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The physiology of the β-amyloid precursor protein intracellular domain AICD

Journal of neurochemistry, 2012-01, Vol.120 (s1), p.109-124

2012

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Correction to: Intraneuronal aggregation of the β‑CTF fragment of APP (C99) induces Aβ‑independent lysosomal-autophagic pathology

Acta neuropathologica, 2023-10, Vol.146 (4), p.659-660

2023

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The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer's disease

Cell death & disease, 2024-05, Vol.15 (5), p.367-367, Article 367

2024

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Is γ-secretase a beneficial inactivating enzyme of the toxic APP C-terminal fragment C99?

The Journal of biological chemistry, 2021-01, Vol.296, p.100489, Article 100489

2021

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p53-Dependent control of cell death by nicastrin: lack of requirement for presenilin-dependent γ-secretase complex

Journal of neurochemistry, 2009-04, Vol.109 (1), p.225-237

2009

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Intraneuronal aggregation of the β-CTF fragment of APP (C99) induces Aβ-independent lysosomal-autophagic pathology

Acta neuropathologica, 2016-08, Vol.132 (2), p.257-276

2016

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Targeting γ-secretase triggers the selective enrichment of oligomeric APP-CTFs in brain extracellular vesicles from Alzheimer cell and mouse models

Translational neurodegeneration, 2019-12, Vol.8 (1), p.35-35, Article 35

2019

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The η-secretase-derived APP fragment ηCTF is localized in Golgi, endosomes and extracellular vesicles and contributes to Aβ production

Cellular and molecular life sciences : CMLS, 2023-04, Vol.80 (4), p.97-97, Article 97

2023

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The Transcription Factor EB Reduces the Intraneuronal Accumulation of the Beta-Secretase-Derived APP Fragment C99 in Cellular and Mouse Alzheimer’s Disease Models

Cells (Basel, Switzerland), 2020-05, Vol.9 (5), p.1204

2020

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The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus

The Journal of neuroscience, 2012-11, Vol.32 (46), p.16243-16255

2012

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p53-dependent control of transactivation of the Pen2 promoter by presenilins

Journal of cell science, 2009-11, Vol.122 (21), p.4003-4008

2009

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β-Amyloid Precursor Protein Intracellular Domain Controls Mitochondrial Function by Modulating Phosphatase and Tensin Homolog–Induced Kinase 1 Transcription in Cells and in Alzheimer Mice Models

Biological psychiatry (1969), 2018-03, Vol.83 (5), p.416-427

2018

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Evidence that the amyloid-β protein precursor intracellular domain, AICD, derives from β-secretase-generated C-terminal fragment

Journal of Alzheimer's disease, 2012-01, Vol.30 (1), p.145

2012

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γ-Secretase-mediated regulation of neprilysin: influence of cell density and aging and modulation by imatinib

Journal of Alzheimer's disease, 2011-01, Vol.27 (3), p.511

2011

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Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP

Neuron (Cambridge, Mass.), 2005-05, Vol.46 (4), p.541-554

2005

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Intraneuronal accumulation of C99 contributes to synaptic alterations, apathy-like behavior, and spatial learning deficits in 3×TgAD and 2×TgAD mice

Neurobiology of aging, 2018-11, Vol.71, p.21-31

2018

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TMP21 Transmembrane Domain Regulates γ-Secretase Cleavage

The Journal of biological chemistry, 2009-10, Vol.284 (42), p.28634-28641

2009

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APH1 Polar Transmembrane Residues Regulate the Assembly and Activity of Presenilin Complexes

The Journal of biological chemistry, 2009-06, Vol.284 (24), p.16298-16307

2009

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Ectodomain shedding of PLA2R1 is mediated by the metalloproteases ADAM10 and ADAM17

The Journal of biological chemistry, 2024-06, p.107480, Article 107480

2024

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Response to Correspondence: Pardossi-Piquard et al., “Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP.” Neuron 46, 541–554

Neuron (Cambridge, Mass.), 2007-02, Vol.53 (4), p.483-486

2007

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The physiology of the β-amyloid precursor protein intracellular domain AICD: Alzheimer's Disease: The Amyloid Cascade Hypothesis - 20 Years On

Journal of neurochemistry, 2012, Vol.120, p.109-124

2012

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The physiology of the [beta]-amyloid precursor protein intracellular domain AICD

Journal of neurochemistry, 2012-01, Vol.120, p.109

2012

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Influence of Genetic Background on Apathy-Like Behavior in Triple Transgenic AD Mice

Current Alzheimer research, 2016-08, Vol.13 (8), p.942

2016

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The physiology of the β-amyloid precursor protein intracellular domain AICD

Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer’s disease models and human brains

Palmitate Is Increased in the Cerebrospinal Fluid of Humans with Obesity and Induces Memory Impairment in Mice via Pro-inflammatory TNF-α

Correction to: Intraneuronal aggregation of the β‑CTF fragment of APP (C99) induces Aβ‑independent lysosomal-autophagic pathology

The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer's disease

Is γ-secretase a beneficial inactivating enzyme of the toxic APP C-terminal fragment C99?

p53-Dependent control of cell death by nicastrin: lack of requirement for presenilin-dependent γ-secretase complex

Intraneuronal aggregation of the β-CTF fragment of APP (C99) induces Aβ-independent lysosomal-autophagic pathology

Targeting γ-secretase triggers the selective enrichment of oligomeric APP-CTFs in brain extracellular vesicles from Alzheimer cell and mouse models

The η-secretase-derived APP fragment ηCTF is localized in Golgi, endosomes and extracellular vesicles and contributes to Aβ production

The Transcription Factor EB Reduces the Intraneuronal Accumulation of the Beta-Secretase-Derived APP Fragment C99 in Cellular and Mouse Alzheimer’s Disease Models

The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus

p53-dependent control of transactivation of the Pen2 promoter by presenilins

β-Amyloid Precursor Protein Intracellular Domain Controls Mitochondrial Function by Modulating Phosphatase and Tensin Homolog–Induced Kinase 1 Transcription in Cells and in Alzheimer Mice Models

Evidence that the amyloid-β protein precursor intracellular domain, AICD, derives from β-secretase-generated C-terminal fragment

γ-Secretase-mediated regulation of neprilysin: influence of cell density and aging and modulation by imatinib

Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP

Intraneuronal accumulation of C99 contributes to synaptic alterations, apathy-like behavior, and spatial learning deficits in 3×TgAD and 2×TgAD mice

TMP21 Transmembrane Domain Regulates γ-Secretase Cleavage

APH1 Polar Transmembrane Residues Regulate the Assembly and Activity of Presenilin Complexes

Ectodomain shedding of PLA2R1 is mediated by the metalloproteases ADAM10 and ADAM17

Response to Correspondence: Pardossi-Piquard et al., “Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP.” Neuron 46, 541–554

The physiology of the β-amyloid precursor protein intracellular domain AICD: Alzheimer's Disease: The Amyloid Cascade Hypothesis - 20 Years On

The physiology of the [beta]-amyloid precursor protein intracellular domain AICD

Influence of Genetic Background on Apathy-Like Behavior in Triple Transgenic AD Mice

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