p(HGNC:PICALM)
although genome-wide association studies have linked LOAD to several other genetic variants, such as TREM2 (triggering receptor expressed on myeloid cells 2),27 clusterin (CLU),28 and phosphatidylinositol-binding clathrin assembly protein (PICALM).28,29 PubMed:26195256
And in AD, the decreasing expression of PICALM in brain endothelium reduces Aβ clearance (Zhao et al. 2015b) PubMed:29626319
A highly significant correlation was found between decreased levels of PICALM and increased levels of LC3-II (p=0.0032) or decreased levels of Beclin-1 (p=0.0295) in the total brain lysates from these diseases (Fig 6D,E). PubMed:27260836
A highly significant correlation was found between decreased levels of PICALM and increased levels of LC3-II (p=0.0032) or decreased levels of Beclin-1 (p=0.0295) in the total brain lysates from these diseases (Fig 6D,E). PubMed:27260836
Phosphatidylinositol binding clathrin assembly protein, PICALM (aka CALM) assembles adaptor protein-2 (AP-2) to clathrin, thus participating in clathrin-mediated endocytosis. We have previously reported that the level of full-length PICALM is decreased in AD brains; PICALM was co-localised with phosphorylated tau in NFTs and in granulovacuolar degenerations (GVDs) in the brains of AD patients and of individuals with Down syndrome but was not observed in amyloid plaques (Ando et al., 2013). PubMed:27260836
In PSP cases, both coiled bodies (Fig. 2 D-F) and NFTs (Fig. 2G-I) in the striatum showed a complete co-localisation of PICALM and phosphotau immunoreactivies. PubMed:27260836
Phosphatidylinositol binding clathrin assembly protein, PICALM (aka CALM) assembles adaptor protein-2 (AP-2) to clathrin, thus participating in clathrin-mediated endocytosis. We have previously reported that the level of full-length PICALM is decreased in AD brains; PICALM was co-localised with phosphorylated tau in NFTs and in granulovacuolar degenerations (GVDs) in the brains of AD patients and of individuals with Down syndrome but was not observed in amyloid plaques (Ando et al., 2013). PubMed:27260836
Overexpression of PICALM in APP/PS1 mice substantially elevates Aβ levels, whereas knockdown reduces the Aβ plaque load, respectively [98] PubMed:29758300
although genome-wide association studies have linked LOAD to several other genetic variants, such as TREM2 (triggering receptor expressed on myeloid cells 2),27 clusterin (CLU),28 and phosphatidylinositol-binding clathrin assembly protein (PICALM).28,29 PubMed:26195256
PICALM, mainly expressed in endothelial cells of vascular walls, contributes to the transport of Aβ across the BBB into blood (Xu et al. 2015) PubMed:29626319
And in AD, the decreasing expression of PICALM in brain endothelium reduces Aβ clearance (Zhao et al. 2015b) PubMed:29626319
And in AD, the decreasing expression of PICALM in brain endothelium reduces Aβ clearance (Zhao et al. 2015b) PubMed:29626319
Phosphatidylinositol binding clathrin assembly protein, PICALM (aka CALM) assembles adaptor protein-2 (AP-2) to clathrin, thus participating in clathrin-mediated endocytosis. We have previously reported that the level of full-length PICALM is decreased in AD brains; PICALM was co-localised with phosphorylated tau in NFTs and in granulovacuolar degenerations (GVDs) in the brains of AD patients and of individuals with Down syndrome but was not observed in amyloid plaques (Ando et al., 2013). PubMed:27260836
Phosphatidylinositol binding clathrin assembly protein, PICALM (aka CALM) assembles adaptor protein-2 (AP-2) to clathrin, thus participating in clathrin-mediated endocytosis. We have previously reported that the level of full-length PICALM is decreased in AD brains; PICALM was co-localised with phosphorylated tau in NFTs and in granulovacuolar degenerations (GVDs) in the brains of AD patients and of individuals with Down syndrome but was not observed in amyloid plaques (Ando et al., 2013). PubMed:27260836
Phosphatidylinositol binding clathrin assembly protein, PICALM (aka CALM) assembles adaptor protein-2 (AP-2) to clathrin, thus participating in clathrin-mediated endocytosis. We have previously reported that the level of full-length PICALM is decreased in AD brains; PICALM was co-localised with phosphorylated tau in NFTs and in granulovacuolar degenerations (GVDs) in the brains of AD patients and of individuals with Down syndrome but was not observed in amyloid plaques (Ando et al., 2013). PubMed:27260836
In PSP cases, both coiled bodies (Fig. 2 D-F) and NFTs (Fig. 2G-I) in the striatum showed a complete co-localisation of PICALM and phosphotau immunoreactivies. PubMed:27260836
A highly significant correlation was found between decreased levels of PICALM and increased levels of LC3-II (p=0.0032) or decreased levels of Beclin-1 (p=0.0295) in the total brain lysates from these diseases (Fig 6D,E). PubMed:27260836
A highly significant correlation was found between decreased levels of PICALM and increased levels of LC3-II (p=0.0032) or decreased levels of Beclin-1 (p=0.0295) in the total brain lysates from these diseases (Fig 6D,E). PubMed:27260836
Overexpression of PICALM in APP/PS1 mice substantially elevates Aβ levels, whereas knockdown reduces the Aβ plaque load, respectively [98] PubMed:29758300
A recent line of work revealed Aβ-promoting function of PICALM by demonstrating that PICALM depletion decreased Aβ generation through disrupting clathrin-mediated endocytosis and internalization of γ-secretase [99,100]. PubMed:29758300
PICALM may also promote amyloid clearance from the brain by internalizing Aβ into endothelial cells and ultimately into to the bloodstream [101] PubMed:29758300
Overexpression of PICALM in APP/PS1 mice substantially elevates Aβ levels, whereas knockdown reduces the Aβ plaque load, respectively [98] PubMed:29758300
A recent line of work revealed Aβ-promoting function of PICALM by demonstrating that PICALM depletion decreased Aβ generation through disrupting clathrin-mediated endocytosis and internalization of γ-secretase [99,100]. PubMed:29758300
A recent line of work revealed Aβ-promoting function of PICALM by demonstrating that PICALM depletion decreased Aβ generation through disrupting clathrin-mediated endocytosis and internalization of γ-secretase [99,100]. PubMed:29758300
However, recent work provides direct evidence that PICALM can also modulate macroautophagy, via its role in SNARE endocytosis to clear tau aggregates [102]. PubMed:29758300
However, recent work provides direct evidence that PICALM can also modulate macroautophagy, via its role in SNARE endocytosis to clear tau aggregates [102]. PubMed:29758300
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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.