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CHMP2B encodes a component of the heteromeric ESCRT-III complex (Endosomal Sorting Complex Required for Transport III) that functions in the recycling or degradation of cell surface receptors. Zusätzlich bieten wir Ihnen CHMP2B Antikörper (67) und CHMP2B Proteine (10) und viele weitere Produktgruppen zu diesem Protein an.
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We directly link TDP-43 (zeige TARDBP ELISA Kits) loss of function toxicity to two genes with rare amyotrophic lateral sclerosis and frontotemporal lobar degeneration-causing mutations, CHMP2B and ErbB4 (zeige ERBB4 ELISA Kits)
these data indicate that the neuronal expression of human CHMP2B(intron5) in areas involved in motor and cognitive functions induces progressive motor alterations associated with dementia symptoms and with histopathological hallmarks reminiscent of both amyotrophic lateral sclerosis and frontotemporal dementia.
Endogenous TMEM106B was partly sequestered in CHMP2B-positive structures. SNP T185 was more associated with CHMP2B than SNP S185, and it enhanced neurotoxicity caused by CHMP2B(Intron5) compared to S185-expressing cells.
Study showed that mutant CHMP2B causes the pathological accumulation of endolysosomal components early in the frontotemporal dementia disease course
Protein kinase CK2 alpha is involved in the phosphorylation of the ESCRT-III subunits CHMP3 and CHMP2B, as well as of VPS4B/SKD1, an ATPase that mediates ESCRT-III disassembly.
Data indicate that knockdown of syntaxin 13 (syx13) further increased the cellular toxicity caused by muaant CHMP2B (CHMP2BIntron5) expression.
CHMP2B immunoreactivity was increased in the dorsal motor nucleus of the vagus nerve in Parkinson's disease and incidental Lewy body disease brains
These findings suggest that endosomal and autophagic pathway is associated with degradation or formation of alpha-synuclein aggregates in alpha-synucleinopathy.
Subjects with CHMP2B mutation show cognitive changes dominated by executive dysfunctions, years before they fulfil diagnostic criteria of FTD (zeige FTL ELISA Kits).
Direct link between disease-causing mutations and the cellular phenotype in cells originating from CHMP2B mutation patients with frontotemporal dementia.
The presence of early microglial changes in our CHMP2B mutant mice indicates neuroinflammation may be a contributing factor to the neurodegeneration observed in FTD (zeige FTL ELISA Kits).
This study showing that CHMP2B resides at synapses and is involved in synaptic plasticity.
Forebrain-specific expression of frontotemporal dementia-associated mutant CHMP2B in mice causes several age-dependent neurodegenerative phenotypes, including social behavioral impairments.
Chmp2b is one of the most highly regulated cell-autonomous targets of Lbx1 (zeige Lbx1 ELISA Kits) in the embryonic mouse neural tube
These data describe the first mouse model of dementia caused by CHMP2B mutation and provide new insights into the mechanisms of CHMP2B-induced neurodegeneration
This gene encodes a component of the heteromeric ESCRT-III complex (Endosomal Sorting Complex Required for Transport III) that functions in the recycling or degradation of cell surface receptors. ESCRT-III functions in the concentration and invagination of ubiquitinated endosomal cargos into intralumenal vesicles. The protein encoded by this gene is found as a monomer in the cytosol or as an oligomer in ESCRT-III complexes on endosomal membranes. It is expressed in neurons of all major regions of the brain. Mutations in this gene result in one form of familial frontotemporal lobar degeneration.
chromatin modifying protein 2B
, charged multivesicular body protein 2b
, chromatin-modifying protein 2b
, VPS2 homolog B
, vacuolar protein-sorting-associated protein 2-2
, chromatin modifying protein 2B, like