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Lysosome dysfunction as a cause of neurodegenerative diseases: Lessons from frontotemporal dementia and amyotrophic lateral sclerosis

Neurobiology of disease, 2021-07, Vol.154, p.105360-105360, Article 105360

2021

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Progranulin deficiency leads to reduced glucocerebrosidase activity

PloS one, 2019-07, Vol.14 (7), p.e0212382-e0212382

2019

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TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

Nature neuroscience, 2018-02, Vol.21 (2), p.228

2018

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Short Aβ peptides attenuate Aβ42 toxicity in vivo

The Journal of experimental medicine, 2018-01, Vol.215 (1), p.283-301

2018

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Substrate-targeting γ-secretase modulators

Nature (London), 2008-06, Vol.453 (7197), p.925-929

2008

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Disulfide bonds and disorder in granulin‐3: An unusual handshake between structural stability and plasticity

Protein science, 2017-09, Vol.26 (9), p.1759-1772

2017

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Molecular Signatures of Neuroinflammation Induced by αSynuclein Aggregates in Microglial Cells

Frontiers in immunology, 2020-01, Vol.11, p.33

2020

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Network analysis of the progranulin-deficient mouse brain proteome reveals pathogenic mechanisms shared in human frontotemporal dementia caused by GRN mutations

Acta neuropathologica communications, 2020-10, Vol.8 (1), p.163-163, Article 163

2020

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Trehalose upregulates progranulin expression in human and mouse models of GRN haploinsufficiency: a novel therapeutic lead to treat frontotemporal dementia

Molecular neurodegeneration, 2016-06, Vol.11 (1), p.46-46, Article 46

2016

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Divergent FUS phosphorylation in primate and mouse cells following double-strand DNA damage

Neurobiology of disease, 2020-12, Vol.146, p.105085-105085, Article 105085

2020

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Lysine 624 of the amyloid precursor protein (APP) is a critical determinant of amyloid β peptide length: support for a sequential model of γ-secretase intramembrane proteolysis and regulation by the amyloid β precursor protein (APP) juxtamembrane region

The Journal of biological chemistry, 2011-11, Vol.286 (46), p.39804-39812

2011

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Diverse compounds mimic Alzheimer disease-causing mutations by augmenting Aβ42 production

Nature medicine, 2005-05, Vol.11 (5), p.545-550

2005

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Complex Relationships between Substrate Sequence and Sensitivity to Alterations in γ‑Secretase Processivity Induced by γ‑Secretase Modulators

Biochemistry (Easton), 2014-04, Vol.53 (12), p.1947-1957

2014

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Possible mechanisms of action of NSAIDs and related compounds that modulate gamma-secretase cleavage

Current topics in medicinal chemistry, 2008, Vol.8 (1), p.47

2008

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Expression of Fused in sarcoma mutations in mice recapitulates the neuropathology of FUS proteinopathies and provides insight into disease pathogenesis

Molecular neurodegeneration, 2012-10, Vol.7 (1), p.53-53, Article 53

2012

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Chronic administration of R-flurbiprofen attenuates learning impairments in transgenic amyloid precursor protein mice

BMC neuroscience, 2007-07, Vol.8 (1), p.54-54, Article 54

2007

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Substrate Sequence Influences γ-Secretase Modulator Activity, Role of the Transmembrane Domain of the Amyloid Precursor Protein

The Journal of biological chemistry, 2011-11, Vol.286 (46), p.39794-39803

2011

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Avoiding Unintended Toxicity

Science (American Association for the Advancement of Science), 2009-05, Vol.324 (5927), p.603-604

2009

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Lysosomal Dysfunction and Other Pathomechanisms in FTLD: Evidence from Progranulin Genetics and Biology

Advances in experimental medicine and biology, 2021-01, Vol.1281, p.219-242

2021

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Intramembrane proteolytic cleavage by human signal peptide peptidase like 3 and malaria signal peptide peptidase

