Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Immunomodulatory mechanisms of Bojungikki-tang through systematic transcriptomic analysis_RPMI8226

ABSTRACT: This study aimed to identify the modes of action (MOA) of water extract of Bojungikki-tang (BJIKT) and major four ingredients in immune cell lines. The four main ingredients were designated as Panax ginseng C. A. Meyer, Astragalus mongholicus Bunge, Atractylodes japonica Koidzumi, and Glycyrrhiza uralensis Fisher, which are the main active herbs of BJIKT. The immune-related cell lines used for transcriptome production are Jurkat (CD4+ T cells), RPMI8226 (B cells), NK-92MI (NK cells), M1MO (macrophages, differentiated from THP-1), and Mature DC (dendritic cells, differentiated from THP-1), respectively. This dataset contains transcriptome expression information for the RPMI8226 cell line.

ORGANISM(S): Homo sapiens

PROVIDER: GSE272089 | GEO | 2026/08/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Immunomodulatory mechanisms of Bojungikki-tang through systematic transcriptomic analysis_M1MO

Project description:This study aimed to identify the modes of action (MOA) of water extract of Bojungikki-tang (BJIKT) and major four ingredients in immune cell lines. The four main ingredients were designated as Panax ginseng C. A. Meyer, Astragalus mongholicus Bunge, Atractylodes japonica Koidzumi, and Glycyrrhiza uralensis Fisher, which are the main active herbs of BJIKT. The immune-related cell lines used for transcriptome production are Jurkat (CD4+ T cells), RPMI8226 (B cells), NK-92MI (NK cells), M1MO (macrophages, differentiated from THP-1), and Mature DC (dendritic cells, differentiated from THP-1), respectively. This dataset contains transcriptome expression information for the M1MO cell line.

2026-08-01 | GSE272091 | GEO

Immunomodulatory mechanisms of Bojungikki-tang through systematic transcriptomic analysis_NK-92MI

2026-08-01 | GSE272090 | GEO

Immunomodulatory mechanisms of Bojungikki-tang through systematic transcriptomic analysis_Jurkat

2026-08-01 | GSE272088 | GEO

Immunomodulatory mechanisms of Bojungikki-tang through systematic transcriptomic analysis_MatureDC

2026-08-01 | GSE272092 | GEO

Bojungikki-Tang Enhances the Efficacy of Pembrolizumab Treatment in Human PBMC-Injected H460 Tumor-Bearing Mice

Project description:Immune checkpoint inhibitors (ICIs) have become a major treatment option for non-small cell lung cancer, but their efficacy is still limited because only a subset of patients responded to ICIs. Bojungikki-Tang (BJIKT), a widely used herbal medicine extracted from 10 medicinal plants, has been largely investigated as a combined treatment with anticancer agents. In this study, we examined the potential anti-tumor effect of co-administration of BJIKT and pembrolizumab in human peripheral blood mononuclear cell (PBMC)-injected H460 tumor-bearing MHC Ⅰ/Ⅱ double knockout NSG mice. We found that combination treatment with BJIKT and pembrolizumab significantly suppressed tumor growth by regulating the activation of immune cells. Immunohistochemistry analysis showed that the combination therapy decreased the exhausted proportion of CD8(+) and CD4(+) T cells expressing PD-1 and LAG-3 markers in the tumor tissues. Our transcriptome analysis indicated that BJIKT strengthened T cell function and TNF signaling and inhibited TGF-β signaling to induce cell cycle arrest and apoptosis. Additionally, BJIKT synergistically exhibited anti-tumor effects along with immune-related pathways when combined with pembrolizumab. Taken together, combination therapy altered immune cells and regulated anti-tumor immune response, paving the way for a more effective understanding of the role of BJIKT in the tumor microenvironment.

