Zobrazeno 1 - 10 of 50 pro vyhledávání: '"Sez6"'
1
Akademický článek
The Sez6 Family Inhibits Complement by Facilitating Factor I Cleavage of C3b and Accelerating the Decay of C3 Convertases
Autor: Wen Q. Qiu, Shaopeiwen Luo, Stefanie A. Ma, Priyanka Saminathan, Herman Li, Jenny M. Gunnersen, Harris A. Gelbard, Jennetta W. Hammond
Publikováno v: Frontiers in Immunology, Vol 12 (2021)
The Sez6 family consists of Sez6, Sez6L, and Sez6L2. Its members are expressed throughout the brain and have been shown to influence synapse numbers and dendritic morphology. They are also linked to various neurological and psychiatric disorders. All
Externí odkaz: https://doaj.org/article/65afac20f5e24796b07dfcf699d2be4c
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2
Akademický článek
Exome sequencing in an Italian family with Alzheimer’s disease points to a role for seizure-related gene 6 (SEZ6) rare variant R615H
Autor: Lara Paracchini, Luca Beltrame, Lucia Boeri, Federica Fusco, Paolo Caffarra, Sergio Marchini, Diego Albani, Gianluigi Forloni
Publikováno v: Alzheimer’s Research & Therapy, Vol 10, Iss 1, Pp 1-20 (2018)
Abstract Background The typical familial form of Alzheimer’s disease (FAD) accounts for about 5% of total Alzheimer’s disease (AD) cases. Presenilins (PSEN1 and PSEN2) and amyloid-β (A4) precursor protein (APP) genes carry all reported FAD-linke
Externí odkaz: https://doaj.org/article/30ede54f6a134ce398fff6dcba2adf24
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3
Akademický článek
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4
Akademický článek
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5
BACE inhibitor treatment of mice induces hyperactivity in a Seizure-related gene 6 family dependent manner without altering learning and memory
Autor: Stefan F. Lichtenthaler, Brian Joel Hrupka, H. J. M. Gijsen, Hiroshi Takeshima, Kathleen Sue Lyn Teng, Jenny M. Gunnersen, Kathryn M. Munro, Amelia Nash
Publikováno v: Scientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
Scientific reports 11(1), 15084 (2021). doi:10.1038/s41598-021-94369-0
Scientific Reports
BACE inhibitors, which decrease BACE1 (β-secretase 1) cleavage of the amyloid precursor protein, are a potential treatment for Alzheimer’s disease. Clinical trials using BACE inhibitors have reported a lack of positive effect on patient symptoms a
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::61e0ac5c9959bc4bfafc3fcfeb50f8b7
https://doaj.org/article/30fc73a123fe4f83943a0c12121c8a83
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6
Amyloid-ß plaque formation and BACE1 accumulation in the brains of a 5xFAD Alzheimer's disease mouse model is associated with altered distribution and not proteolysis of BACE1 substrates Sez6 and Sez6L
Autor: Kristina Dominko, Ana Rastija, Kosara Smiljanic, Aleksandra Mladenovic, Lucija Lešnjaković, Selma Kanazir, Desanka Milanovic, Silva Hecimovic
Publikováno v: Mechanisms of Ageing and Development
The formation of amyloid-ß peptides (Aß), that accumulate in Alzheimer's disease (AD) brains, involves proteolytic processing of the amyloid precursor protein (APP) firstly by ß-secretase (BACE1). Since BACE1 cleaves a plethora of other substrates
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::40b101dd6cf3005ba464cf75b12f866e
http://fulir.irb.hr/7675/7/MAD-D-22-00218_R1.pdf
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7
Akademický článek
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8
Akademický článek
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9
The Sez6 Family Inhibits Complement by Facilitating Factor I Cleavage of C3b and Accelerating the Decay of C3 Convertases
Autor: Priyanka Saminathan, Wen Q. Qiu, Jenny M. Gunnersen, Jennetta W. Hammond, Stefanie A. Ma, Shaopeiwen Luo, Herman Li, Harris A. Gelbard
Publikováno v: Frontiers in Immunology, Vol 12 (2021)
Frontiers in Immunology
The Sez6 family consists of Sez6, Sez6L, and Sez6L2. Its members are expressed throughout the brain and have been shown to influence synapse numbers and dendritic morphology. They are also linked to various neurological and psychiatric disorders. All
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1b187e1ffda366bdf272c00ef0a6f8ec
https://doi.org/10.3389/fimmu.2021.607641
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10
Exome sequencing in an Italian family with Alzheimer’s disease points to a role for seizure-related gene 6 (SEZ6) rare variant R615H
Autor: Sergio Marchini, Paolo Caffarra, Diego Albani, Lucia Boeri, Federica Fusco, Luca Beltrame, Lara Paracchini, Gianluigi Forloni
Publikováno v: Alzheimer’s Research & Therapy, Vol 10, Iss 1, Pp 1-20 (2018)
Alzheimer's Research & Therapy
Background The typical familial form of Alzheimer’s disease (FAD) accounts for about 5% of total Alzheimer’s disease (AD) cases. Presenilins (PSEN1 and PSEN2) and amyloid-β (A4) precursor protein (APP) genes carry all reported FAD-linked mutatio
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6e98fe3984daa7abd59dd851710589d6
http://link.springer.com/article/10.1186/s13195-018-0435-2
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