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Article ; Online: The complexity of a monogenic neurodegenerative disease: More than two decades of therapeutic driven research into Niemann-Pick type C disease.

Hammond, Natalie / Munkacsi, Andrew B / Sturley, Stephen L

Biochimica et biophysica acta. Molecular and cell biology of lipids

2019 Volume 1864, Issue 8, Page(s) 1109–1123

Abstract: Niemann-Pick type C (NP-C) disease is a rare and fatal neurodegenerative disease typified by aberrations in intracellular lipid transport. Cholesterol and other lipids accumulate in the late endosome/lysosome of all diseased cells thereby causing ... ...

Abstract	Niemann-Pick type C (NP-C) disease is a rare and fatal neurodegenerative disease typified by aberrations in intracellular lipid transport. Cholesterol and other lipids accumulate in the late endosome/lysosome of all diseased cells thereby causing neuronal and visceral atrophy. A cure for NP-C remains elusive despite the extensive molecular advances emanating from the identification of the primary genetic defect in 1997. Penetration of the blood-brain barrier and efficacy in the viscera are prerequisites for effective therapy, however the rarity of NP-C disease is the major impediment to progress. Disease diagnosis is challenging and establishment of appropriate test populations for clinical trials difficult. Fortunately, disease models that span the diversity of microbial and metazoan life have been utilized to advance the quest for a therapy. The complexity of lipid storage in this disorder and in the model systems, has led to multiple theories on the primary disease mechanism and consequently numerous and varied proposed interventions. Here, we conduct an evaluation of these studies.
MeSH term(s)	Animals ; Biomedical Research ; History, 20th Century ; History, 21st Century ; Humans ; Models, Biological ; Neurodegenerative Diseases ; Niemann-Pick Disease, Type C/diagnosis ; Niemann-Pick Disease, Type C/etiology ; Niemann-Pick Disease, Type C/history ; Niemann-Pick Disease, Type C/therapy ; Rare Diseases
Language	English
Publishing date	2019-04-17
Publishing country	Netherlands
Document type	Historical Article ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbalip.2019.04.002
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Article ; Online: Identification and characterization of protein interactions with the major Niemann-Pick type C disease protein in yeast reveals pathways of therapeutic potential.

Hammond, Natalie / Snider, Jamie / Stagljar, Igor / Mitchell, Kevin / Lagutin, Kirill / Jessulat, Matthew / Babu, Mohan / Teesdale-Spittle, Paul H / Sheridan, Jeffrey P / Sturley, Stephen L / Munkacsi, Andrew B

Genetics

2023 Volume 225, Issue 1

Abstract: Niemann-Pick type C (NP-C) disease is a rare lysosomal storage disease caused by mutations in NPC1 (95% cases) or NPC2 (5% cases). These proteins function together in cholesterol egress from the lysosome, whereby upon mutation, cholesterol and other ... ...

Abstract	Niemann-Pick type C (NP-C) disease is a rare lysosomal storage disease caused by mutations in NPC1 (95% cases) or NPC2 (5% cases). These proteins function together in cholesterol egress from the lysosome, whereby upon mutation, cholesterol and other lipids accumulate causing major pathologies. However, it is not fully understood how cholesterol is transported from NPC1 residing at the lysosomal membrane to the endoplasmic reticulum (ER) and plasma membrane. The yeast ortholog of NPC1, Niemann-Pick type C-related protein-1 (Ncr1), functions similarly to NPC1; when transfected into a mammalian cell lacking NPC1, Ncr1 rescues the diagnostic hallmarks of cholesterol and sphingolipid accumulation. Here, we aimed to identify and characterize protein-protein interactions (PPIs) with the yeast Ncr1 protein. A genome-wide split-ubiquitin membrane yeast two-hybrid (MYTH) protein interaction screen identified 11 ER membrane-localized, full-length proteins interacting with Ncr1 at the lysosomal/vacuolar membrane. These highlight the importance of ER-vacuole membrane interface and include PPIs with the Cyb5/Cbr1 electron transfer system, the ceramide synthase complex, and the Sec61/Sbh1 protein translocation complex. These PPIs were not detected in a sterol auxotrophy condition and thus depend on normal sterol metabolism. To provide biological context for the Ncr1-Cyb5 PPI, a yeast strain lacking this PPI (via gene deletions) exhibited altered levels of sterols and sphingolipids including increased levels of glucosylceramide that mimic NP-C disease. Overall, the results herein provide new physical and genetic interaction models to further use the yeast model of NP-C disease to better understand human NP-C disease.
MeSH term(s)	Animals ; Humans ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Niemann-Pick Disease, Type C/drug therapy ; Niemann-Pick Disease, Type C/genetics ; Niemann-Pick Disease, Type C/metabolism ; Natural Cytotoxicity Triggering Receptor 1/metabolism ; Proteins/genetics ; Cholesterol ; Sterols/metabolism ; Mammals
Chemical Substances	Natural Cytotoxicity Triggering Receptor 1 ; Proteins ; Cholesterol (97C5T2UQ7J) ; Sterols
Language	English
Publishing date	2023-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2167-2
ISSN	1943-2631 ; 0016-6731
ISSN (online)	1943-2631
ISSN	0016-6731
DOI	10.1093/genetics/iyad129
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Article: Exacerbating and reversing lysosomal storage diseases: from yeast to humans.

