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BOS1 Bos1p

Bos1p, BOS1, Gosr2, GS27
This gene encodes a trafficking membrane protein which transports proteins among the medial- and trans-Golgi compartments. Due to its chromosomal location and trafficking function, this gene may be involved in familial essential hypertension. Three transcript variants encoding three different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: BET1, CAN, HAD, v-SNARE, YPT1
Papers on Bos1p
Overexpression of native Saccharomyces cerevisiae ER-to-Golgi SNARE genes increased heterologous cellulase secretion.
Van Zyl et al., Stellenbosch, South Africa. In Appl Microbiol Biotechnol, Jan 2016
Co-overexpression of the most promising exocytic SNARE components identified in literature for secretory enhancement of the cellulolytic proteins tested (SSO1 for Sf-Cel3A and SNC1 for Te-Cel7A) with the most effective ER-to-Golgi SNARE components identified in this study (SED5 for both Sf-Cel3A and Te-Cel7A) yielded variable results, with Sf-Cel3A improved by 131 % and Te-Cel7A yielding no improvement.
Endogenous microRNAs in human microvascular endothelial cells regulate mRNAs encoded by hypertension-related genes.
Liang et al., Milwaukee, United States. In Hypertension, Oct 2015
The result indicated significant suppression of the abundance of mRNA encoded by ADM by endogenous miR-181a-5p, ATP2B1 by the miR-27 family, FURIN by miR-125a-5p, FGF5 by the let-7 family, GOSR2 by miR-27a-3p, JAG1 by miR-21-5p, SH2B3 by miR-30a-5p, miR-98, miR-181a-5p, and the miR-125 family, TBX3 by the miR-92 family, ADRA1B by miR-22-3p, ADRA2A by miR-30a-5p and miR-30e-5p, ADRA2B by miR-30e-5p, ADRB1 by the let-7 family and miR-98, EDNRB by the miR-92 family, and NOX4 by the miR-92 family, miR-100-5p, and miR-99b-5p (n=3-9; P<0.05 versus scrambled anti-miR).
A genetic variant in the seed region of miR-4513 shows pleiotropic effects on lipid and glucose homeostasis, blood pressure, and coronary artery disease.
Dehghan et al., Rotterdam, Netherlands. In Hum Mutat, 2014
We sought to identify miR-4513 target genes that may mediate these associations and revealed five genes (PCSK1, BNC2, MTMR3, ANK3, and GOSR2) through which these effects might be taking place.
De novo donor HLA-specific antibodies predict development of bronchiolitis obliterans syndrome after lung transplantation.
Smith et al., Brighton, United Kingdom. In J Heart Lung Transplant, 2014
RESULTS: De novo DSA was associated with development of BOS Stage 1 (BOS1; hazard ratio [HR] = 2.302, p = 0.0015), BOS2 (HR = 3.627, p < 0.0001) and BOS3 (HR = 5.736, p < 0.0001).
Development of a two-step high-resolution melting (HRM) analysis for screening sequence variants associated with resistance to the QoIs, benzimidazoles and dicarboximides in airborne inoculum of Botrytis cinerea.
Pappas et al., Vólos, Greece. In Fems Microbiol Lett, 2014
Three and five different genotypes were detected and classified according to their melting profiles in BenA and bos1 genes associated with resistance to benzimidazoles and dicarboximides, respectively.
EYA1-related disorders: two clinical cases and a literature review.
Martini et al., Padova, Italy. In Int J Pediatr Otorhinolaryngol, 2014
RESULTS: Diagnostic criteria indicated that the two patients were affected by BOS1 (Branchio-Otic Syndrome 1).
Gene-age interactions in blood pressure regulation: a large-scale investigation with the CHARGE, Global BPgen, and ICBP Consortia.
Rao et al., Saint Louis, United States. In Am J Hum Genet, 2014
Index SNPs in the EHBP1L1 (DBP and MAP), CASZ1 (SBP and MAP), and GOSR2 (PP) loci exhibited the largest age interactions, with opposite directions of effect in the young versus the old.
Characterization of iprodione resistance in Botrytis cinerea from strawberry and blackberry.
Schnabel et al., In Phytopathology, 2014
Sequence analysis of the target gene bos1, which codes for a class III histidine kinase, revealed that the MR phenotype was associated with Q369P and N373S mutations and that the LR phenotype was associated with either a I365S or a I365N mutation.
Ramsay Hunt syndrome: clinical characterization of progressive myoclonus ataxia caused by GOSR2 mutation.
de Koning et al., Groningen, Netherlands. In Mov Disord, 2014
Recently, a mutation in the GOSR2 gene (c.430G>T,
Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.
Johnson et al., In Nature, 2011
This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology.
A mutation in the Golgi Qb-SNARE gene GOSR2 causes progressive myoclonus epilepsy with early ataxia.
Berkovic et al., Adelaide, Australia. In Am J Hum Genet, 2011
This p.Gly144Trp mutation is equivalent to a loss of function and results in failure of GOSR2 protein to localize to the cis-Golgi.
GOSR2 Lys67Arg is associated with hypertension in whites.
Boerwinkle et al., Houston, United States. In Am J Hypertens, 2009
We found evidence that a SNP in GOSR2 is modestly associated with hypertension in whites from the ARIC study and the WGHS.
Targeting of Arf-1 to the early Golgi by membrin, an ER-Golgi SNARE.
Donaldson et al., Bethesda, United States. In J Cell Biol, 2005
These studies suggest that membrin recruits Arf-1 to the early Golgi and reveal distinct kinetic cycles for Arf-1 at early and late Golgi determined by different sets of Arf regulators and effectors.
Branchiootorenal Spectrum Disorders
Smith, Seattle, United States. In Unknown Journal, 1999
Molecular genetic testing of EYA1 (BOR1, BOS1) detects mutations in approximately 40% of individuals with the clinical diagnosis of BOR/BOS.
Nucleation of COPII vesicular coat complex by endoplasmic reticulum to Golgi vesicle SNAREs.
Schekman et al., Berkeley, United States. In Science, 1998
Protein trafficking from the endoplasmic reticulum (ER) to the Golgi apparatus involves specific uptake into coat protein complex II (COPII)-coated vesicles of secretory and of vesicle targeting (v-SNARE) proteins.
A SNARE involved in protein transport through the Golgi apparatus.
Hong et al., Singapore, Singapore. In Nature, 1997
This protein, which behaves like a SNARE and has been named GS27 (for Golgi SNARE of 27K), is identical to membrin, a protein implicated earlier in ER-to-Golgi transport.
Ypt1p implicated in v-SNARE activation.
Ferro-Novick et al., New Haven, United States. In Nature, 1995
Here we show that Bos1p, the v-SNARE of yeast endoplasmic reticulum-to-Golgi transport vesicles, pairs with another integral membrane protein of similar topology (Sec22p) on vesicles.
Bos1p, an integral membrane protein of the endoplasmic reticulum to Golgi transport vesicles, is required for their fusion competence.
Ferro-Novick et al., New Haven, United States. In Cell, 1993
BOS1 encodes an integral endoplasmic reticulum (ER) membrane protein and genetically interacts with three other yeast genes (BET1, SEC22, and YPT1) whose products are required for membrane traffic between the ER and the Golgi apparatus.
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