Only in Titles

Search results for: EED

paperclip

#36943785   2023/03/21 To Up

Assessing environmental enteric dysfunction via multiplex assay and its relation to growth and development among HIV-exposed uninfected Tanzanian infants.

Environmental enteric dysfunction (EED) may contribute to poor growth and development in young children. While validated EED biomarkers are currently lacking, multiplex assays are able to capture multiple domains of the condition. The purpose of this exploratory study was to examine the relationship between biomarkers of EED and subsequent growth and development among Tanzanian HIV-exposed uninfected (HEU) infants.
Jacqueline M Lauer, Miles A Kirby, Alfa Muhihi, Nzovu Ulenga, Said Aboud, Enju Liu, Robert K M Choy, Michael B Arndt, Jianqun Kou, Wafaie Fawzi, Andrew Gewirtz, Christopher R Sudfeld, Karim P Manji, Christopher P Duggan

2920 related Products with: Assessing environmental enteric dysfunction via multiplex assay and its relation to growth and development among HIV-exposed uninfected Tanzanian infants.

0.1ml (1mg/ml)10,000 assays1000 tests10 mg1 kit(96 Wells)1 kit(96 Wells)100ug100ul16 Arrays/Slide

Related Pathways

paperclip

#36923952   2023/02/21 To Up

Gene-repressing epigenetic reader EED unexpectedly enhances cyclinD1 gene activation.

Epigenetically switched, proliferative vascular smooth muscle cells (SMCs) form neointima, engendering stenotic diseases. Histone-3 lysine-27 trimethylation (H3K27me3) and acetylation (H3K27ac) marks are associated with gene repression and activation, respectively. The polycomb protein embryonic ectoderm development (EED) reads H3K27me3 and also enhances its deposition, hence is a canonical gene repressor. However, herein we found an unexpected role for EED in activating the pro-proliferative gene (cyclinD1). EED overexpression in SMCs increased mRNA, seemingly contradicting its gene-repressing function. However, consistently, EED co-immunoprecipitated with gene-activating H3K27ac reader BRD4, and they co-occupied at both mitogen-activated and mitogen-repressed ( anti-proliferative gene), as indicated by chromatin immunoprecipitation qPCR. These results were abolished by an inhibitor of either the EED/H3K27me3 or BRD4/H3K27ac reader function. In accordance, elevating BRD4 increased H3K27me3. , while EED was upregulated in rat and human neointimal lesions, selective EED inhibition abated angioplasty-induced neointima and reduced cyclinD1 in rat carotid arteries. Thus, results uncover a previously unknown role for EED in activation, likely via its cooperativity with BRD4 that enhances each other's reader function; i.e., activating pro-proliferative while repressing anti-proliferative . As such, this study confers mechanistic implications for the epigenetic intervention of neointimal pathology.
Mengxue Zhang, Jing Li, Qingwei Wang, Go Urabe, Runze Tang, Yitao Huang, Jose Verdezoto Mosquera, K Craig Kent, Bowen Wang, Clint L Miller, Lian-Wang Guo

1378 related Products with: Gene-repressing epigenetic reader EED unexpectedly enhances cyclinD1 gene activation.