The FASEB journal, 2006-08, Vol.20 (10), p.1671-1679

2006

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Transient pharmacologic lowering of Aβ production prior to deposition results in sustained reduction of amyloid plaque pathology

Molecular neurodegeneration, 2012-08, Vol.7 (1), p.39-39

2012

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An NSAID-like Compound, FT-9, Preferentially Inhibits γ-Secretase Cleavage of the Amyloid Precursor Protein Compared to Its Effect on Amyloid Precursor-like Protein 1

Biochemistry (Easton), 2009-11, Vol.48 (46), p.10894-10904

2009

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N‐terminal phosphorylation of Fused in Sarcoma (FUS) protein results in distinct changes to the cellular proteome that differ from the P525L model of pathology

Alzheimer's & dementia, 2020-12, Vol.16, p.n/a

2020

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N‐terminal phosphorylation of Fused in Sarcoma (FUS) protein results in distinct changes to the cellular proteome that differ from the P525L model of pathology: Developing topics

Alzheimer's & dementia, 2020-12, Vol.16 (S3)

2020

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Lysosome dysfunction as a cause of neurodegenerative diseases: Lessons from frontotemporal dementia and amyotrophic lateral sclerosis

Progranulin deficiency leads to reduced glucocerebrosidase activity

TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

Short Aβ peptides attenuate Aβ42 toxicity in vivo

Chimeric Peptide Species Contribute to Divergent Dipeptide Repeat Pathology in c9ALS/FTD and SCA36

Substrate-targeting γ-secretase modulators

Disulfide bonds and disorder in granulin‐3: An unusual handshake between structural stability and plasticity

Molecular Signatures of Neuroinflammation Induced by αSynuclein Aggregates in Microglial Cells

Network analysis of the progranulin-deficient mouse brain proteome reveals pathogenic mechanisms shared in human frontotemporal dementia caused by GRN mutations

Trehalose upregulates progranulin expression in human and mouse models of GRN haploinsufficiency: a novel therapeutic lead to treat frontotemporal dementia

Divergent FUS phosphorylation in primate and mouse cells following double-strand DNA damage

Lysine 624 of the amyloid precursor protein (APP) is a critical determinant of amyloid β peptide length: support for a sequential model of γ-secretase intramembrane proteolysis and regulation by the amyloid β precursor protein (APP) juxtamembrane region

Diverse compounds mimic Alzheimer disease-causing mutations by augmenting Aβ42 production

Complex Relationships between Substrate Sequence and Sensitivity to Alterations in γ‑Secretase Processivity Induced by γ‑Secretase Modulators

Possible mechanisms of action of NSAIDs and related compounds that modulate gamma-secretase cleavage

Expression of Fused in sarcoma mutations in mice recapitulates the neuropathology of FUS proteinopathies and provides insight into disease pathogenesis

Chronic administration of R-flurbiprofen attenuates learning impairments in transgenic amyloid precursor protein mice

Substrate Sequence Influences γ-Secretase Modulator Activity, Role of the Transmembrane Domain of the Amyloid Precursor Protein

Avoiding Unintended Toxicity

Lysosomal Dysfunction and Other Pathomechanisms in FTLD: Evidence from Progranulin Genetics and Biology

Intramembrane proteolytic cleavage by human signal peptide peptidase like 3 and malaria signal peptide peptidase

Transient pharmacologic lowering of Aβ production prior to deposition results in sustained reduction of amyloid plaque pathology

An NSAID-like Compound, FT-9, Preferentially Inhibits γ-Secretase Cleavage of the Amyloid Precursor Protein Compared to Its Effect on Amyloid Precursor-like Protein 1

N‐terminal phosphorylation of Fused in Sarcoma (FUS) protein results in distinct changes to the cellular proteome that differ from the P525L model of pathology

N‐terminal phosphorylation of Fused in Sarcoma (FUS) protein results in distinct changes to the cellular proteome that differ from the P525L model of pathology: Developing topics

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