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anti-Human Reelin Antibodies:
anti-Mouse (Murine) Reelin Antibodies:
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Mouse (Murine) Monoclonal Reelin Primary Antibody for IHC (p), IHC - ABIN153124
Saegusa, Woo, Fujimoto, Kemmochi, Shimamoto, Hirose, Mitsumori, Nishikawa, Shibutani: Sustained production of Reelin-expressing interneurons in the hippocampal dentate hilus after developmental exposure to anti-thyroid agents in rats. in Reproductive toxicology (Elmsford, N.Y.) 2010
Show all 11 Pubmed References
Human Monoclonal Reelin Primary Antibody for IHC (p), IP - ABIN153123
Ogawa, Wang, Ohishi, Taniai, Akane, Suzuki, Mitsumori, Shibutani: Reversible aberration of neurogenesis targeting late-stage progenitor cells in the hippocampal dentate gyrus of rat offspring after maternal exposure to acrylamide. in Archives of toxicology 2012
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 Antibodies) 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 Antibodies)(+) 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 Antibodies) 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 Antibodies) mutations.
We screened for mutations in RELN or VLDLR (show VLDLR Antibodies) 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 Antibodies)-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 presence of reelin was elevated in junctional areas as in dysplastic nevi. VLDLR (show VLDLR Antibodies) presented positive values in 16 cases (16/ 32) and ApoER2 (show LRP8 Antibodies) was weak positive in 7 cases.
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 Antibodies) 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 Antibodies) as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD (show CHRD Antibodies) 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 Antibodies) 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 Antibodies) Hippocampus Integrity in mice.
Sex-associated and brain region-specific differences in reelin expression appear long before Abeta (show APP Antibodies)-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.
Developmental gene expression pattern of reelin, dab1 (show DAB1 Antibodies), vldlr (show VLDLR Antibodies), and apoer2 (show LRP8 Antibodies) 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