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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Integral membrane protein 2B

FBD, BRI2, ITM2B, integral membrane protein 2B, Abri
Amyloid precursor proteins are processed by beta-secretase and gamma-secretase to produce beta-amyloid peptides which form the characteristic plaques of Alzheimer disease. This gene encodes a transmembrane protein which is processed at the C-terminus by furin or furin-like proteases to produce a small secreted peptide which inhibits the deposition of beta-amyloid. Mutations which result in extension of the C-terminal end of the encoded protein, thereby increasing the size of the secreted peptide, are associated with two neurogenerative diseases, familial British dementia and familial Danish dementia. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: APP, CAN, ACID, V1a, HAD
Papers on FBD
Oxidative stress and mitochondria-mediated cell death mechanisms triggered by the familial Danish dementia ADan amyloid.
Rostagno et al., New York City, United States. In Neurobiol Dis, Jan 2016
The main amyloid subunit composing FDD lesions, a 34-amino acid de-novo generated peptide ADan, is the direct result of a genetic defect at the 3'-end of the BRI2 gene and the physiologic action of furin-like proteolytic processing at the C-terminal region of the ADan precursor protein.
BRI2 and BRI3 are functionally distinct phosphoproteins.
da Cruz E Silva et al., Aveiro, Portugal. In Cell Signal, Jan 2016
The functional significance of these complexes is apparent given that both BRI proteins are substrates of PP1, thus simultaneously this is the first report of BRI2 and BRI3 as phosphoproteins.
Interaction of ApoE3 and ApoE4 isoforms with an ITM2b/BRI2 mutation linked to the Alzheimer disease-like Danish dementia: Effects on learning and memory.
D'Adamio et al., New York City, United States. In Neurobiol Learn Mem, Dec 2015
Mutations in Amyloid β Precursor Protein (APP) and in genes that regulate APP processing - such as PSEN1/2 and ITM2b/BRI2 - cause familial dementia, such Familial Alzheimer disease (FAD), Familial Danish (FDD) and British (FBD) dementias.
Reduced Fertility and Altered Epididymal and Sperm Integrity in Mice Lacking ADAM7.
Cho et al., Kwangju, South Korea. In Biol Reprod, Sep 2015
Western blot analyses revealed reduced levels of integral membrane protein 2B (ITM2B) and ADAM2 in sperm from Adam7-null mice, suggesting a requirement for ADAM7 in normal expression of sperm membrane proteins involved in sperm functions.
Lessons from a Rare Familial Dementia: Amyloid and Beyond.
Walsh et al., Dublin, Ireland. In J Parkinsons Dis Alzheimers Dis, Aug 2015
Contemporaneous other studies suggested that loss of the ABri precursor protein (BRI2) may underlie the cognitive deficits in FBD.
The Familial British Dementia Mutation Promotes Formation of Neurotoxic Cystine Cross-linked Amyloid Bri (ABri) Oligomers.
Walsh et al., Dublin, Ireland. In J Biol Chem, Aug 2015
Post-translational processing of wild type BRI2 and FBD-BRI2 result in the production of a 23-residue long Bri peptide and a 34-amino acid long ABri peptide, respectively, and ABri is found deposited in the brains of individuals with FBD.
Differential Inhibition of Signal Peptide Peptidase Family Members by Established γ-Secretase Inhibitors.
Golde et al., Philadelphia, United States. In Plos One, 2014
We use a recombinant substrate based on the amino-terminus of BRI2 fused to amyloid β 1-25 (Aβ1-25) (FBA) to develop facile, cost-effective SPP/SPPL protease assays.
Generalised Anxiety Disorder--A Twin Study of Genetic Architecture, Genome-Wide Association and Differential Gene Expression.
Spector et al., London, United Kingdom. In Plos One, 2014
Significant differential expression of two exons with the ITM2B gene within the discordant MZ subset was observed, a finding that was replicated in an independent cohort.
Role of BRI2 in dementia.
