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Taken together, these results suggest that the exonic deletion of RELN plays a pathological role, implicating functional changes in the dopaminergic and GABAergic systems, in the pathophysiology of schizophrenia.
our findings provide direct evidence for the impaired Reelin-DAB1 transduction cascade in a patient with deleterious variants in the RELN gene, suggest, for the first time, an abnormal interplay between Reelin-DAB1 and mTORC1 signaling pathways in a patient with nonsyndromic ASD
hypomethylation of the RELN promoter could contribute to the development of cognitive deficits in schizophrenia
New potential risk variant in the RELN locus for dyslexia.
The results suggest that polymorphism rs7341475 in the reelin gene may be associated with the variability of positive symptomatology in schizophrenic men
Our findings strengthen the association of TGFB1 (rs1800472) with otosclerosis and support a relationship between RELN and familial otosclerosis only, which may explain previous variable replications.
Both RELN and its main downstream effector DAB1 are silenced in glioblastoma as compared to non-neoplastic tissue and mRNA expression is inversely correlated with malignancy grade. RELN expression is positively correlated with patient survival in 2 large, independent clinically annotated datasets. RELN silencing occurs via promoter hypermethylation as shown by database mining and bisulfite sequencing of the RELN promoter.
The relationship between TGF-beta1 and RELN and uncovered the important role of RELN in suppressing cell migration in HCC cells.
RELN-del triggered an impaired reelin signal and decreased the expression levels of genes relevant for cell movement in human neurons
RELN expression is increased in AD brain at advanced Braak stages and after Abeta treatment.
Study found a positive link between RELN SNP rs2229864 and ASD risk, but not a significant association between RELN SNPs rs736707 and autism risk. A significant rs736707-rs2229864 haplotype was found. Individuals with a CC haplotype were more likely to have autistic spectrum disorders, whereas individuals with a CT haplotype had more possibility to be typical development controls.
A two-hit loss involving VHL predicted for clear-cell renal cell carcinoma(ccRCC ) and a better prognosis, whereas mutations in PTEN, TP53, or RELN predicted for Sarcomatoid clear-cell renal cell carcinoma and worse prognosis.
we determined that Reelin protein and mRNA levels increased in CJD human samples and in mouse models of human prion disease in contrast to murine models of prion infection. However, changes in Reelin expression appeared only at late terminal stages of the disease, which prevent their use as an efficient diagnostic biomarker.
In primary-culture fetal astrocytes, streptozotocin down-regulated the expression of Reelin 410 and 180 kDa , while alpha-boswellic acid upregulated it. Interruption in astroglial Reelin/Akt/Tau signaling pathways may have a role in Alzheimer disease.
In frontal cortex extracts, an increase in Reelin mRNA, and in soluble and insoluble (guanidine-extractable) Reelin protein, was associated with late Braak stages of Alzheimer's disease (AD), while expression of its receptor, ApoER2, did not change.
This study detected significant reductions in the mRNAs associated with RELN and GAD1 in the frontal cortex (FC) of autism spectrum disorder.
There results suggest that reelin played essential roles in the development of lymphoma and might be a potential drug target in lymphoma
This review addresses recent advances in the field of nonneuronal reelin signaling.
methylation status of the promoter proximal cytosine-phospho-guanine dinucleotides determines the expression of RELN in myeloma cells.
Meta-analyses of 12 RELN gene single nucleotide polymorphisms (SNPs) and related neuropsychiatric disorders (schizophrenia, autistic spectrum disorders, attention-deficit hyperactivity disorder, Alzheimer's disease and bipolar disorders) with subgroup analyses based on ethnicity. Findings suggest a role of RELN SNPs in psychiatric diseases.
data provide evidence of a local increase of aromatase expression by reelin. Regarding reproduction, this crosstalk may contribute to follicular stability and counteract luteinization in ovaries.
The combined results indicate that the direct interaction between L1 and Reelin as well as the Reelin-mediated generation of L1-80 contribute to brain development at early developmental stages.
Data indicate a role of Reelin in the development and function of the brain.
We show that the compartmentalized presence of Reelin is essential for the directionality, but not the actual migratory process or speed, of migrating granule cells leading to their characteristic lamination in the dentate gyrus
controls positioning of brainstem serotonergic raphe neurons
Dextran sulphate sodium (DSS)-colitis activates reelin production. DSS-colitis decreases the methylation of the reelin promoter region.
results highlight a role for reelin in maintaining intestinal epithelial cell homeostasis and providing resistance against colon pathology.
These results indicate that Reelin is an important regulator of GPIb-mediated platelet activation and may represent a new therapeutic target for the prevention and treatment of cardio- and cerebrovascular diseases
ITSN1 is a component of Reelin signaling that acts predominantly by facilitating the VLDLR-Dab1 axis to direct neuronal migration in the cortex and hippocampus and to augment synaptic plasticity.
These results suggest that CTR-dependent Reelin functions are required for some specific normal brain functions and that DeltaC-KI mice recapitulate some aspects of neuropsychiatric disorders, such as schizophrenia, bipolar disorder, and autism spectrum disorder.
Reelin directly promotes N-cadherin-dependent neuronal adhesion, causing neuronal aggregation.
The results of this study reveal that the Reelin/Dab1 pathway contributes to the fine tuning of the density of perisynaptic astroglial ensheathment of synapses established on newborn Granule Cells, with overactivation of the pathway resulting in reduced ensheathment and Reelin-downregulation leading to increased ensheathment.
Model selection was performed on different model structures and a comprehensive mechanistic model of the early Reelin signaling cascade is provided in this work
found that Reelin protein with intact C-terminal region binds preferentially toPurkinje cells
This study demonstrated that both the loss of reelin protein expression, caused by genetic mutation, and prenatal pesticide exposure can alter the shape and connectivity of neurons in several brain regions.
CHD7 is necessary for maintaining an open, accessible chromatin state at the Reln locus. Taken together, this study shows that Reln gene expression is regulated by chromatin remodeling, identifies CHD7 as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD protein can control brain development
ADAMTS-3 was identified as the protease that cleaves and inactivates Reelin in the cerebral cortex and hippocampus. ADAMTS-3 was expressed in the excitatory neurons of the embryonic and postnatal cerebral cortex and hippocampus.
RELN R2290C heterozygous neurospheres reveals up-regulation of Protein Disulfide Isomerase A1, best known as an endoplasmic reticulum-chaperone protein
In the vertebrate visual system, Reelin gradient is important for laminar targeting and for attracting retinal ganglion cell axons.
Developmental gene expression pattern of reelin, dab1, vldlr, and apoer2 in the central nervous system of zebrafish was compared, and their remarkable expression was detected in the developing laminar structures and also non-laminated structures.
A peak in Reelin mRNA and protein expression is present in the pig embryonic brain during the period of major neurogenesis and neuronal migration.
This gene encodes a large secreted extracellular matrix protein thought to control cell-cell interactions critical for cell positioning and neuronal migration during brain development. This protein may be involved in schizophrenia, autism, bipolar disorder, major depression and in migration defects associated with temporal lobe epilepsy. Mutations of this gene are associated with autosomal recessive lissencephaly with cerebellar hypoplasia. Two transcript variants encoding distinct isoforms have been identified for this gene. Other transcript variants have been described but their full length nature has not been determined.
extracellular matrix serine protease
, reelin, extracellular