Results 71 to 80 of about 35,583 (221)

Metabolism of Presenilin 1: Influence of Presenilin 1 on Amyloid Precursor Protein Processing

Neurobiology of Aging, 1998
To create model systems to examine presenilin 1 (PS1) metabolism in vivo, we generated transgenic mice expressing wild-type and A246E mutant human PS1. Our data indicate that both wild-type and mutant PS1 is endoproteolytically cleaved into 27 kDa N- and 17 kDa C-terminal fragments, which are the principal PS1 species found in normal mammalian brain ...
openaire   +2 more sources

Novel presenilin 1 and 2 double knock-out cell line for in vitro validation of PSEN1 and PSEN2 mutations

Neurobiology of Disease, 2020
Mutations in APP (amyloid precursor protein), PSEN1 (presenilin 1) or PSEN2 (presenilin 2) are the main cause of early-onset familial forms of Alzheimer's disease (autosomal dominant AD or ADAD).
Anna A. Pimenova, Alison M. Goate
doaj   +1 more source

In Silico Structure‐Guided Design of Peptide Candidates Targeting γ‐Secretase Subunit Assembly

Proteins: Structure, Function, and Bioinformatics, EarlyView.
ABSTRACT The γ‐secretase complex is a membrane‐embedded protease essential for intramembrane cleavage of substrates such as Notch receptors and the amyloid precursor protein (APP), processes central to cancer progression and Alzheimer's disease (AD) pathology.
Selcen Arı Yuka, Kübra Telli, Alper Yılmaz   +2 more
wiley   +1 more source

Impact of aging : sporadic, and genetic risk factors on vulnerability to apoptosis in Alzheimer's disease [PDF]

, 2003
The identification of specific genetic (presenilin-1 [PS1] and amyloid precursor protein [APP] mutations) and environmental factors responsible for Alzheimer's disease (AD) has revealed evidence for a shared pathway of neuronal death.
Czech, Christian, Eckert, Anne, Frölich, Lutz, Kratzsch, Tilmann, Leutner, Silke, Maurer, Konrad, Müller, Walter E., Peters, Jürgen, Pradier, Laurent, Schindowski, Katharina, Steiner, Barbara, Touchet, Natalie   +11 more
core   +1 more source

Increased expression of inflammasome signaling genes and proteins in selective brain regions in the intermediate stage of Alzheimer's disease

Brain Pathology, EarlyView.
Neuritic plaques increase in the intermediate stage of Alzheimer's neuropathological change. The intermediate stage of Alzheimer's disease was investigated by transcriptomics and immunohistochemistry. This revealed that inflammasome sensors NLRP1, NLRP3, and AIM2 oligomerize with ASC speck to form the inflammasome complex and initiate the downstream ...
Juan Pablo de Rivero Vaccari, David A. Davis, Andrew P. Sawaya, Susanna P. Garamszegi, Xiaoyan Sun, Ayled Barreda, Helen M. Bramlett, Sakir Humayun Gultekin, W. Dalton Dietrich, Robert W. Keane, Regina T. Vontell   +10 more
wiley   +1 more source

Targeting the Notch receptor dimerization domain to inhibit Notch signalling—A new avenue of therapeutics

The FEBS Journal, EarlyView.
Notch signalling is an evolutionarily conserved signalling pathway that directs cell growth and differentiation across multiple tissue types, and its regulation must be controlled across the lifespan. Aberrant Notch signalling due to genetic mutations that occur within the negative regulatory region of the Notch 1 gene is linked to the development of ...
Gerard F Hoyne
wiley   +1 more source

Assembly, trafficking and function of gamma-secretase [PDF]

, 2006
gamma-Secretase catalyzes the final cleavage of the beta-amyloid precursor protein to generate amyloid-beta peptide, the principal component of amyloid plaques in the brains of patients suffering from Alzheimer's disease.
Baumeister R, Christian Haass, Christoph Kaether, Edbauer D, Fullekrug J, Harald Steiner, Levy-Lahad E, Levy-Lahad E, Pasternak SH, Steiner H   +9 more
core   +1 more source

Direct association of presenilin‐1 with β‐catenin

FEBS Letters, 1998
Families bearing mutations in the presenilin‐1 (PS1) gene develop Alzheimer's disease (AD). However, the mechanism through which PS1 causes AD is unclear. The co‐immunoprecipitation with PS1 in transfected COS‐7 cells indicates that PS1 directly interacts with endogenous β‐catenin, and the interaction requires residues 322–450 of PS1 and 445–676 of β ...
Murayama, Miyuki, Tanaka, Shoji, Palacino, James, Murayama, Ohoshi, Honda, Toshiyuki, Sun, Xiaoyan, Yasutake, Kaori, Nihonmatsu, Naomi, Wolozin, Benjamin, Takashima, Akihiko   +9 more
openaire   +2 more sources

Proteostasis of organelles in aging and disease

The FEBS Journal, EarlyView.
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi, Cansu Doğan, Dunja Petrović, Gülce Perçin, Seda Koyuncu, David Vilchez   +5 more
wiley   +1 more source

Transcriptional Regulation of the Mouse Presenilin-1 Gene [PDF]

Journal of Biological Chemistry, 1997
The presenilin-1 (PS-1) gene encodes at least three separate mRNA transcripts from its 12 exons, which are spread over 50 kilobase pairs of mouse DNA. The first transcript begins with exon 1A, whereas the other transcripts begin with exon 1B. Different portions of exon 1B are spliced to give long and short mRNAs.
N, Mitsuda, A D, Roses, M P, Vitek
openaire   +2 more sources