Teunissen et al., Amsterdam, Netherlands. In J Alzheimers Dis, 2013
Similarly, FBD and FDD originate from mutations in the BRI2 gene (or ITM2b), causing amyloid angiopathy and neurofibrillary tangles analogous to those observed in AD.
Risks of misinterpretation in the evaluation of the effect of fruit-based drinks in postprandial studies.
Palmery et al., Roma, Italy. In Gastroenterol Res Pract, 2013
It has been suggested that some fruit-based drinks (FBD) may delay the onset of postprandial stress, which is involved in the pathogenesis of many diseases.
Exploitation of latent allostery enables the evolution of new modes of MAP kinase regulation.
Lim et al., San Francisco, United States. In Cell, 2013
One activator (Ste5-VWA) provides pathway insulation and dates to the divergence of Fus3 from its paralog, Kss1; a second activator (Ste5-FBD) that tunes mating behavior is, in contrast, not conserved in most lineages.
The α-helical content of the transmembrane domain of the British dementia protein-2 (Bri2) determines its processing by signal peptide peptidase-like 2b (SPPL2b).
Haass et al., München, Germany. In J Biol Chem, 2012
The alpha-helical content of the transmembrane domain of the British dementia protein-2 (Bri2) determines its processing by signal peptide peptidase-like 2b (SPPL2b).
BRI2 protein regulates β-amyloid degradation by increasing levels of secreted insulin-degrading enzyme (IDE).
Coomaraswamy et al., Tübingen, Germany. In J Biol Chem, 2011
BRI2 protein regulates beta-amyloid degradation by increasing levels of secreted insulin-degrading enzyme (IDE).
Glycosylation of BRI2 on asparagine 170 is involved in its trafficking to the cell surface but not in its processing by furin or ADAM10.
Efthimiopoulos et al., Athens, Greece. In Glycobiology, 2011
BRI2 is N-glycosylated at Asn170 and show that this post-translational modification is essential for its expression at the cell surface but not for its proteolytic processing.
BRICHOS domain associated with lung fibrosis, dementia and cancer--a chaperone that prevents amyloid fibril formation?
Presto et al., Uppsala, Sweden. In Febs J, 2011
The BRICHOS domain was initially defined from sequence alignments of the Bri protein associated with familial dementia, chondromodulin associated with chondrosarcoma and surfactant protein C precursor (proSP-C) associated with respiratory distress syndrome and interstitial lung disease (ILD).
APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant.
D'Adamio et al., United States. In Embo J, 2011
Knock-in mice with familial Danish dementia, a mouse model congruous to human disease since they carry one mutant and one wild-type Bri2 allele, show that the Danish mutation causes loss of Bri2 protein, synaptic plasticity and memory impairment.
Increased AβPP processing in familial Danish dementia patients.
D'Adamio et al., United States. In J Alzheimers Dis, 2010
Neurological effects of the Danish form of BRI2 dementia caused by toxic amyloid Abeta protein precursor metabolites suggest that familial Danish and Alzheimer's dementias share common pathogenic mechanisms.
Modeling familial British and Danish dementia.
Vidal et al., Indianapolis, United States. In Brain Struct Funct, 2010
Familial British dementia (FBD) and familial Danish dementia (FDD) are two autosomal dominant neurodegenerative diseases caused by mutations in the BRI ( 2 ) gene.
Thalidomide and thalidomide analogues for maintenance of remission in Crohn's disease.
Stokkers et al., Manchester, United Kingdom. In Cochrane Database Syst Rev, 2008
SEARCH STRATEGY: MEDLINE (1966 to September 2008), EMBASE (1984 to September 2008), the Cochrane Central Register of Controlled Trials from the Cochrane Library (Issue 3, 2008) and the IBD/FBD Review Group Specialized Trials Register were searched to identify relevant studies.
A stop-codon mutation in the BRI gene associated with familial British dementia.
Ghiso et al., New York City, United States. In Nature, 1999
A point mutation at the stop codon of BRI therefore results in the generation of the ABri peptide, which is deposited as amyloid fibrils causing neuronal disfunction and dementia.
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