THEMIS2

Last update 08 May 2025

Basic Info

Synonyms

C1orf38, ICB-1, ICB1

+ [6]

Introduction

May constitute a control point in macrophage inflammatory response, promoting LPS-induced TLR4-mediated TNF production (PubMed:20644716). Determines the threshold for activation of B cells by low-affinity and low-avidity ligands via PLCG2 activation and its downstream pathways (By similarity).

100 Clinical Results associated with THEMIS2

100 Translational Medicine associated with THEMIS2

0 Patents (Medical) associated with THEMIS2

Literatures (Medical) associated with THEMIS2

01 Jun 2024·The Journal of Immunology

THEMIS2 Impairs Antitumor Activity of NK Cells by Suppressing Activating NK Receptor Signaling

Article

Author: Nabekura, Tsukasa ; Deborah, Elfira Amalia ; Shibuya, Akira ; Shibuya, Kazuko

AbstractNK cells are cytotoxic innate lymphocytes that play a critical role in antitumor immunity. NK cells recognize target cells by using a repertoire of activating NK receptors and exert the effector functions. Although the magnitude of activation signals through activating NK receptors controls NK cell function, it has not been fully understood how these activating signals are modulated in NK cells. In this study, we found that a scaffold protein, THEMIS2, inhibits activating NK receptor signaling. Overexpression of THEMIS2 attenuated the effector function of human NK cells, whereas knockdown of THEMIS2 enhanced it. Mechanistically, THEMIS2 binds to GRB2 and phosphorylated SHP-1 and SHP-2 at the proximity of activating NK receptors DNAM-1 and NKG2D. Knockdown of THEMIS2 in primary human NK cells promoted the effector functions. Furthermore, Themis2-deficient mice showed low metastatic burden in an NK cell–dependent manner. These findings demonstrate that THEMIS2 has an inhibitory role in the antitumor activity of NK cells, suggesting that THEMIS2 might be a potential therapeutic target for NK cell–mediated cancer immunotherapy.

01 Jun 2023·Cell Chemical Biology

IFNα primes cancer cells for Fusicoccin-induced cell death via 14-3-3 PPI stabilization

Article

Author: Kaschani, Farnusch ; Higuchi, Yusuke ; Choidas, Axel ; Centorrino, Federica ; Menninger, Sascha ; Wolf, Alexander ; Andrei, Sebastian A ; Ninck, Sabrina ; Heilmann, Geronimo ; Ottmann, Christian ; Eickhoff, Jan ; Kaiser, Markus ; Kato, Nobuo ; Klebl, Bert ; Andlovic, Blaž ; Arkin, Michelle ; Brunsveld, Luc

The natural product family of the fusicoccanes (FCs) has been shown to display anti-cancer activity, especially when combined with established therapeutic agents. FCs stabilize 14-3-3 protein-protein interactions (PPIs). Here, we tested combinations of a small library of FCs with interferon α (IFNα) on different cancer cell lines and report a proteomics approach to identify the specific 14-3-3 PPIs that are induced by IFNα and stabilized by FCs in OVCAR-3 cells. Among the identified 14-3-3 target proteins are THEMIS2, receptor interacting protein kinase 2 (RIPK2), EIF2AK2, and several members of the LDB1 complex. Biophysical and structural biology studies confirm these 14-3-3 PPIs as physical targets of FC stabilization, and transcriptome as well as pathway analyses suggest possible explanations for the observed synergistic effect of IFNα/FC treatment on cancer cells. This study elucidates the polypharmacological effects of FCs in cancer cells and identifies potential targets from the vast interactome of 14-3-3s for therapeutic intervention in oncology.

30 Jan 2023·Disease Markers

Screening of Biomarkers in Liver Tissue after Bariatric Surgery Based on WGCNA and SVM-RFE Algorithms

Article

Author: Liu, Zhixin ; Jiang, Yicheng ; Yang, Haojun ; Wang, Yu ; Chen, Shuai ; Jiao, Yuwen ; Tang, Liming

As the most common chronic liver disease around the world, nonalcoholic fatty liver disease (NAFLD) has a close connection with obesity, diabetes, and metabolic syndrome. Bariatric surgery (BS) is considered to be the most effective treatment for NAFLD. However, the regulatory mechanism of hepatic lipid metabolism after BS remains poorly elucidated. By analyzing two transcriptome datasets regarding liver tissues after BS, namely, GSE83452 and GSE106737, we acquired 110 differentially expressed genes (DEGs). By further analysis of DEGs in terms of the weighted gene coexpression network analysis (WGCNA) and support vector machine-recursive feature elimination (SVM-RFE) algorithms, we identified four crucial genes participating in the regulation of hepatic lipid metabolism: SRGN, THEMIS2, SGK1, and FPR3. In addition, the results of gene set enrichment analysis (GSEA) showed that BS can activate immune-related regulatory pathways and change immune cell infiltration levels. Finally, through cellular level studies, we found that the silencing of SRGN affects the expression of SREBP-1, SIRT1, and FAS during adipogenesis in the liver and the formation of lipid droplets in the liver. In summary, the immune system in the liver is activated after BS, and SRGN participates in the regulation of hepatic lipid metabolism.

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THEMIS2

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