2024-03-05 | GSE260575 | GEO

Immunomodulatory mechanisms of Bojungikki-tang through systematic transcriptomic analysis_NK-92MI

Project description:Immunomodulatory mechanisms of Bojungikki-tang through systematic transcriptomic analysis_NK-92MI

| PRJNA1135097 | ENA

Homo sapiens isolate:RPMI8226 | breed:RPMI8226 | cultivar:RPMI8226

Project description:Homo sapiens isolate:RPMI8226 | breed:RPMI8226 | cultivar:RPMI8226 Raw sequence reads

| PRJNA350365 | ENA

Human immune cell proteomic library

Project description:Comprehensive human immune cell proteomic spectral library which contain CD4+T cell, CD8+ T cell, NK cell, B cell, PBMC, Daudi, Jurkat, stimulated Jurkat, Molt-4, Ramos, and THP-1 were generated. This library includes 10,544 proteins groups, and 127,106 peptides.

2023-12-12 | MSV000093644 | MassIVE

Unveiling a Novel in-vitro Model of Skin Inflamm-Aging: Validation of Terminalia chebula Extract and Supermolecular Bakuchiol for Reversal of Inflamm-Aging

Project description:Introduction: Sensitive skin is characterized by skin barrier disruption which is usually prone to react to external stimuli including UV, air pollution as well as cosmetic allergens. Sensitive skin tends to react with oxidative stress factors that could further lead to skin inflammation resulting in inflamm-aging. But almost no inflamm-aging models for sensitive skin, so it is worth constructing a method to screen anti-inflammaging ingredients and products. Methods: An in-vitro macrophages-fibroblasts model was established to evaluate the anti-inflammaging effect of ingredients. M1 phenotype and aging-associated gene expression were recorded by qPCR test to validate the inflamm-aging model. RNA sequencing was used to further elaborate the inflamm-aging mechanism of two validated ingredients. Results and conclusion: A novel in-vitro model of sensitive skin inflamm-aging was constructed by applying M1 phenotype of THP-1 culture medium supernatant to introduce the cellular senescence of the fibroblast cells, which could be used to screen out anti-inflammaging ingredients. In this model, supramolecular bakuchiol could promote collagen COL1A1 and COL3A3 production and inhibit inflammatory factors by increasing anti-inflammatory gene transcription (PTX3, ADAM33, and PDLIM1), while Terminalia chebula extract can inhibit cell senescence by reducing transcription of MAP4K2, and inflammatory factors CCL3 accumulation.

2025-04-16 | GSE286316 | GEO

NKCLR3 impairs natural killer cell cytotoxicity by epigenetically targeting the Natural Cytotoxicity Triggering Receptor 1 (NCR1) [lncRNA-seq]

Project description:Natural killer cells (NK cells) play a critical role in the surveillance of tumor immunity. However, NK cell-based immunotherapy, including autologous and allogeneic NK cell reinfusion, has not brought significant clinical benefits to patients. To identify factors that control the intrinsic cytotoxicity of NK cells, we utilized the histone deacetylase inhibitor valproic acid (VPA) to develop a NK cell cytotoxicity suppression model. With RNA-seq and functional assays, we identified a previously uncharacterized lncRNA, NKCLR3 (NK cytotoxicity-associated long noncoding RNA 3), as a negative regulatory factor of NK cell-mediated cytotoxicity. NKCLR3 was significantly upregulated in VPA-treated NK cells and was negatively associated with the cytotoxicity of NK cells. Knockdown of NKCLR3 enhanced antitumor activity in NK-92MI cells. Using reverse transcription-associated capture sequencing (RAT-seq), we found that NKCLR3 functioned by targeting the Natural cytotoxicity triggering receptor 1 (NCR1) gene, which encodes the activating receptor NKp46 involved in the natural cytotoxicity. Mechanistic studies revealed that NKCLR3 interacted with the regulatory elements of NCR1 and blocked the formation of an intrachromosomal interaction that is required for optimal expression of NCR1. In addition, NKCLR3 inhibited the synthesis of NCR1 enhancer RNA. Through these dual mechanisms, NKCLR3 induced a suppressive epigenotype in the NCR1 promoter and suppressed the expression of the NCR1 gene. Thus, the NKCLR3-NCR1 axis identified in this study may serve as a novel target to improve therapeutic intervention of NK cells in tumor immunotherapy.

2025-01-01 | GSE285271 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data