Rajakumar, Tamayanthi / Munkacsi, Andrew B / Sturley, Stephen L

Microbial cell (Graz, Austria)

2017 Volume 4, Issue 9, Page(s) 278–293

Abstract: Lysosomal storage diseases (LSDs) arise from monogenic deficiencies in lysosomal proteins and pathways and are characterized by a tissue-wide accumulation of a vast variety of macromolecules, normally specific to each genetic lesion. Strategies for ... ...

Abstract	Lysosomal storage diseases (LSDs) arise from monogenic deficiencies in lysosomal proteins and pathways and are characterized by a tissue-wide accumulation of a vast variety of macromolecules, normally specific to each genetic lesion. Strategies for treatment of LSDs commonly depend on reduction of the offending metabolite(s) by substrate depletion or enzyme replacement. However, at least 44 of the ~50 LSDs are currently recalcitrant to intervention. Murine models have provided significant insights into our understanding of many LSD mechanisms; however, these systems do not readily permit phenotypic screening of compound libraries, or the establishment of genetic or gene-environment interaction networks. Many of the genes causing LSDs are evolutionarily conserved, thus facilitating the application of models system to provide additional insight into LSDs. Here, we review the utility of yeast models of 3 LSDs: Batten disease, cystinosis, and Niemann-Pick type C disease. We will focus on the translation of research from yeast models into human patients suffering from these LSDs. We will also discuss the use of yeast models to investigate the penetrance of LSDs, such as Niemann-Pick type C disease, into more prevalent syndromes including viral infection and obesity.
Language	English
Publishing date	2017-08-25
Publishing country	Austria
Document type	Journal Article ; Review
ZDB-ID	2814756-X
ISSN	2311-2638
ISSN	2311-2638
DOI	10.15698/mic2017.09.588
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Article: The complexity of a monogenic neurodegenerative disease: More than two decades of therapeutic driven research into Niemann-Pick type C disease

Hammond, Natalie / Munkacsi, Andrew B / Sturley, Stephen L

Biochimica et biophysica acta. 2019 Aug., v. 1864, no. 8

2019

Abstract	Niemann-Pick type C (NP-C) disease is a rare and fatal neurodegenerative disease typified by aberrations in intracellular lipid transport. Cholesterol and other lipids accumulate in the late endosome/lysosome of all diseased cells thereby causing neuronal and visceral atrophy. A cure for NP-C remains elusive despite the extensive molecular advances emanating from the identification of the primary genetic defect in 1997. Penetration of the blood-brain barrier and efficacy in the viscera are prerequisites for effective therapy, however the rarity of NP-C disease is the major impediment to progress. Disease diagnosis is challenging and establishment of appropriate test populations for clinical trials difficult. Fortunately, disease models that span the diversity of microbial and metazoan life have been utilized to advance the quest for a therapy. The complexity of lipid storage in this disorder and in the model systems, has led to multiple theories on the primary disease mechanism and consequently numerous and varied proposed interventions. Here, we conduct an evaluation of these studies.
Keywords	animal organs ; Animalia ; atrophy ; blood-brain barrier ; cholesterol ; clinical trials ; disease diagnosis ; disease models ; genetic disorders ; lysosomes ; neurodegenerative diseases ; neurons ; therapeutics
Language	English
Dates of publication	2019-08
Size	p. 1109-1123.
Publishing place	Elsevier B.V.
Document type	Article
ISSN	1388-1981
DOI	10.1016/j.bbalip.2019.04.002
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Article ; Online: Lipid droplet formation on opposing sides of the endoplasmic reticulum.

