gamma-secretase-activating protein isoform X7 [Mus musculus]
Protein Classification
List of domain hits
| Name | Accession | Description | Interval | E-value | ||||
| GSAP super family | cl45535 | gamma-secretase-activating protein and similar proteins; Gamma-secretase activating protein, ... |
5-196 | 3.44e-71 | ||||
gamma-secretase-activating protein and similar proteins; Gamma-secretase activating protein, also called GSAP or PION, selectively increases amyloid-beta production through a mechanism involving its interaction with both gamma-secretase and its substrate, the amyloid-beta precursor protein C-terminal fragment (APP-CTF). GSAP cleavage via caspase-3 is regulated and depends upon the availability of 5-lipoxygenase. Alzheimer's disease (AD), the most prevalent cause of dementia, is associated with accumulation of amyloid-beta peptide which is a major characteristic of the AD brain and responsible for some of its clinical manifestations. The anticancer drug imatinib had been shown to inhibit amyloid-beta formation without affecting Notch cleavage, by preventing GSAP interaction with the gamma-secretase substrate, APP-CTF. Thus, GSAP can serve as an amyloid-beta-lowering therapeutic target without affecting other key functions of gamma-secretase. The actual alignment was detected with superfamily member cd23105: Pssm-ID: 438516 Cd Length: 514 Bit Score: 236.85 E-value: 3.44e-71
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| GSAP-16 | pfam14959 | gamma-Secretase-activating protein C-term; GSAP, or gamma-secretase-activating protein, also ... |
341-448 | 2.25e-49 | ||||
gamma-Secretase-activating protein C-term; GSAP, or gamma-secretase-activating protein, also known as PION, regulates gamma-secretase activity. The holo-protein is a large, approx 850 residue protein that is rapidly cleaved to an active 16 kDa C-terminal fragment that is the stable, predominant form. GSAP is expressed in inclusion bodies and is important in brain function. It dramatically and selectively increases neurotoxic beta-Amyloid production in the brain through a mechanism involving its interactions with both gamma-secretase and its substrate, the amyloid precursor protein C-terminal fragment (APP-CTF). Accumulation of neurotoxic beta-Amyloid is a major hallmark of Alzheimer's disease. Formation of beta-Amyloid is catalyzed by gamma-secretase, a protease with numerous substrates that catalyzes the intra-membrane cleavage of integral membrane proteins such as Notch receptors and APP (beta-amyloid precursor protein). The secondary structure of GSAP is largely alpha-helical, lacking well-defined tertiary structure. GSAP represents a type of gamma-secretase regulator that directs enzyme specificity by interacting with a specific substrate. : Pssm-ID: 464405 Cd Length: 108 Bit Score: 165.87 E-value: 2.25e-49
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| Name | Accession | Description | Interval | E-value | ||||
| GSAP | cd23105 | gamma-secretase-activating protein and similar proteins; Gamma-secretase activating protein, ... |
5-196 | 3.44e-71 | ||||
gamma-secretase-activating protein and similar proteins; Gamma-secretase activating protein, also called GSAP or PION, selectively increases amyloid-beta production through a mechanism involving its interaction with both gamma-secretase and its substrate, the amyloid-beta precursor protein C-terminal fragment (APP-CTF). GSAP cleavage via caspase-3 is regulated and depends upon the availability of 5-lipoxygenase. Alzheimer's disease (AD), the most prevalent cause of dementia, is associated with accumulation of amyloid-beta peptide which is a major characteristic of the AD brain and responsible for some of its clinical manifestations. The anticancer drug imatinib had been shown to inhibit amyloid-beta formation without affecting Notch cleavage, by preventing GSAP interaction with the gamma-secretase substrate, APP-CTF. Thus, GSAP can serve as an amyloid-beta-lowering therapeutic target without affecting other key functions of gamma-secretase. Pssm-ID: 438516 Cd Length: 514 Bit Score: 236.85 E-value: 3.44e-71
