Entada acaciifolia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA168514 | ENA |
REPOSITORIES: ENA
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Project description:Being a sessile organism, plants are constantly confronted by various biotic (pest and pathogen) and abiotic (drought, salinity, flood, extreme temperatures, etc.) stresses. In response to these environmental stresses, plants have developed numerous defense mechanisms. One of the basal defense responses in plants are mediated by trypsin inhibitors (TIs). Putranjiva roxburghii trypsin inhibitor (PRTI), a potent trypsin inhibitor from P. roxburghii showing sequence similarity with a group of genes known to have defense and storage function such as wound inducible (WIN) proteins, vegetative storage proteins (VSPs), and Bark storage protein (BSPs) was overexpressed in Citrus aurantifolia. PRTI overexpressing lines were tolerant to various abiotic stresses (salinity, drought, and alkalinity) and two pests namely, Scirtothrips citri and Papilio demoleus. The molecular insights underlying the heterologous overexpression of PRTI at the transcriptomic level reveals the upregulation of stress responsive genes and involvement of hormonal signal transduction and transporters. Further, genes related to DNA repair, amino acid synthesis, and development were also found to be upregulated. Our study also reveals the nuclear-cytoplasmic localization and alteration phytohormone profile by PRTI overexpression in transgenic lines as compared to wild-type which clearly indicates the role of abscisic acid ABA in stress tolerance.
2022-12-31 | GSE208104 | GEO
Project description:<p>The purpose of this study is to identify genetic predictors of ACE inhibitor-associated angioedema. In addition to preventing the formation of the pressor angiotensin II, ACE inhibitors prevent the carboxyl-terminal degradation of the vasoactive substances bradykinin and substance P. Angioedema is hypothesized to result from defective amino-terminal degradation of bradykinin or substance P in patients in whom ACE is inhibited. For example, activity of dipeptidyl peptidase IV (DPP-IV), the enzyme responsible for the inactivation of substance P when ACE is inhibited, is decreased in patients with angioedema. In preliminary studies, we have identified SNPs in the DPP4 gene that associate with DPP-IV activity and, in blacks, with risk of angioedema.</p> <p>This project will use genome-wide genotyping to compare 250 cases and 568 ACE inhibitor-exposed control subjects (131 cases and 288 controls ascertained at Vanderbilt and 70 cases and 280 controls ascertained at the Marshfield Clinic). We plan a 2-stage analysis of associations between SNPs and angioedema - first, we will study DPP4 SNPs for association with angioedema and, second, we will explore associations using the full GWAS data set. Depending on the platform, additional DPP4 SNPs will be used to fully tag common genetic variants in both African American and European American samples. Based on the HapMap data, there are 14 tagging SNPs in people of European descent and 34 in Yoruba (selection criteria MAF>0.05 and r2>0.8).</p> <p>Cases were defined as having ACE inhibitor-associated angioedema if they had had swelling of the lips, throat, tongue or face while taking an ACE inhibitor but had never had angioedema while not taking an ACE inhibitor. For simplicity, intestinal edema was excluded. Control subjects were treated for at least 6 months with an ACE inhibitor without angioedema. Because black Americans are known to be overrepresented among patients with ACE inhibitor-associated angioedema, control subjects were prespecified to be 50% black American, 50% white American, and 50% female. At Vanderbilt, the medical history, including the history of angioedema, was confirmed by a research nurse or physician using a detailed case report form. Characteristics of Vanderbilt cases appear in the Table. At Marshfield, medical history will be confirmed by chart review. The Marshfield cohort is 98% white American and 57% female with a mean age of 47.2 years.</p>
| phs000438 | dbGaP
Project description:Trypsin-induced head-to-tail cyclization in a scorpion venom trypsin inhibitor peptide
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Project description:IκBs exert a principal function as cytoplasmic inhibitors of the NF-kB transcription factors. Additional functions for specific IκB homologues have also been described including their association to chromatin to directly regulate gene transcription. Phosphorylated and SUMOylated IκBα (pS-IκBα) specifically binds histones H2A and H4 in the stem and progenitor compartment of skin and intestine, but the mechanisms that control the recruitment of nuclear pS-IκBα to the chromatin are largely unstudied. We here show thatserine 32-36 phosphorylation of IκBα favors its binding with nucleosomes and demonstrated that p-IκBαassociation to H4 is favored by acetylation at specific H4 lysine (K) residues. Acetylated N-terminal tail of H4 is lost during intestinal cell differentiation due to histone cleavage at amino acids 17-19 by the action of trypsin or chymotrypsin, which interferes p-IκBα association to chromatin. Paradoxically, pharmacologic or genetic inhibition of trypsin and chymotrypsin activity in HT29 cells increased p-IκBα chromatin binding, associated to impaired goblet cell differentiation, which was comparable to IκBα deletion. Together our results indicate that dynamic binding of IκBα to chromatin is a requirement for intestinal cell differentiation and provide a molecular base for the restricted nuclear distribution of p-IκBα at specific stem cell compartments.
2021-06-21 | GSE167087 | GEO
Project description:We created isogenic mutiple myeloma and mouse embryonic fibroblast cell lines disrupted for KDM6A using CRISPR editing and Cre-mediated deletion. To detect KDM6A we inserted a dual HA tag sequence into the C-terminal of KDM6A by CRISPR-mediated editing. We also created one isogenic cell line harboring a jmjD-dead KDM6A where 2 amino acids essential for KDM6A enzymatic activity, H1146 and E1148 , were replaced with alanine residues
2024-10-01 | GSE244510 | GEO