Prion pathogenesis is independent of caspase-12. - Wikidata - awgldk - TriplyDB

Prion pathogenesis is independent of caspase-12.

Prion pathogenesis is independent of caspase-12.

http://www.wikidata.org/entity/Q42068269

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Sustained translational repression by eIF2α-P mediates prion neurodegeneration Unfolded Protein Response and Macroautophagy in Alzheimer's, Parkinson's and Prion Diseases Protein disulfide isomerases in neurodegeneration: from disease mechanisms to biomedical applications Expression of mutant or cytosolic PrP in transgenic mice and cells is not associated with endoplasmic reticulum stress or proteasome dysfunction Heat shock proteins: cellular and molecular mechanisms in the central nervous system.Heat shock factor 1 regulates lifespan as distinct from disease onset in prion disease.Cytoplasmic prion protein induces forebrain neurotoxicity Prion protein misfolding affects calcium homeostasis and sensitizes cells to endoplasmic reticulum stress.The intricate mechanisms of neurodegeneration in prion diseases.Prion infections and anti-PrP antibodies trigger converging neurotoxic pathways.Striatal pathology underlies prion infection-mediated hyperactivity in mice.Synaptic dysfunction in prion diseases: a trafficking problem?Endoplasmic reticulum stress, inflammation, and perinatal brain damage The Endoplasmic Reticulum Chaperone GRP78/BiP Modulates Prion Propagation in vitro and in vivo.Endoplasmic reticulum and the unfolded protein response: dynamics and metabolic integration Disturbance of endoplasmic reticulum proteostasis in neurodegenerative diseases.Abnormal calcium homeostasis and protein folding stress at the ER: A common factor in familial and infectious prion disorders.Mechanisms of prion-induced neurodegeneration.The Protein-disulfide Isomerase ERp57 Regulates the Steady-state Levels of the Prion Protein.Dysfunction of the PI3K-Akt-GSK-3 pathway is a common feature in cell culture and in vivo models of prion disease.The Endoplasmic Reticulum Unfolded Protein Response in Neurodegenerative Disorders and Its Potential Therapeutic Significance ER Stress and Neurodegenerative Disease: A Cause or Effect Relationship?What Is Our Current Understanding of PrPSc-Associated Neurotoxicity and Its Molecular Underpinnings?

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P2860

Prion pathogenesis is independent of caspase-12.

http://www.wikidata.org/entity/Q42068269

description

2007 nî lūn-bûn

@nan

2007年の論文

@ja

2007年論文

@yue

2007年論文

@zh-hant

2007年論文

@zh-hk

2007年論文

@zh-mo

2007年論文

@zh-tw

2007年论文

@wuu

2007年论文

@zh

2007年论文

@zh-cn

name

Prion pathogenesis is independent of caspase-12.

@en

Prion pathogenesis is independent of caspase-12.

@nl

type

label

Prion pathogenesis is independent of caspase-12.

@en

Prion pathogenesis is independent of caspase-12.

@nl

prefLabel

Prion pathogenesis is independent of caspase-12.

@en

Prion pathogenesis is independent of caspase-12.

@nl

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Prion pathogenesis is independent of caspase-12.

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P2093

Andrew D Steele

http://www.w3.org/2001/XMLSchema#string

Andrew W Borkowski

http://www.w3.org/2001/XMLSchema#string

Caroline H Yi

http://www.w3.org/2001/XMLSchema#string

Claudio Hetz

http://www.w3.org/2001/XMLSchema#string

Junying Yuan

http://www.w3.org/2001/XMLSchema#string

Robert H Wollmann

http://www.w3.org/2001/XMLSchema#string

Walker S Jackson

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P2860

Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta

Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1

Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alpha

Involvement of caspase-4 in endoplasmic reticulum stress-induced apoptosis and Abeta-induced cell death

Enhanced bacterial clearance and sepsis resistance in caspase-12-deficient mice

The power of automated high-resolution behavior analysis revealed by its application to mouse models of Huntington's and prion diseases.

Overexpressed protein disulfide isomerase in brains of patients with sporadic Creutzfeldt-Jakob disease.

Perturbation of endoplasmic reticulum homeostasis facilitates prion replication.

Bax deletion prevents neuronal loss but not neurological symptoms in a transgenic model of inherited prion disease.

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243-247

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10.4161/PRI.1.4.5551

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4

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1

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Susan Lindquist

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19164919

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Prion protein family

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2634538

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