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| GSAP-16 | pfam14959 | gamma-Secretase-activating protein C-term; GSAP, or gamma-secretase-activating protein, also ... |
341-448 | 2.25e-49 | ||||
gamma-Secretase-activating protein C-term; GSAP, or gamma-secretase-activating protein, also known as PION, regulates gamma-secretase activity. The holo-protein is a large, approx 850 residue protein that is rapidly cleaved to an active 16 kDa C-terminal fragment that is the stable, predominant form. GSAP is expressed in inclusion bodies and is important in brain function. It dramatically and selectively increases neurotoxic beta-Amyloid production in the brain through a mechanism involving its interactions with both gamma-secretase and its substrate, the amyloid precursor protein C-terminal fragment (APP-CTF). Accumulation of neurotoxic beta-Amyloid is a major hallmark of Alzheimer's disease. Formation of beta-Amyloid is catalyzed by gamma-secretase, a protease with numerous substrates that catalyzes the intra-membrane cleavage of integral membrane proteins such as Notch receptors and APP (beta-amyloid precursor protein). The secondary structure of GSAP is largely alpha-helical, lacking well-defined tertiary structure. GSAP represents a type of gamma-secretase regulator that directs enzyme specificity by interacting with a specific substrate. Pssm-ID: 464405 Cd Length: 108 Bit Score: 165.87 E-value: 2.25e-49
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| Name | Accession | Description | Interval | E-value | ||||
| GSAP | cd23105 | gamma-secretase-activating protein and similar proteins; Gamma-secretase activating protein, ... |
5-196 | 3.44e-71 | ||||
gamma-secretase-activating protein and similar proteins; Gamma-secretase activating protein, also called GSAP or PION, selectively increases amyloid-beta production through a mechanism involving its interaction with both gamma-secretase and its substrate, the amyloid-beta precursor protein C-terminal fragment (APP-CTF). GSAP cleavage via caspase-3 is regulated and depends upon the availability of 5-lipoxygenase. Alzheimer's disease (AD), the most prevalent cause of dementia, is associated with accumulation of amyloid-beta peptide which is a major characteristic of the AD brain and responsible for some of its clinical manifestations. The anticancer drug imatinib had been shown to inhibit amyloid-beta formation without affecting Notch cleavage, by preventing GSAP interaction with the gamma-secretase substrate, APP-CTF. Thus, GSAP can serve as an amyloid-beta-lowering therapeutic target without affecting other key functions of gamma-secretase. Pssm-ID: 438516 Cd Length: 514 Bit Score: 236.85 E-value: 3.44e-71
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| GSAP-16 | pfam14959 | gamma-Secretase-activating protein C-term; GSAP, or gamma-secretase-activating protein, also ... |
341-448 | 2.25e-49 | ||||
gamma-Secretase-activating protein C-term; GSAP, or gamma-secretase-activating protein, also known as PION, regulates gamma-secretase activity. The holo-protein is a large, approx 850 residue protein that is rapidly cleaved to an active 16 kDa C-terminal fragment that is the stable, predominant form. GSAP is expressed in inclusion bodies and is important in brain function. It dramatically and selectively increases neurotoxic beta-Amyloid production in the brain through a mechanism involving its interactions with both gamma-secretase and its substrate, the amyloid precursor protein C-terminal fragment (APP-CTF). Accumulation of neurotoxic beta-Amyloid is a major hallmark of Alzheimer's disease. Formation of beta-Amyloid is catalyzed by gamma-secretase, a protease with numerous substrates that catalyzes the intra-membrane cleavage of integral membrane proteins such as Notch receptors and APP (beta-amyloid precursor protein). The secondary structure of GSAP is largely alpha-helical, lacking well-defined tertiary structure. GSAP represents a type of gamma-secretase regulator that directs enzyme specificity by interacting with a specific substrate. Pssm-ID: 464405 Cd Length: 108 Bit Score: 165.87 E-value: 2.25e-49
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