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Genetic deletion of brevican, one of the main components, resulted in a massive degradation of extracellular matrix baskets at inner hair cells, a significant impairment in spatial coupling of pre- and postsynaptic elements and mild impairment of hearing.
intrachromosomal deletion generating a fusion between BCAN and NTRK1 drives the formation of aggressive high-grade gliomas and confers sensitivity to entrectinib
The synaptic plasticity occurs in the hippocampus of freely behaving mice that lack brevican, the informational content stored by synaptic plasticity is not the same.
This study found that mice with reduced brevican levels show enhanced locomotor activity to acute cocaine and a progressive increase in expression of cocaine CPP during forced abstinence.
The extracellular matrix molecule brevican is an integral component of the machinery mediating fast synaptic transmission at the calyx of Held
This study provided evidence that the brevican modulates synaptogenesis and long-term synapse stability. The mutant neurons display reduced frequencies of mEPSCs and mIPSCs.
these results imply that Bral2-brevican interaction may play a key role in synaptic stabilization and the structural integrity of brain perineuronal nets
defective brevican processing observed in amyloid beta-bearing mice may contribute to deficient neural plasticity
Results indicate that reactive gliosis differs between the spinal cord dorsal root entry zone and dorsal column and that Brevican and Versican may participate in the inhibitory properties of the dorsal root entry zone.
Brevican is not essential for learning and memory, but plays a role in long-term potentiation in mice
Brevican and the ADAMTS-cleaved fragment of brevican were most broadly distributed in neuropil in the brain.
The proteoglycan brevican binds to fibronectin after proteolytic cleavage and promotes glioma cell motility
This study show that brevican plays a crucial role in determining the specialization of the hyaluronan-binding nodal matrix assemblies in large diameter nodes.
Data indicate that median methylation levels of BCAN, HOXD1, KCTD8, KLF11, NXPH1, POU4F1, SIM1, and TCF7L1 were >/=30% higher than in normal samples, representing potential biomarkers for tumor diagnosis.
High Brevican is associated with the invasive phenotype of low-grade astrocytoma.
gene locus at chromosome 1q21-23.
Authors describe the expression of BEHAB/brevican in human brain and characterize two novel glioma-specific isoforms which are generated by differential glycosylation and are absent from normal adult brain and other neuropathologies.
These results demonstrate for the first time that ADAMTS-5 is capable of degrading brevican and is overexpressed in glioblastoma cells, and suggest that ADAMTS-5 may play a role in glioma cell invasion through the cleavage of brevican.
This gene encodes a member of the lectican family of chondroitin sulfate proteoglycans that is specifically expressed in the central nervous system. This protein is developmentally regulated and may function in the formation of the brain extracellular matrix. This protein is highly expressed in gliomas and may promote the growth and cell motility of brain tumor cells. Alternate splicing results in multiple transcript variants.
brevican core protein
, brevican core protein-like
, brevican soluble core protein
, Brevican core protein
, brain-enriched hyaluronan-binding protein
, brevican (brain specific proteoglycan in the aggrecan family)
, chondroitin sulfate proteoglycan 7
, chondroitin sulfate proteoglycan BEHAB
, chondroitin sulfate proteoglycan BEHAB/brevican