FUT5 Antibody
- Known as:
- FUT5 Antibody
- Catalog number:
- XW-8096
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- FUT5 Antibody
Related genes to: FUT5 Antibody
- Gene:
- FUT5 NIH gene
- Name:
- fucosyltransferase 5
- Previous symbol:
- -
- Synonyms:
- FUC-TV
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-17
- Date modifiied:
- 2015-11-23
Related products to: FUT5 Antibody
Related articles to: FUT5 Antibody
- Pertussis (whooping cough) is caused by the bacterium Bordetella pertussis. Among the virulence factors produced by B. pertussis, pertussis toxin (PT) is responsible for key disease symptoms, including impacts on the immune system. PT is an AB5 toxin, consisting of a single catalytic A subunit and five B subunits. The B pentamer recognizes cell surface glycans and facilitates intracellular delivery of the catalytic A subunit. PT also impacts host cell signaling via mechanisms that do not depend on the catalytic activity of the A subunit. In particular, PT promotes signaling through the T-cell receptor (TCR), leading to activation of extracellular signal-regulated kinase (ERK) cascades. PT prefers to bind sialylated and N-linked glycans, but other aspects of PT's glycan binding specificity remain underexplored. Here we report that the absence of fucose on mammalian cell surfaces leads to increased binding by PT. Using pharmacological inhibitors in a human bronchial epithelial cell line, we observe that sialylation and N-linked glycosylation promote PT binding while fucosylation interferes with PT binding. Similarly, CHO and Colo205 cells deficient in fucosylation exhibited enhanced PT binding as compared to the corresponding wild-type cell lines. Genetic knockout of FUT3/FUT5/FUT6 or of FUT8 led to increased PT binding, suggesting that specific fucosylated epitopes mediate protection from PT. The functional impact of altered PT binding was examined in Jurkat T cells, where removal of cell surface non-core fucose led to increased PT-dependent ERK phosphorylation. In sum, our study identifies a role for fucosylation in protecting mammalian cells from PT. - Source: PubMed
Konada Rohit Sai ReddyNischan NicoleSilva AuroraKohler Jennifer J - Recurrent tuberculosis (TB) accounts for 30% of the annual TB burden in Cape Town. To better understand mechanisms behind recurrences, we assessed the association between neighborhood factors and the cumulative number of TB episodes per individual between 2003 and 2015. We used TB notification data, previously geocoded, and probabilistically linked with 2011 Census data at the neighborhood level. Individuals were grouped by follow-up time after their first TB episode: 5-10 years (FUT5-10) and over 10 years (FUT10+). Ordinal regressions adjusted for age and sex examined associations, with robust standard errors for neighborhood clustering. A secondary analysis from 2009 onward included HIV status, restricted to individuals with at least five years of follow-up. In the FUT10+ cohort, 9.6% had two TB episodes and 2.1% had three or more; this was 7.9% and 1.3% in FUT5-10, and 7.4% and 1.3% in the secondary analysis cohort (SAC). A higher cumulative number of episodes was associated with neighborhood household size across cohorts (FUT10+ aOR = 1.23 (95% CI 1.15-1.31), FUT5-10 aOR = 1.26 (95% CI 1.16-1.37), annual neighborhood TB incidence (FUT10+ aOR = 1.13 (95% CI 1.06-1.20), FUT5-10 aOR = 1.11 (95% CI 1.04-1.19)), neighborhood socioeconomic index (FUT10+ aOR = 0.98 (95% CI 0.95-1.01), FUT5-10 aOR = 0.94 (95% CI 0.91-0.97), SAC aOR = 0.93 (95% CI 0.88-0.98)) and HIV infection (SAC aOR = 1.83 (95% CI 1.59-2.10)). These findings highlight that neighborhood-level risk factors contribute to recurrence and suggest the role of reinfection in recurrent TB. Targeting neighborhoods with high TB incidence, larger households, and lower socioeconomic status may improve screening and reduce TB burden in Cape Town. - Source: PubMed
Publication date: 2026/02/13
