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Last update 08 May 2025

TWEAKR

Last update 08 May 2025

Basic Info

Synonyms

CD266, FGF-inducible 14, Fibroblast growth factor-inducible immediate-early response protein 14

+ [7]

Introduction

Receptor for TNFSF12/TWEAK. Weak inducer of apoptosis in some cell types. Promotes angiogenesis and the proliferation of endothelial cells. May modulate cellular adhesion to matrix proteins.

Drugs associated with TWEAKR

GrB-Fc-IT4

Target

GRB x TWEAKR

Mechanism

GRB modulators [+1]

Active Org.

The University of Texas MD Anderson Cancer Center

Originator Org.

The University of Texas MD Anderson Cancer Center

Active Indication

Ovarian Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ASP1531

Target

TWEAKR

Mechanism

TWEAKR antagonists

Active Org.

Astellas Pharma, Inc.

Originator Org.

Astellas Pharma, Inc.

Active Indication

Cachexia [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

TSCP-2

Target

TRAIL receptor x TWEAKR

Mechanism

TRAIL receptor modulators [+1]

Active Org.

KAHR Medical Ltd.

Originator Org.

KAHR Medical Ltd.

Active Indication

Rheumatoid Arthritis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with TWEAKR

NCT00738764

/ CompletedPhase 1

A Phase 1, Multicenter, Open-Label, Dose Escalation Trial of PDL192 in Subjects With Advanced Solid Tumors

This is a phase 1, multicenter, open-label, dose escalation trial of PDL192 in subjects with advanced solid tumors.

Start Date01 Jul 2008

Sponsor / Collaborator

Abbott Laboratories

100 Clinical Results associated with TWEAKR

100 Translational Medicine associated with TWEAKR

0 Patents (Medical) associated with TWEAKR

703

Literatures (Medical) associated with TWEAKR

31 Dec 2025·Future Science OA

TWEAK/Fn14 axis may promote vascular smooth muscle cell senescence via p38 signaling pathway: preliminary evidence

Article

Author: Wei, Chunyang ; Wang, Yanfu ; Miao, Zhuang ; Qi, Guoxian ; Liu, Xiaoying ; Zhang, Hua

AIMThe primary objective of this study is to investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), on the process of vascular smooth muscle cell (VSMC) senescence.METHODSRat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated. Additionally, the role of p38 phosphorylation pathway in the effect of TWEAK on VSMCs senescence was assessed.RESULTSExpressions of TWEAK and Fn14 were significantly elevated in senescent VSMCs. TWEAK activated the p38 phosphorylation pathway and promoted the SA-β-gal staining and P53 expression.CONCLUSIONThese preliminary findings suggest that the TWEAK/Fn14 axis may play a crucial role in promoting VSMC senescence.

31 Dec 2025·Journal of the International Society of Sports Nutrition

Bioinformatic identification of important roles of COL1A1 and TNFRSF12A in cartilage injury and osteoporosis

Article

Author: Wang, Xichun ; Gong, Shiguo ; Liu, Muzi ; Zhang, Zihong ; Sheng, Xin

OBJECTIVEThe aim of this study was to identify the key regulatory mechanisms of cartilage injury and osteoporosis through bioinformatics methods, and to provide a new theoretical basis and molecular targets for the diagnosis and treatment of the disease.METHODSMicroarray data for cartilage injury (GSE129147) and osteoporosis (GSE230665) were first downloaded from the GEO database. Differential expression analysis was applied to identify genes that were significantly up-or down-regulated in the cartilage injury and osteoporosis samples. These genes were subjected to GO enrichment analysis and KEGG pathway analysis. In addition, we employed SVA and RRA methods to merge the two sets of data, eliminating batch effects and enhancing the statistical power of the analysis. Through WGCNA, we identified gene modules that were closely associated with disease phenotypes and then screened for key genes that intersected with differentially expressed genes. The diagnostic value of these genes as potential biomarkers was evaluated by ROC analysis. Moreover, we performed an immune infiltration analysis to explore the correlation between these core genes and immune cell infiltration.RESULTSWe performed GO enrichment analysis and KEGG pathway analysis of genes significantly up-or down-regulated in cartilage injury and osteoporosis samples. Important biological processes, cellular components and molecular functions, and key metabolic or signaling pathways associated with osteoporosis and cartilage injury were identified. Through WGCNA, we identified gene modules that were closely associated with the disease phenotype, from which we then screened for key genes that intersected with differentially expressed genes. Ultimately, we focused on two identified core genes, COL1A1 and TNFRSF12A, and assessed the diagnostic value of these genes as potential biomarkers by ROC analysis. Meanwhile, GSVA provided an in-depth view of the role of these genes in disease-specific biological pathways. Immune infiltration analysis further revealed the possible key role of COL1A1 and TNFRSF12A in regulating immune cell infiltration in osteoporosis and cartilage injury.CONCLUSIONCOL1A1 and TNFRSF12A as key regulatory molecules in osteoporosis and cartilage injury.

01 Apr 2025·Hepatology

Integrative single-cell and spatial transcriptomic analyses identify a pathogenic cholangiocyte niche and TNFRSF12A as therapeutic target for biliary atresia

Article

Author: Jiang, Hong ; Liang, Peishi ; Luo, Zhenhua ; Wu, Sihan ; Zhong, Zhihai ; Chen, Huadong ; Liu, Juncheng ; Xiao, Man-Huan ; Tang, Yanlai ; Li, Wei ; Feng, Xuyang ; Ma, Dong ; Wang, Fen ; Huang, Zaoli

Background and Aims:Biliary atresia (BA) is a devastating fibroinflammatory biliary disease that is the leading indication for pediatric liver transplants worldwide. Although cholangiocytes are the primary target cells, the pathogenic mechanisms involving cholangiocytes remain elusive. Here, we aimed to characterize the pathogenic role of cholangiocytes in BA.Approach and Results:Integration of single-cell RNA sequencing of 12 liver tissues (from 9 BA and 3 controls) and the spatial transcriptome of another four liver sections (from 2 BA and 2 controls) provided a comprehensive spatial liver cell atlas of BA. In particular, we identified a cholangiocyte-enriched spatial niche with infiltration of activated HSCs, activated portal fibroblasts, macrovascular endothelial cells, and TREM2+ macrophages that were elevated in the portal triad of BA. This niche was positively correlated with bile duct profiles, liver fibrosis, and poor survival in 2 independent cohorts of patients with BA. Using integrative bioinformatics analyses to mine the cell-cell communication and regulatory network in BA cholangiocytes, we uncovered the fibroinflammatory phenotype of cholangiocytes with TNFSF12-TNFRSF12A as a significant signal. Genetic ablation or blockade of TNFRSF12A suppresses liver injury, inflammation, and bile duct profiles in a mouse model of disease. Using human biliary organoids, we revealed that BA organoids expressed higher levels of CCL2 in response to TNFSF12 stimulation and promoted monocyte chemotaxis via the CCL2-CCR2 axis.Conclusions:Pathogenic cholangiocytes-enriched niche identifies TNFRSF12A as a potential therapeutic target for BA.

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TWEAKR

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