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Appears in Networks 4

In-Edges 3

act(complex(GO:"gamma-secretase complex")) association p(HGNC:PSEN1, var("?")) View Subject | View Object

Finally, some patients express mutant presenilin proteins 1 and 2 (PS1 and PS2) that can change the processing of APP by altering gamma secretase activity, thereby promoting the generation of amyloidogenic Abeta (Hardy and Selkoe, 2002). PubMed:14556719

path(MESH:"Alzheimer Disease") association p(HGNC:PSEN1, var("?")) View Subject | View Object

Furthermore, presenilin-1, the most common mutation associated with early-onset familial AD (FAD), plays an essential role in calcium homeostasis and maintaining acidic lysosomal pH, with FAD-associated mutations disrupting calcium-dependent vATPase function in lysosomes [7,18–20] PubMed:29758300

Out-Edges 10

p(HGNC:PSEN1, var("?")) increases p(HGNC:APP, frag("672_713")) View Subject | View Object

Transgenic mice over-expressing PSs with FAD mutations show significantly increased Abeta42 levels, suggesting that PS mutations probably induce AD by producing more of the hydrophobic Abeta42 form (Duff et al. 1996; Qian et al. 1998) PubMed:22122372

p(HGNC:PSEN1, var("?")) association act(complex(GO:"gamma-secretase complex")) View Subject | View Object

Finally, some patients express mutant presenilin proteins 1 and 2 (PS1 and PS2) that can change the processing of APP by altering gamma secretase activity, thereby promoting the generation of amyloidogenic Abeta (Hardy and Selkoe, 2002). PubMed:14556719

p(HGNC:PSEN1, var("?")) increases a(CHEBI:"amyloid-beta") View Subject | View Object

Finally, some patients express mutant presenilin proteins 1 and 2 (PS1 and PS2) that can change the processing of APP by altering gamma secretase activity, thereby promoting the generation of amyloidogenic Abeta (Hardy and Selkoe, 2002). PubMed:14556719

p(HGNC:PSEN1, var("?")) association path(MESH:"Alzheimer Disease") View Subject | View Object

Furthermore, presenilin-1, the most common mutation associated with early-onset familial AD (FAD), plays an essential role in calcium homeostasis and maintaining acidic lysosomal pH, with FAD-associated mutations disrupting calcium-dependent vATPase function in lysosomes [7,18–20] PubMed:29758300

p(HGNC:PSEN1, var("?")) decreases act(a(MESH:"Vacuolar Proton-Translocating ATPases")) View Subject | View Object

Furthermore, presenilin-1, the most common mutation associated with early-onset familial AD (FAD), plays an essential role in calcium homeostasis and maintaining acidic lysosomal pH, with FAD-associated mutations disrupting calcium-dependent vATPase function in lysosomes [7,18–20] PubMed:29758300

p(HGNC:PSEN1, var("?")) increases path(MESH:"Alzheimer Disease") View Subject | View Object

That presenilin 1 mutations, which are a cause of early-onset familial AD, impede lysosome proteolysis and accelerate neuritic dystrophy also supports a primary role for failure of proteolytic clearance (Lee et al. 2010). PubMed:22908190

p(HGNC:PSEN1, var("?")) decreases bp(GO:"lysosomal protein catabolic process") View Subject | View Object

That presenilin 1 mutations, which are a cause of early-onset familial AD, impede lysosome proteolysis and accelerate neuritic dystrophy also supports a primary role for failure of proteolytic clearance (Lee et al. 2010). PubMed:22908190

p(HGNC:PSEN1, var("?")) decreases act(a(HBP:Neurites)) View Subject | View Object

That presenilin 1 mutations, which are a cause of early-onset familial AD, impede lysosome proteolysis and accelerate neuritic dystrophy also supports a primary role for failure of proteolytic clearance (Lee et al. 2010). PubMed:22908190

p(HGNC:PSEN1, var("?")) decreases bp(GO:"pH reduction") View Subject | View Object

These observations suggest how PS1 mutations, which impede lysosomal acidification (Lee et al. 2010), may markedly accelerate and amplify neuritic dystrophy in AD PubMed:22908190

p(HGNC:PSEN1, var("?")) decreases act(a(MESH:Neurites)) View Subject | View Object

These observations suggest how PS1 mutations, which impede lysosomal acidification (Lee et al. 2010), may markedly accelerate and amplify neuritic dystrophy in AD PubMed:22908190

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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.