Sturley, Stephen L / Hussain, M Mahmood

Journal of lipid research

2012 Volume 53, Issue 9, Page(s) 1800–1810

Abstract: In animal cells, the primary repositories of esterified fatty acids and alcohols (neutral lipids) are lipid droplets that form on the lumenal and/or cytoplasmic side of the endoplasmic reticulum (ER) membrane. A monolayer of amphipathic lipids, ... ...

Abstract	In animal cells, the primary repositories of esterified fatty acids and alcohols (neutral lipids) are lipid droplets that form on the lumenal and/or cytoplasmic side of the endoplasmic reticulum (ER) membrane. A monolayer of amphipathic lipids, intermeshed with key proteins, serves to solubilize neutral lipids as they are synthesized and desorbed. In specialized cells, mobilization of the lipid cargo for delivery to other tissues occurs by secretion of lipoproteins into the plasma compartment. Serum lipoprotein assembly requires an obligate structural protein anchor (apolipoprotein B) and a dedicated chaperone, microsomal triglyceride transfer protein. By contrast, lipid droplets that form on the cytoplasmic face of the ER lack an obligate protein scaffold or any required chaperone/lipid transfer protein. Mobilization of neutral lipids from the cytosol requires regulated hydrolysis followed by transfer of the products to different organelles or export from cells. Several proteins play a key role in controlling droplet number, stability, and catabolism; however, it is our premise that their formation initiates spontaneously, solely as a consequence of neutral lipid synthesis. This default pathway directs droplets into the cytoplasm where they accumulate in many lipid disorders.
MeSH term(s)	Animals ; Endoplasmic Reticulum/metabolism ; Humans ; Intracellular Membranes/metabolism ; Lipid Metabolism ; Lipoproteins/metabolism ; Proteome/metabolism
Chemical Substances	Lipoproteins ; Proteome
Language	English
Publishing date	2012-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.R028290
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Article ; Online: Exacerbating and reversing lysosomal storage diseases

Tamayanthi Rajakumar / Andrew B. Munkacsi / Stephen L. Sturley

Microbial Cell, Vol 4, Iss 9, Pp 278-

from yeast to humans

2017 Volume 293

Abstract	Lysosomal storage diseases (LSDs) arise from monogenic deficiencies in lysosomal proteins and pathways and are characterized by a tissue-wide accumulation of a vast variety of macromolecules, normally specific to each genetic lesion. Strategies for treatment of LSDs commonly depend on reduction of the offending metabolite(s) by substrate depletion or enzyme replacement. However, at least 44 of the ~50 LSDs are currently recalcitrant to intervention. Murine models have provided significant insights into our understanding of many LSD mechanisms; however, these systems do not readily permit phenotypic screening of compound libraries, or the establish-ment of genetic or gene-environment interaction networks. Many of the genes causing LSDs are evolutionarily conserved, thus facilitating the application of models system to provide additional insight into LSDs. Here, we review the utility of yeast models of 3 LSDs: Batten disease, cystinosis, and Niemann-Pick type C disease. We will focus on the translation of research from yeast models into human patients suffering from these LSDs. We will also discuss the use of yeast models to investigate the penetrance of LSDs, such as Niemann-Pick type C disease, into more prevalent syndromes including viral infection and obesity.
Keywords	lysosomal storage disease ; Niemann Pick Type-C disease ; gene modifier ; exacerbate-reverse ; yeast ; HIV ; Ebola ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2017-08-01T00:00:00Z
Publisher	Shared Science Publishers OG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Potential COVID-19 therapeutics from a rare disease: weaponizing lipid dysregulation to combat viral infectivity.

Sturley, Stephen L / Rajakumar, Tamayanthi / Hammond, Natalie / Higaki, Katsumi / Márka, Zsuzsa / Márka, Szabolcs / Munkacsi, Andrew B

Journal of lipid research

2020 Volume 61, Issue 7, Page(s) 972–982

Abstract: ... from the late endosome/lysosome (LE/L). The NP-C disease-causing gene (NPC1) has been strongly associated ... with viral infection, both as a filovirus receptor (e.g., Ebola) and through LE/L lipid trafficking. This suggests ...

