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Human Reelin ELISA Kit for Sandwich ELISA - ABIN821736
Hornig, Sturm, Fiebich, Tebartz van Elst: Increased Blood-Reelin-Levels in First Episode Schizophrenia. in PLoS ONE 2015
Human Reelin ELISA Kit for Sandwich ELISA - ABIN418446
Cuchillo-Ibañez, Mata-Balaguer, Balmaceda, Arranz, Nimpf, Sáez-Valero: The β-amyloid peptide compromises Reelin signaling in Alzheimer's disease. in Scientific reports 2016
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.
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 (show HELLS ELISA Kits) 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 (show ERBB2 ELISA Kits)(+) 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 (show ERBB2 ELISA Kits) 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 (show LGI1 ELISA Kits) mutations.
We screened for mutations in RELN or VLDLR (show VLDLR ELISA Kits) 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 (show VLDLR ELISA Kits)-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.
The results of this study reveal that the Reelin/Dab1 (show DAB1 ELISA Kits) 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 (show CHD3 ELISA Kits) 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 (show CHD3 ELISA Kits) as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD (show CHRD ELISA Kits) 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 (show P4HB ELISA Kits) 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 (show CA1 ELISA Kits) Hippocampus Integrity in mice.
Sex-associated and brain region-specific differences in reelin expression appear long before Abeta (show APP ELISA Kits)-plaque formation in AbetaPP mutant Alzheimer disease model.
Developmental gene expression pattern of reelin, dab1 (show DAB1 ELISA Kits), vldlr (show VLDLR ELISA Kits), and apoer2 (show LRP8 ELISA Kits) 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