Topic
DAB1
About: DAB1 is a research topic. Over the lifetime, 703 publications have been published within this topic receiving 54412 citations. The topic is also known as: DAB1, reelin adaptor protein.
Papers published on a yearly basis
Papers
TL;DR: The reeler phenotype seems to reflect a failure of early events associated with brain lamination which are normally controlled by reelin.
Abstract: The autosomal recessive mouse mutation reeler leads to impaired motor coordination, tremors and ataxia. Neurons in affected mice fail to reach their correct locations in the developing brain, disrupting the organization of the cerebellar and cerebral cortices and other laminated regions. Here we use a previously characterized reeler allele (rl(tg)) to close a gene, reelin, deleted in two reeler alleles. Normal but not mutant mice express reelin in embryonic and postnatal neurons during periods of neuronal migration. The encoded protein resembles extracellular matrix proteins involved in cell adhesion. The reeler phenotype thus seems to reflect a failure of early events associated with brain lamination which are normally controlled by reelin.
1,782 citations
TL;DR: It is suggested that VLDLR and ApoER2 participate in transmitting the extracellular Reelin signal to intracellular signaling processes initiated by mDab1, a cytosolic protein that activates tyrosine kinases.
1,294 citations
TL;DR: The selective down-regulation of RELN and GAD(67) in prefrontal cortex of patients with schizophrenia and bipolar disorder who have psychosis is consistent with the hypothesis that these parameters are vulnerability factors in psychosis; this plus the loss of the correlation between these 2 parameters that exists in nonpsychotic subjects support the hypotheses that these changes may be liability factors underlying psychosis.
Abstract: Background Reelin (RELN) is a glycoprotein secreted preferentially by cortical γ-aminobutyric acid-ergic (GABAergic) interneurons (layers I and II) that binds to integrin receptors located on dendritic spines of pyramidal neurons or on GABAergic interneurons of layers III through V expressing the disabled-1 gene product (DAB1), a cytosolic adaptor protein that mediates RELN action. To replicate earlier findings that RELN and glutamic acid decarboxylase (GAD) 67 , but not DAB1 expression, are down-regulated in schizophrenic brains, and to verify whether other psychiatric disorders express similar deficits, we analyzed, blind, an entirely new cohort of 60 postmortem brains, including equal numbers of patients matched for schizophrenia, unipolar depression, and bipolar disorder with nonpsychiatric subjects. Methods Reelin, GAD 65 , GAD 67 , DAB1, and neuron-specific–enolase messenger RNAs (mRNAs) and respective proteins were measured with quantitative reverse transcriptase–polymerase chain reaction (RT-PCR) or Western blot analyses. Reelin-positive neurons were identified by immunohistochemistry using a monoclonal antibody. Results Prefrontal cortex and cerebellar expression of RELN mRNA, GAD 67 protein and mRNA, and prefrontal cortex RELN-positive cells was significantly decreased by 30% to 50% in patients with schizophrenia or bipolar disorder with psychosis, but not in those with unipolar depression without psychosis when compared with nonpsychiatric subjects. Group differences were absent for DAB1,GAD 65 and neuron-specific–enolase expression implying that RELN and GAD 67 down-regulations were unrelated to neuronal damage. Reelin and GAD 67 were also unrelated to postmortem intervals, dose, duration, or presence of antipsychotic medication. Conclusions The selective down-regulation of RELN and GAD 67 in prefrontal cortex of patients with schizophrenia and bipolar disorder who have psychosis is consistent with the hypothesis that these parameters are vulnerability factors in psychosis; this plus the loss of the correlation between these 2 parameters that exists in nonpsychotic subjects support the hypothesis that these changes may be liability factors underlying psychosis.
1,267 citations
TL;DR: It is shown that Reelin binds directly and specifically to the ectodomains of VLDLR and ApoER2 in vitro and that blockade of V LDLR and apoE receptor 2 correlates with loss of Reelin-induced tyrosine phosphorylation of Disabled-1 in cultured primary embryonic neurons.
947 citations
TL;DR: Findings revealed that the selective expression of a distinct molecule on Cajal-Retzius neurons is critical for the normal lamination of cortical neurons in the mammalian neocortex.
926 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 10 |
| 2024 | 5 |
| 2023 | 13 |
| 2022 | 26 |
| 2021 | 14 |
| 2020 | 11 |