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Human Monoclonal SORL1 Primary Antibody pour ELISA, WB - ABIN1724683
Scherzer, Offe, Gearing, Rees, Fang, Heilman, Schaller, Bujo, Levey, Lah: Loss of apolipoprotein E receptor LR11 in Alzheimer disease. dans Archives of neurology 2004
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Human Monoclonal SORL1 Primary Antibody pour ICC, IHC - ABIN1724674
Gabrielsson, Olofsson, Sjögren, Jernås, Elander, Lönn, Rudemo, Carlsson: Evaluation of reference genes for studies of gene expression in human adipose tissue. dans Obesity research 2005
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Dog (Canine) Polyclonal SORL1 Primary Antibody pour ELISA - ABIN546707
Jacobsen, Madsen, Jacobsen, Nielsen, Gliemann, Petersen: Activation and functional characterization of the mosaic receptor SorLA/LR11. dans The Journal of biological chemistry 2001
Mouse (Murine) Polyclonal SORL1 Primary Antibody pour ELISA, WB - ABIN184579
Kim, Lee, Lee, Kim, Song, Huh, Lee, Kim, Kim, Hong, Shim, Chang: Implication of mouse Vps26b-Vps29-Vps35 retromer complex in sortilin trafficking. dans Biochemical and biophysical research communications 2010
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Data describe a transcript that encodes a truncated sorLA receptor, suggesting novel neuronal functions for sorLA and that alternative transcription provides a mechanism for SORL1 activity regulation.
SORLA co-precipitates with HER2 in cancer cells and regulates HER2 subcellular distribution by promoting recycling of the endosomal receptor back to the plasma membrane. Depletion of SORLA triggers HER2 targeting to late endosomal/lysosomal compartments and impairs HER2-driven signalling and in vivo tumour growth.
rare variant in SORL1 gene previously associated with Alzheimer's disease in genome-wide association studies and meta-analyses was associated with lower total capital EM, Cyrillicsmall o, Cyrilliccapital ES, Cyrilliccapital A, Cyrillic scores in the random sample of elderly people that suggests declined cognitive functions in the carriers of this variant in elderly
The levels of sLR11, abundantly expressed in carotid atherosclerotic plaques, are highly associated with increased plaque score
sLR11 binds to CSF-HDL and competes with Abeta in binding to apoE in CSF-HDL
Study, demonstrates that the Alzheimer disease (AD) related variant SORL1 A528T contributes to susceptibility to Parkinson disease with dementia and shows a weak association with an AD-like CSF biomarker signature.
The change Trp848Ter and a splice-site variant in SORL1 are likely correlated with Familial Alzheimer's Disease.
Data show that amyloid precursor protein (APP) dimerization affects its interaction with LDL receptor related protein 1 (LRP1) and LDL-receptor related protein SorLA (SorLA), suggesting that APP dimerization modulates its interplay with sorting molecules and in turn its localization and processing.
The sorting-related receptor with A-type repeats (SorLA) is a well-studied pathogenic factor for Alzheimer's and belongs to the Vps10p domain receptor family, which also encompasses sortilin and SorCS1-3.
A meta-analysis identified empirical data assessing effects of a single nucleotide polymorphisms of SORL1 on Alzheimer's disease based on 14 studies involving 37941 cases and 49727 control studies; showed increased risk between single nucleotide polymorphisms (rs641120, rs1010159) and Alzheimer's disease susceptibility in Asian populations, single nucleotide polymorphisms rs641120 was detected as a decreased risk in both.
This study found one SORL1 RNA transcript strongly regulated by SORL1-BDNF interactions in elderly without pathological AD and showing stronger associations with diffuse than neuritic Abeta plaques.
The findings of this study suggested that three genetic variants rs2070045, rs1699102, and rs3824968 could significantly regulate SORL1 expression in human brain tissues.
We conclude that rs1784933 and rs1805192 minor alleles, gene- gene interaction between rs1784933 and rs1805192, gene- environment interaction between rs1784933 and alcohol drinking, and haplotype containing the rs1784933- A and rs689021- C alleles are all associated with increased LOAD risk.
Show reduced sortilin-related receptor (SORL1) expression only in neural stem cells of a patient carrying two copies of APOE4 allele with increased amyloid beta/SORL1 localization along the degenerated neurites.
This study shown rare Genetic Variant in SORL1 May Increase Penetrance of Alzheimer's Disease in a Family with Several Generations of APOE-varepsilon4 Homozygosity.
The C allele in SORL1 was found to be a protective factor for late-onset Alzheimer's disease in both Caucasian and Han Chinese.
