Pearson correlation between biological quadruplicates for each condition and time point

Autor: Henning Urlaub, Inga Zerr, Oleksandr Yagensky, Tamara Rabe, John Jia En Chua, Saima Zafar, Saravanan Gunaseelan, Wolfgang Härtig, Mahdokht Kohansal-Nodehi
Jazyk: angličtina
Rok vydání: 2019
Předmět:
0301 basic medicine
Mouse
Proteome
Gene Expression
Alzheimer's disease
Hebp1
human
mouse
neuron
neuroscience
rat
pathology [Alzheimer Disease]
Mice
0302 clinical medicine
Biology (General)
analysis [Proteome]
Caspase
biology
General Neuroscience
Neurodegeneration
General Medicine
Cell biology
medicine.anatomical_structure
biosynthesis [Heme-Binding Proteins]
Disease Progression
Medicine
Signal transduction
Research Article
Human
Genetically modified mouse
QH301-705.5
Science
Heme binding protein 1
Mice
Transgenic
physiopathology [Alzheimer Disease]
General Biochemistry
Genetics and Molecular Biology
03 medical and health sciences
Heme-Binding Proteins
Alzheimer Disease
medicine
Animals
Humans
General Immunology and Microbiology
Wild type
Neurotoxicity
medicine.disease
030104 developmental biology
biology.protein
Rat
Neuron
ddc:600
030217 neurology & neurosurgery
Neuroscience
Zdroj: eLife, Vol 8 (2019)
eLife
eLife 8, e47498 (2019). doi:10.7554/eLife.47498
Popis: Alzheimer’s disease is the most prevalent neurodegenerative disorder leading to progressive cognitive decline. Despite decades of research, understanding AD progression at the molecular level, especially at its early stages, remains elusive. Here, we identified several presymptomatic AD markers by investigating brain proteome changes over the course of neurodegeneration in a transgenic mouse model of AD (3×Tg-AD). We show that one of these markers, heme-binding protein 1 (Hebp1), is elevated in the brains of both 3×Tg-AD mice and patients affected by rapidly-progressing forms of AD. Hebp1, predominantly expressed in neurons, interacts with the mitochondrial contact site complex (MICOS) and exhibits a perimitochondrial localization. Strikingly, wildtype, but not Hebp1-deficient, neurons showed elevated cytotoxicity in response to heme-induced apoptosis. Increased survivability in Hebp1-deficient neurons is conferred by blocking the activation of the mitochondrial-associated caspase signaling pathway. Taken together, our data highlight a role of Hebp1 in progressive neuronal loss during AD progression.
Databáze: OpenAIRE
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