Dearden Elivan Leth FrankMolemans MarjanAbrahams ShumsonesaBerkowitz NatachaMohr-Holland ErikaWood RobinHermans Sabine - Pertussis (whooping cough) is caused by the bacterium . Among the virulence factors produced by pertussis toxin (PT) is responsible for key disease symptoms, including impacts on the immune system. PT is an AB toxin, consisting of a single catalytic A subunit and five B subunits. The B pentamer recognizes cell surface glycans and facilitates intracellular delivery of the catalytic A subunit. PT also impacts host cell signaling via mechanisms that do not depend on the catalytic activity of the A subunit. In particular, PT promotes signaling through the T-cell receptor (TCR), leading to activation of extracellular signal-regulated kinase (ERK) cascades. PT prefers to bind sialylated and N-linked glycans, but other aspects of PT's glycan binding specificity remain underexplored. Here we report that the absence of fucose on mammalian cell surfaces leads to increased binding by PT. Using pharmacological inhibitors in a human bronchial epithelial cell line, we observe that sialylation and N-linked glycosylation promote PT binding while fucosylation interferes with PT binding. Similarly, CHO and Colo205 cells deficient in fucosylation exhibited enhanced PT binding as compared to the corresponding wild-type cell lines. Genetic knockout of FUT3/FUT5/FUT6 or of FUT8 led to increased PT binding, suggesting that specific fucosylated epitopes mediate protection from PT. The functional impact of altered PT binding was examined in Jurkat T cells, where removal of cell surface non-core fucose led to increased PT-dependent ERK phosphorylation. In sum, our study identifies a role for fucosylation in protecting mammalian cells from PT. - Source: PubMed
Publication date: 2025/12/04
Konada Rohit Sai ReddyNischan NicoleSilva AuroraKohler Jennifer J - Root System Architecture (RSA) plays an essential role in influencing maize yield by enhancing anchorage and nutrient uptake. Analyzing maize RSA dynamics holds potential for ideotype-based breeding and prediction, given the limited understanding of the genetic basis of RSA in maize. Here, we obtained 16 root morphology-related traits (R-traits), 7 weight-related traits (W-traits), and 108 slice-related microphenotypic traits (S-traits) from the meristem, elongation, and mature zones by cross-sectioning primary, crown, and lateral roots from 316 maize lines. Significant differences were observed in some root traits between tropical/subtropical and temperate lines, such as primary and total root diameters, root lengths, and root area. Additionally, root anatomy data were integrated with genome-wide association study (GWAS) to elucidate the genetic architecture of complex root traits. GWAS identified 809 genes associated with R-traits, 261 genes linked to W-traits, and 2577 key genes related to 108 slice-related traits. We confirm the function of a candidate gene, (), in regulating root development and heat tolerance in maize. The different haplotypes found in tropical/subtropical and temperate lines are associated with primary root features and hold promising applications in molecular breeding. Furthermore, we performed machine learning prediction models of RSA using root slice traits, achieving high prediction accuracy. Collectively, our study offers a valuable tool for dissecting the genetic architecture of RSA, along with resources and predictive models beneficial for molecular design breeding and genetic enhancement. - Source: PubMed
Publication date: 2025/03/13
Guo WeijunWang FanhuaLv JianyueYu JiaWu YueWuriyanghan HadaLe LiangPu Li - Endometriosis (EM) is a widely recognized disorder in gynecological endocrinology. Although hormonal therapies are frequently employed for EM, their side effects and outcome limitations underscore the need to explore the genetic basis and potential drug targets for developing innovative therapeutic approaches. This study aimed to identify both cerebrospinal fluid (CSF) and plasma protein markers as promising therapeutic targets for EM. - Source: PubMed
Publication date: 2025/01/22
Chen PengWei XinLi Xiao-KeZhou Yi-HangLiu Qi-FangOu-Yang Ling