Abstract	The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 has resulted in the death of more than 328,000 persons worldwide in the first 5 months of 2020. Herculean efforts to rapidly design and produce vaccines and other antiviral interventions are ongoing. However, newly evolving viral mutations, the prospect of only temporary immunity, and a long path to regulatory approval pose significant challenges and call for a common, readily available, and inexpensive treatment. Strategic drug repurposing combined with rapid testing of established molecular targets could provide a pause in disease progression. SARS-CoV-2 shares extensive structural and functional conservation with SARS-CoV-1, including engagement of the same host cell receptor (angiotensin-converting enzyme 2) localized in cholesterol-rich microdomains. These lipid-enveloped viruses encounter the endosomal/lysosomal host compartment in a critical step of infection and maturation. Niemann-Pick type C (NP-C) disease is a rare monogenic neurodegenerative disease caused by deficient efflux of lipids from the late endosome/lysosome (LE/L). The NP-C disease-causing gene (NPC1) has been strongly associated with viral infection, both as a filovirus receptor (e.g., Ebola) and through LE/L lipid trafficking. This suggests that NPC1 inhibitors or NP-C disease mimetics could serve as anti-SARS-CoV-2 agents. Fortunately, there are such clinically approved molecules that elicit antiviral activity in preclinical studies, without causing NP-C disease. Inhibition of NPC1 may impair viral SARS-CoV-2 infectivity via several lipid-dependent mechanisms, which disturb the microenvironment optimum for viral infectivity. We suggest that known mechanistic information on NPC1 could be utilized to identify existing and future drugs to treat COVID-19.
MeSH term(s)	Androstenes/therapeutic use ; Angiotensin-Converting Enzyme 2 ; Anticholesteremic Agents/therapeutic use ; Antiviral Agents/therapeutic use ; Betacoronavirus/drug effects ; Betacoronavirus/metabolism ; Betacoronavirus/pathogenicity ; COVID-19 ; Cholesterol/metabolism ; Coronavirus Infections/diagnosis ; Coronavirus Infections/drug therapy ; Coronavirus Infections/epidemiology ; Drug Repositioning/methods ; Humans ; Hydroxychloroquine/therapeutic use ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Lysosomes/drug effects ; Lysosomes/metabolism ; Lysosomes/virology ; Niemann-Pick C1 Protein ; Niemann-Pick Disease, Type C/drug therapy ; Niemann-Pick Disease, Type C/genetics ; Niemann-Pick Disease, Type C/metabolism ; Niemann-Pick Disease, Type C/pathology ; Pandemics ; Peptidyl-Dipeptidase A/genetics ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral/diagnosis ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/epidemiology ; Protein Binding ; Receptors, Virus/antagonists & inhibitors ; Receptors, Virus/genetics ; Receptors, Virus/metabolism ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/genetics ; Spike Glycoprotein, Coronavirus/metabolism
Chemical Substances	Androstenes ; Anticholesteremic Agents ; Antiviral Agents ; Intracellular Signaling Peptides and Proteins ; NPC1 protein, human ; Niemann-Pick C1 Protein ; Receptors, Virus ; Spike Glycoprotein, Coronavirus ; 3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one (3039-71-2) ; Hydroxychloroquine (4QWG6N8QKH) ; Cholesterol (97C5T2UQ7J) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Keywords	covid19
Language	English
Publishing date	2020-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.R120000851
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Article: Niemann-Pick type C pathogenesis and treatment: from statins to sugars.

Madra, Moneek / Sturley, Stephen L

Clinical lipidology

2011 Volume 5, Issue 3, Page(s) 387–395

Abstract: The isolation of the causative genes for Niemann-Pick type C disease, a panethnic lysosomal lipid storage disorder, has provided models of how sterols and other lipids such as glycosphingolipids traverse the membranes of eukaryotic cells. Unfortunately, ... ...

Abstract	The isolation of the causative genes for Niemann-Pick type C disease, a panethnic lysosomal lipid storage disorder, has provided models of how sterols and other lipids such as glycosphingolipids traverse the membranes of eukaryotic cells. Unfortunately, these molecular advances have yet to reciprocate with a cure for this devastating neurodegenerative disorder where neuronal replenishment will most likely yield the greatest benefit. In the meantime, stabilizing treatment strategies based on the removal of presumably toxic metabolites are in place. For example, the small molecule inhibition of glucosylceramide synthase by miglustat limits ganglioside accumulation and is now the only approved treatment of Niemann-Pick type C. In addition, 2-hydroxypropyl-B-cyclodextrin, a lipid chelator, relieves the lysosomal to endoplasmic reticulum blockage and markedly increases the life expectancy of the murine model. Ultimately, these strategies, targeting the primary biochemical lesion in these cells, and others will likely be combined to provide a synergistic cocktail approach to treating this disease.
Language	English
Publishing date	2011-01-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2601614-X
ISSN	1758-4302 ; 1758-4299
ISSN (online)	1758-4302
ISSN	1758-4299
DOI	10.2217/clp.10.19
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Article ; Online: Making, baking, and breaking: the synthesis, storage, and hydrolysis of neutral lipids.