Report altered hippocampal functional connectivity in carriers with risk APOE epsilon4 or SORL1 G-allele, which may predispose these risk-allele carriers to be susceptible for Alzheimer disease.
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.
Its genetic variation contributes to pathogenesis of Alzheimer disease.
SORL1 variations influence the atrophy of specific Alzheimer disease-related brain structures, suggesting the potential role of SORL1 in the neurodegeneration of cognitive related regions.
These results demonstrate a novel role for SORLA as a physiological and pathological EphA4 modulator.
Results demonstrate that the lack of SORLA results in accumulation of phosphorylated synapsins in cortex and hippocampus. Authors propose an underlying molecular mechanism by demonstrating that SORLA interacts with phosphorylated synapsins through 14-3-3 adaptor proteins to deliver synapsins to calpain-mediated proteolytic degradation.
Analysis of the molecular mechanism for the association of SORL1 with obesity: there is a genetic link between neurodegeneration and metabolism that converges on the receptor SORLA
SorLA ectodomain, released from the cell membrane upon enzymatic cleavage of full-length SorLA, may act as an IL-6 carrier protein that stabilizes IL-6 and its capacity for trans signaling.
We identify binding and trafficking interactions between two of these factors, SORLA and SNX27, and demonstrate that SNX27 can direct trafficking of SORLA and the Abeta precursor APP to the cell surface to limit the production of Abeta. Diversion APP to the cell surface through modulation of this molecular complex may represent a complimentary strategy for future development in AD treatment.
LR11 regulated vascular smooth muscle cell proliferation during the progression of hypoxia-induced medial thickening in mice.
Therefore, SORL1 activation by 6-shogaol provides neuronal cell survival through the inhibition of Abeta production. These results indicate that 6-shogaol should be regarded as an SORL1 activator and a potential preventive agent for the treatment of AD.
Data strongly suggest an involvement of LR11 in mediating the harmful effects of a high-fat diet on CVD progression.
Mice lacking LR11 are protected from diet-induced obesity associated with an increased browning of white adipose tissue and hypermetabolism.
using massively parallel reporter assays, we dissect the enhancer activity of three liver eExons (SORL1 exon 17, TRAF3IP2 exon 2, PPARG exon 6) at single nucleotide resolution in the mouse liver
Data indicate that activation of alpha(2A) adrenergic receptor (alpha(2A)AR) signaling disrupts transgenic amyloid precursor protein (APP) interaction with sorting-related receptor with A repeat (SorLA) in cells and brain.
SORLA-mediated trafficking of TrkB enhances the response of neurons to BDNF.
SorLA acts as sorting receptor for the GDNF/GFRalpha1 complex, directing it from the cell surface to endosomes.
sLR11 regulates the hypoxia-enhanced adhesion of HSPCs via an uPAR-mediated pathway that stabilizes the hematological pool size by controlling cell attachment to the BM niche.
SorLA expression might be critical not only for amyloid-related pathology but also for other cellular processes altered in Alzheimer disease.
overexpression of SorLA increased migration of THP-1 monocytes to monocyte chemoattractant protein-1 with a coincident increase in UPAR expression.
Sorcs1 deficiency might be a common genetic risk factor underlying the predisposition to Alzheimer disease that is associated with type 2 diabetes.
These data suggest a novel regulatory pathway whereby intracellular trafficking of SPAK by the sorting receptor SORLA is crucial for proper NKCC2 activation and for maintenance of renal ion balance.
These findings demonstrate that the beneficial effects ascribed to BDNF in APP metabolism act through induction of Sorla that encodes a negative regulator of neuronal APP processing.
LR11, which is expressed in the intimal SMCs, is important in the process of the migration and proliferation of SMCs in vivo.
This gene encodes a mosaic protein that belongs to at least two families: the vacuolar protein sorting 10 (VPS10) domain-containing receptor family, and the low density lipoprotein receptor (LDLR) family. The encoded protein also contains fibronectin type III repeats and an epidermal growth factor repeat. The encoded protein is translated as a preproprotein and likely plays roles in endocytosis and sorting. There may be an association between expression of this locus and Alzheimer's Disease.
sortilin-related receptor, L(DLR class) A repeats containing
, sortilin-related receptor, L(DLR class) A repeats-containing
, sortilin-related receptor-like
, LDLR relative with 11 ligand-binding repeats
, low-density lipoprotein receptor relative with 11 ligand-binding repeats
, mosaic protein LR11
, sortilin-related receptor
, sorting protein-related receptor containing LDLR class A repeats