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Human Polyclonal PICALM Primary Antibody for 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
Show all 5 Pubmed References
Human Polyclonal PICALM Primary Antibody for IHC, IHC (p) - ABIN4345441
Hu, Wu, Feng, Li, Wang, Qi, Du: Cellular protein profiles altered by PRRSV infection of porcine monocytes-derived dendritic cells. in Veterinary microbiology 2019
The data of this study suggest a possible role of PICALM methylation in Alzheimer's Disease, particularly related to cognitive function.
the PICALM rs3851179 polymorphism was associated with Alzheimer's disease; the APOE epsilon4 status did not influence the relationship (Meta-Analysis)
the Single nucleotide polymorphisms rs11136000 of CLU, rs541458 of PICALM, and rs1554948 of TNK1 according to the three age groups 50-65 years (group 1), 66-80 years (group 2), and 80+ years (group 3) in 569 older subjects without cognitive impairment (NoCI) and 520 Alzheimer's disease (AD) patients, were studied.
interactive effects of rs541458 x age existed with regard to executive function and processing speed after controlling for gender, years of education and APOE epsilon4 status.
IN PICALM rs3851179 polymorphism, the age- dependent increase in the P3 latency was more pronounced in the PICALM GG carriers than in the carriers of the PICALM AA and PICALM AG genotypes.
There were significant differences in genotype and allele frequencies for the SNP PICALM rs3851179 between Brazilian Alzheimer and Parkinson disease cases and controls, but none for CR1 rs6656401 and CLU rs11136000 intronic polymorphisms.
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 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 were significantly associated with AD.
Hippocampal shape features derived from the diffeomorphic metric-based shape analysis led to the identification of significant CLU-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.
Depletion of PICALM in brain-derived cells has significant effects on the processing of APP, probably by reducing clathrin-mediated endocytosis. In particular, it affects the production of beta-C-terminal fragment which is increasingly considered to be an important mediator in Alzheimer's disease independent of Abeta.
reduction of CALM decreases Ab deposition as well as brain levels of insoluble Ab42 in vivo These results suggest that CALM expression modifies Alzheimer disease (AD)risk by regulating Aamyloid-beta protein pathology
PICALM is involved with late onset Alzheimer's disease. [review]
Our finding suggests that PICALM rs3851179 could contribute to cognitive impairment in older patients with Parkinson disease
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 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 internalization and subsequent Abeta generation. PICALM contributes to amyloid plaque load in brain likely via its effect on Abeta metabolism.
These results indicate that CALM is required for erythroid maturation and transferrin 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 region of Mmu14 and Stmn2, but not Cr1 or Clu or Picalm have roles in prion 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