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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.
review of role in Alzheimer's disease
Significant association between rs17458357 , rs2572683,rs12555895 within the RELN gene and accelerated decline in Cognition performance in Chinese elderly male Gout population.
This study demonstrated that RELN DNA methylation might contribute to the pathogenesis of schizophrenia.
The present investigation, performed on a study sample from a population with one of the highest suicide rates in the world, indicated an association between rs2965087 in the reelin gene and the expression of suicidal threats a month before suicide in contrast to other symptoms of depression.
Reelin is was low in primary breast cancer tissue, but higher in Her2(+) breast cancers (but not triple-negative ones) metastasizing to the brain, especially in the tumor periphery adjacent to surrounding astrocytes. In the neural niche, astrocytes epigenetically regulate Reelin expression and its interaction with Her2 leading to increased proliferation and survival fitness.
Heterozygous RELN mutations cause a typical Autosomal Dominant Lateral Temporal Lobe Epilepsy syndrome, indistinguishable from that associated with LGI1 mutations.
We screened for mutations in RELN or VLDLR and compared the phenotype of these patients with that of previously reported patients. differences in clinical severity, involvement of the cerebellar hemispheres, together with the severity of the neocortical defect, enables RELN-mutated patients to be distinguished from VLDLR-mutated patients.
Reelin signaling is a critical player in the modulation of synaptic function.
Reelin was expressed by human hepatic stellate cells/myofibroblasts and the number of these cells increased significantly in the lobule as the liver fibrosis progressed, suggesting a role for Reelin in the activation of hepatic stellate cells/myofibroblasts during liver injury.
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
A C-terminal region truncation of the reelin protein causes abnormal phenotypes in the cerebral cortex and hippocampus.
This study demonstrated that Reelin Maintain Postnatal CA1 Hippocampus Integrity in mice.
Sex-associated and brain region-specific differences in reelin expression appear long before Abeta-plaque formation in AbetaPP mutant Alzheimer disease model.
These findings suggest that circulating Reelin promotes atherosclerosis by increasing vascular inflammation, and that reducing or inhibiting circulating Reelin may present a novel approach for the prevention of cardiovascular disease.
A new transgenic mouse model demonstrates that Reelin is a molecule which is critical for proper cortical development.
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