephen L Buchwald, Susan Lindquist,

α-Synuclein (α-syn) is a small lipid-binding protein implicated in several neurodegenerative diseases, including Parkinson's disease, whose pathobiology is conserved from yeast to man. There are no therapies targeting these underlying cellular pathologies, or indeed those of any major neurodegenerative disease. Using unbiased phenotypic screens as an alternative to target-based approaches, ... Read more >>

Science (Science (New York, N.Y.))
[2013, 342(6161):979-983]

Cited: 116 times

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