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A Disc1 peptide binds to GSK3beta, and Disc1 directs early brain development and neurogenesis, by promoting beta-catenin-mediated Wnt signaling and inhibiting GSK3beta activity.
Disc1 and nrg1 (show NRG1 ELISA Kits) function in controlling development of oligodendrocytes and neurones from olig2 (show OLIG2 ELISA Kits)-expressing precursor cells.
Disc1 functions in the transcriptional repression of foxd3 (show FOXD3 ELISA Kits) and sox10 (show SOX10 ELISA Kits), thus mediating cranial neural crest cell migration and differentiation.
This population-based case-control study was carried out to determine whether polymorphisms in DISC1 and NRG1 (show NRG1 ELISA Kits) genes could be associated with schizophrenia in the Chinese population.
This study demonstrated that the Increased density of DISC1-immunoreactive oligodendroglial cells in fronto-parietal white matter of patients with paranoid schizophrenia.
The present findings, at least in part, provide some clues for further investigating the association of DISC1 variants with SCZ susceptibility
DISC1 may be involved in sleep regulation
Polymorphisms in DISC1 play a role in vulnerability to opioid dependence in a Polish sample.
Hypoxic preconditioning decreases NF-kappaB (show NFKB1 ELISA Kits) activity via DISC1.
Results suggest that DISC1 interacts with BA (show APP ELISA Kits)CE1 and promotes lysosomal degradation of (show APP ELISA Kits) BAC (show PSEN1 ELISA Kits)E1, thus reducing the generation of Abeta
It is anterogradely transported to the neurite tips, together with Lis1, and functions in neurite extension via suppression of GSK3beta activity.
DISC1 disruption affects expression of neural cell fate markers and Wnt (show WNT2 ELISA Kits) signaling.
These results uncover an unexpected role for DISC1 in normal beta-cell physiology and suggest that DISC1 dysregulation contributes to T2D independently of its importance for cognition.
abnormality in hippocampal activity at the goal zone during the task may underlie the learning deficit observed in the DISC1 mutant mice.
Missense mutation in DISC1 C-terminal coiled-coil has GSK3beta signaling and sex-dependent behavioral effects in mice
Systematic investigation suggests that DISC1 is present in several cellular compartments, including synapses, where it interacts with a wider molecular network to mediate cellular and synaptic function.
Hypoxic preconditioning decreases NF-kappaB (show NFKB1 ELISA Kits) activity via Disc1.
Results indicate that DISC1 attenuates Abeta (show APP ELISA Kits) generation and cognitive deficits of APP (show APP ELISA Kits)/PS1 (show PSEN1 ELISA Kits) transgenic mice through promoting lysosomal degradation of BACE1 (show BACE ELISA Kits)
These results suggest that alteration of CB1R (show CNR1 ELISA Kits)-mediated signaling in DN-DISC1 mice may underlie susceptibility to detrimental effects of adolescent cannabis exposure on adult behaviors.
These results suggest a mechanism by which cross-talk between DISC1 and NRG1 (show NRG1 ELISA Kits)-ErbB4 (show ERBB4 ELISA Kits) signalling may contribute to these deficits.
Study found that DISC1 influences APP (show APP ELISA Kits) C-terminal processing and Abeta (show APP ELISA Kits) peptide generation, affects surface expression and internalization of APP (show APP ELISA Kits) in neurons
DISC1 regulates the expression of brain neurotrophin (show BDNF ELISA Kits) VGF (show VGF ELISA Kits) through the PI3K/AKT (show AKT1 ELISA Kits)/CREB (show CREB1 ELISA Kits) pathway.
This gene encodes a protein with multiple coiled coil motifs which is located in the nucleus, cytoplasm and mitochondria. The protein is involved in neurite outgrowth and cortical development through its interaction with other proteins. This gene is disrupted in a t(1\;11)(q42.1\;q14.3) translocation which segregates with schizophrenia and related psychiatric disorders in a large Scottish family. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
disrupted in schizophrenia 1 protein
, disrupted in schizophrenia 1
, disrupted in schizophrenia 1 homolog