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Human Polyclonal PICALM Primary Antibody für ICC, IF - ABIN4345438
Zhao, Sagare, Ma, Halliday, Kong, Kisler, Winkler, Ramanathan, Kanekiyo, Bu, Owens, Rege, Si, Ahuja, Zhu, Miller, Schneider, Maeda, Maeda, Sugawara, Ichida, Zlokovic: Central role for PICALM in amyloid-β blood-brain barrier transcytosis and clearance. in Nature neuroscience 2015
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The PICALM rs3851179 polymorphism significantly affects the default mode network network in mild cognitive impairment
No association for PICALM with Alzheimer's disease in south-Indian population.
this updated meta-analysis highlights the involvement of PICALM rs3851179 variant in Alzheimer's disease susceptibility in Chinese population.
suggest that there is a close relationship between abnormal PICALM processing, tau pathology and impairment of autophagy in human neurodegenerative diseases
There was no significant association between single nucleotide polymorphisms (SNPS) of GAB2 (zeige GAB2 Antikörper) rs2373115 (G > T) and PICALM rs541458 (C > T) and Alzheimer's disease (AD). The allele T of rs3851179 in PICALM was associated with a 13 % increase in the risk of AD. Seven SNPs on SORL1 (zeige SORL1 Antikörper) were significantly associated with AD.
Hippocampal shape features derived from the diffeomorphic metric-based shape analysis led to the identification of significant CLU (zeige CLU Antikörper)-PICALM interaction effects on hippocampal morphology in young healthy adults, which were not identified by volume measurement and voxel-wise analysis.
This study provided preliminary evidences supporting that PICALM variations render protections by facilitating reserve capacities of posterior cingulate in non-demented elderly.
rs3851179 in PICALM was associated with an increased risk of gestational diabetes. The frequency of the Alzheimer's disease risk-associated C allele was significantly higher in the gestational diabetes group compared to controls. The C allele of the PICALM SNP was protective for impaired glucose tolerance.
Alzheimer's disease risk PICALM GG genotype suggests changes in the cortical excitatory-inhibitory balance, which are heightened during normal aging.
Study concludes that the novel clathrin interaction sites identified here in CALM and AP180 have a major role in how these proteins interface with clathrin. This work advances the case that AP180 and CALM are required to use a combination of standard clathrin N-terminal domain binding motifs and the sequence identified here for optimal binding and assembling clathrin.
Confinement within the presynaptic bouton is mediated in part by synaptic vesicle protein association with the clathrin-based endocytic machinery to limit diffusional spread of newly exocytosed SV proteins.
the PICALM PIP2 binding domain is necessary for transferrin receptor endocytosis in erythroblasts and absolutely essential for erythroid development from mouse hematopoietic stem/progenitor cells in an erythroid culture system.
During leukemogenesis, CALM-AF10 (zeige MLLT10 Antikörper) plays critical roles in the cytoplasm.
These data reveal that PICALM plays a critical role in iron homeostasis.
PICALM, an adaptor protein involved in clathrin-mediated endocytosis, regulates APP (zeige APP Antikörper) internalization and subsequent Abeta (zeige APP Antikörper) generation. PICALM contributes to amyloid plaque load in brain likely via its effect on Abeta (zeige APP Antikörper) metabolism.
These results indicate that CALM is required for erythroid maturation and transferrin (zeige Tf Antikörper) internalization in mice.
In leukemia cells, full-length CALM-AF10 localized to the nucleus with no consistent effect on growth factor endocyctosis, and suppressed histone H3 lysine 79 methylation regardless of the presence of clathrin
the Rarb (zeige RARB Antikörper) region of Mmu14 and Stmn2 (zeige STMN2 Antikörper), but not Cr1 (zeige TDGF1 Antikörper) or Clu (zeige CLU Antikörper) or Picalm have roles in prion (zeige PRNP Antikörper) disease
fit14R & fit15R are nonsense point mutations in the mouse PICALM gene. They are splice-donor alterations causing transcripts less abundant transcripts missing exons 4 & 17, respectively. The protein is truncated near the N or C termini, respectively.
This gene encodes a clathrin assembly protein, which recruits clathrin and adaptor protein complex 2 (AP2) to cell membranes at sites of coated-pit formation and clathrin-vesicle assembly. The protein may be required to determine the amount of membrane to be recycled, possibly by regulating the size of the clathrin cage. The protein is involved in AP2-dependent clathrin-mediated endocytosis at the neuromuscular junction. A chromosomal translocation t(10\;11)(p13\;q14) leading to the fusion of this gene and the MLLT10 gene is found in acute lymphoblastic leukemia, acute myeloid leukemia and malignant lymphomas. The polymorphisms of this gene are associated with the risk of Alzheimer disease. Multiple alternatively spliced transcript variants encoding different isoforms have been found for this gene.
clathrin assembly lymphoid myeloid leukemia protein
, phosphatidylinositol-binding clathrin assembly protein
, clathrin assembly lymphoid myeloid leukemia
, clathrin-assembly lymphoid leukemia protein
, clathrin-assembly lymphoid myeloid leukemia protein