TRIB1

Last update 08 May 2025

Basic Info

Synonyms

C8FW, G-protein-coupled receptor-induced gene 2 protein, GIG-2

+ [8]

Introduction

Adapter protein involved in protein degradation by interacting with COP1 ubiquitin ligase (PubMed:27041596). The COP1-binding motif is masked by autoinhibitory interactions with the protein kinase domain (PubMed:26455797). Serves to alter COP1 substrate specificity by directing the activity of COP1 toward CEBPA (PubMed:27041596). Binds selectively the recognition sequence of CEBPA (PubMed:26455797). Regulates myeloid cell differentiation by altering the expression of CEBPA in a COP1-dependent manner (By similarity). Controls macrophage, eosinophil and neutrophil differentiation via the COP1-binding domain (By similarity). Interacts with MAPK kinases and regulates activation of MAP kinases, but has no kinase activity (PubMed:15299019, PubMed:26455797).

100 Clinical Results associated with TRIB1

100 Translational Medicine associated with TRIB1

0 Patents (Medical) associated with TRIB1

320

Literatures (Medical) associated with TRIB1

01 Mar 2025·The Plant Journal

Cryptochrome 1 promotes photomorphogenesis in Arabidopsis by displacing substrates from the COP1 ubiquitin ligase

Article

Author: Trimborn, Laura ; Hoecker, Ute ; Urquiza‐García, Uriel ; Kuttig, Franziska ; Lederer, Patrick ; Ponnu, Jathish ; Korsching, Kris R. ; Yu, Pengxin ; Zurbriggen, Matias D.

SUMMARYIn blue light, cryptochrome photoreceptors inhibit the key repressor of light signaling, the COP1/SPA ubiquitin ligase, to promote photomorphogenic responses. This inhibition relies on the direct interaction between COP1 and cryptochromes. Here, we analyzed the molecular mechanism of CRY1‐mediated inhibition of COP1. We show that the VP motif in the C‐terminal domain of CRY1 is essential for the COP1‐CRY1 interaction in Arabidopsis. Phenotypic analysis of transgenic Arabidopsis plants harboring a mutation in the VP motif reveals that the VP motif of CRY1 is required for blue light‐induced responses, such as seedling de‐etiolation and anthocyanin biosynthesis. Via its VP motif, CRY1 inhibits the interaction between COP1 and the COP1 substrate transcription factors PAP2 and HY5. Replacing the VP motif of CRY1 with that of the human COP1 interactor TRIB1 produces a functional photoreceptor in transgenic plants. Since HY5, PAP2 and CRY1 interact with COP1 through their respective VP motifs, our results demonstrate that CRY1 inhibits the activity of COP1 by competitively displacing substrates from COP1. Taken together with previous results showing VP‐dependent substrate displacement by photoactivated CRY2 and UVR8 photoreceptors, our results highlight the conservation of this mechanism across multiple photoreceptors.

01 Mar 2025·Phytomedicine

Notoginsenoside R1 alleviates blue light-induced corneal injury and wound healing delay by binding to and inhibiting TRIB1

Article

Author: Tong, Jianping ; Wang, Xinglin ; Li, Yuanyuan ; Chen, Kuangqi ; Shen, Chang ; Wang, Yinhao ; Li, Xiang ; Xia, Yutong ; Li, Xiuyi ; Chen, Zhitong ; Song, Dongjie ; Yu, Xin ; Li, Jiafeng ; Shen, Ye

BACKGROUNDWith the escalating use of digital devices, blue light (BL) exposure has emerged as a critical concern due to its potential to cause ocular damage. This study explores the protective effects of notoginsenoside R1 (NR1), a bioactive compound from Panax notoginseng (Burkill) F.H. Chen (Sanqi), against BL-induced corneal epithelial injury.PURPOSEThis research aims to investigate the protective effects of NR1 on BL-induced corneal injury and wound healing delay.METHODSHuman corneal epithelial cells (hCECs) were pretreated with NR1 (0-50 μM) or N-acetylcysteine (NAC, 10 mM), then exposed to BL (570 μW/cm²) for 24 h. Cell viability, proliferation, migration, and ROS levels were assessed using various techniques. In mice, NR1 (25 μM and 50 μM) and NAC (0.3 %) eye drops were administered during BL exposure. Corneal injury, healing rates, cell proliferation, migration, ROS, and inflammation were evaluated. RNA-sequencing, bioinformatics, and molecular binding validation identified tribbles homolog 1 (TRIB1) as a key molecule mitigating BL damage with NR1. Functional studies via gene silencing, overexpression, and pharmacological modulation further explored TRIB1's role in BL exposure.RESULTSNR1 significantly reduced BL-induced inflammation, ROS production, and inhibited migration and proliferation in hCECs and murine corneas. It also alleviated BL-induced corneal injury and delayed healing in mice. NR1 inhibited TRIB1 upregulation, a marker of BL-induced injury and healing delay. Overexpression of TRIB1 negated NR1's therapeutic effects on hCECs, while TRIB1 silencing mitigated functional impairment. In mice, increased Trib1 expression caused corneal injury and delayed healing, reversed by NR1 treatment.CONCLUSIONNR1 shows potential as a therapeutic agent by inhibiting TRIB1 elevation in response to BL exposure, providing a novel promising target for corneal injury and wound healing delay induced by BL, and offering a comprehensive strategy for clinical pharmacological intervention.

01 Feb 2025·Advanced Science

Bacteroides Fragilis Exacerbates T2D Vascular Calcification by Secreting Extracellular Vesicles to Induce M2 Macrophages

Article

Author: Liu, Jianghua ; Gao, Yan ; Chen, Cong ; Cao, Jingsong ; Liang, Zhengfeng ; He, Yuqi ; Ouyang, Shuhui ; Wang, Lili

AbstractVascular calcification (VC) in type 2 diabetes (T2D) poses a serious threat to the life and health of patients. However, its pathogenesis remains unclear, resulting in a lack of effective treatment for the root cause. It is found that both intestinal Bacteroides fragilis (BF) and peripheral M2 monocytes/macrophages are significantly elevated in patients with T2D VC. M2 macrophages are identified as a significant risk factor for T2D VC. Both BF and their extracellular vesicles (EV) promote T2D VC and facilitate macrophage M2 polarization. Macrophages clearance significantly antagonized BF EV‐induced T2D VC in mice. Mechanistically, EV‐rich double‐stranded DNA (dsDNA) activates stimulator of interferon response cGAMP interactor 1 (Sting), promotes myocyte enhancer factor 2D (Mef2d) phosphorylation, upregulates tribbles pseudokinase 1 (Trib1) expression, and induces macrophage M2 polarization. Concurrently, Mef2d activated by the EV targets and upregulates the expression of pro‐calcification factor Serpine1, thereby exacerbating T2D VC. Clinical studies have shown that Serpine1 is significantly elevated in the peripheral blood of patients with T2D VC and is closely associated with T2D VC. In summary, this study reveals that intestinal BF promotes Trib1 expression through the EV‐Sting‐Mef2d pathway to induce macrophage M2 polarization and upregulates serpin family E member 1 (Serpine1) expression, thereby aggravating T2D VC. The findings provide a new theoretical and experimental bases for optimizing the strategies for prevention and treatment of T2D VC.

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TRIB1

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