Ruggles, Kelly V / Turkish, Aaron / Sturley, Stephen L

Annual review of nutrition

2013 Volume 33, Page(s) 413–451

Abstract: The esterification of amphiphilic alcohols with fatty acids is a ubiquitous strategy implemented by eukaryotes and some prokaryotes to conserve energy and membrane progenitors and simultaneously detoxify fatty acids and other lipids. This key reaction is ...

Abstract	The esterification of amphiphilic alcohols with fatty acids is a ubiquitous strategy implemented by eukaryotes and some prokaryotes to conserve energy and membrane progenitors and simultaneously detoxify fatty acids and other lipids. This key reaction is performed by at least four evolutionarily unrelated multigene families. The synthesis of this "neutral lipid" leads to the formation of a lipid droplet, which despite the clear selective advantage it confers is also a harbinger of cellular and organismal malaise. Neutral lipid deposition as a cytoplasmic lipid droplet may be thermodynamically favored but nevertheless is elaborately regulated. Optimal utilization of these resources by lipolysis is similarly multigenic in determination and regulation. We present here a perspective on these processes that originates from studies in model organisms, and we include our thoughts on interventions that target reductions in neutral lipids as therapeutics for human diseases such as obesity and diabetes.
MeSH term(s)	Animals ; Biological Evolution ; Cholesterol Esters/metabolism ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/metabolism ; Diet, High-Fat/adverse effects ; Dietary Fats/metabolism ; Esterification ; Homeostasis ; Humans ; Lipid Metabolism ; Obesity/etiology ; Obesity/metabolism ; Triglycerides/metabolism
Chemical Substances	Cholesterol Esters ; Dietary Fats ; Triglycerides
Language	English
Publishing date	2013
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	406980-8
ISSN	1545-4312 ; 0199-9885
ISSN (online)	1545-4312
ISSN	0199-9885
DOI	10.1146/annurev-nutr-071812-161254
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Article ; Online: Saturated with fat: new perspectives on lipotoxicity.

Garbarino, Jeanne / Sturley, Stephen L

Current opinion in clinical nutrition and metabolic care

2009 Volume 12, Issue 2, Page(s) 110–116

Abstract: Purpose of review: To present current perspectives on the mediators and mechanisms of cyto-lipotoxic events and their relevance to human health.: Recent findings: The relatively recent isolation of lipid acyltransferase genes from yeast to mice and ... ...

Abstract	Purpose of review: To present current perspectives on the mediators and mechanisms of cyto-lipotoxic events and their relevance to human health. Recent findings: The relatively recent isolation of lipid acyltransferase genes from yeast to mice and humans has resulted in a paradigm shift that now establishes all fatty acids as toxic, albeit in tissue specific patterns and by different mechanisms. Furthermore, the dysregulation of glucose homeostasis in combination with excess fatty acids provides a synergistic effect leading to glucolipotoxicity and cell death. These findings are relevant to the development of disease states associated with the pathogenesis of the metabolic syndrome. Summary: In an era when an astounding number of people are diagnosed with metabolic disorders, it is imperative that we understand the consequences of a chronic metabolic surplus. Excessive fat, saturated or otherwise, has to be accommodated. Multiple aspects of this homeostasis are emerging, some of which are described here.
MeSH term(s)	Adipose Tissue/metabolism ; Cell Death/physiology ; Dietary Fats/adverse effects ; Fatty Acids/metabolism ; Glucose/metabolism ; Homeostasis ; Humans ; Hyperlipidemias/metabolism ; Lipid Metabolism ; Metabolic Syndrome/metabolism ; Obesity/metabolism
Chemical Substances	Dietary Fats ; Fatty Acids ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2009-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1460178-3
ISSN	1473-6519 ; 1363-1950
ISSN (online)	1473-6519
ISSN	1363-1950
DOI	10.1097/MCO.0b013e32832182ee
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