Last update 19 Sep 2024

TWEAKR

Last update 19 Sep 2024

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

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

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

BIIB-036

Target

TWEAKR

Mechanism

TWEAKR antagonists

Active Org.-

Originator Org.

Biogen, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhaseDiscontinued

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

667

Literatures (Medical) associated with TWEAKR

01 Aug 2024·Viral Immunology

Monocyte Transcriptome in Different Phases of Chronic Hepatitis B Virus Infection Uncovers Potential Functional Roles

Article

Author: Chaudhary, Kiran ; Jain, Kshama ; Muniyasamy, Abaranjitha ; Sinha, Prakriti ; Upadhyay, Pramod ; Mohan, K Varsha ; Bhardwaj, Vaishali

The hepatitis B virus (HBV) chronic infection goes through different phases, i.e., immune tolerant (IT), immune clearance (IC), and inactive carrier (IN) resulting from the interplay of viral replication and immune response. Although the adaptive immune response is central to viral control, roles of the innate immune cells are less prominent. We explored monocyte transcriptome in these different phases of HBV infection to understand the nature of its involvement and identify unique differentially expressed genes (DEGs) in each phase. CD14+ peripheral blood monocytes were isolated from patients in the IT, IC, and IN phases and from healthy subjects and their RNA was sequenced. The significant DEGs were studied through gene annotation databases to understand differentially modulated pathways. The DEGs were further validated by qRT-PCR to identify genes that were uniquely expressed in each phase. It was found that TNFRSF12A was upregulated in all the HBV samples. The IN phase had six uniquely upregulated genes, i.e., PI3, EMP1, STX1A, RRAD, SPINK1, and SNORD3B-2. E2F7 was most consistently downregulated in the IT phase, and in the IC phase, IL23A and PI3 were specifically downregulated. Cut-off values were generated by ROC curve analysis to differentiate between the groups based on their expression levels. The monocyte functions are majorly suppressed in the IT and IC phases and are, however, somewhat metabolically active in the IN phase.

01 Jun 2024·Heliyon

Identification of immune-related tumor antigens and immune subtypes in osteosarcoma

Article

Author: Xu, Gongping ; Zhang, Mingshu ; Xi, Chunyang ; Yu, Enming

PurposeThe development of tumor vaccines has become a hot topic in immunotherapy for osteosarcoma (OS); however, more tumor antigens with stronger immunogenicity need to be identified.MethodsWe downloaded six sets of gene expression profile data from online databases. The overexpressed genes were analyzed, intersected, and used to calculate the immune infiltration abundance in the TARGET OS dataset based on their expression matrix. Potential tumor antigen genes were identified based on whether they exhibited a high correlation with the antigen-presenting cells (APCs). A total of 1330 immune-related genes (IRGs) from the ImmPort website were retrieved based on their expression, and the Consensus Cluster method was used to obtain immune subtypes of the OS samples. Prognosis, immune microenvironment, and sensitivity to drugs were compared among the immune subtypes.ResultsIn total, 680 genes were overexpressed in at least two datasets, of which TREM2, TNFRSF12A, and THY1 were positively correlated with different APCs. Based on the expression matrix of 1330 IRGs in TARGET-OS, two immune subtypes, IS1 and IS2, were identified. The prognosis of the IS1 subtype was better than that of IS2, the expression of immune checkpoint (ICP)-related genes was higher in patients with the IS1 subtype, and immune cell infiltration and sensitivity to 16 drugs were generally higher in IS1 subtype patients.ConclusionWe identified three APC-correlated genes that can be considered to code for potential novel tumor antigens for OS vaccines. Two immune subtypes in patients with OS were identified to implement personalized treatments using mRNA vaccines.

01 May 2024·Experimental Cell Research

PLAU promotes cell proliferation and migration of head and neck cancer via STAT3 signaling pathway

Article

Author: Zhang, Shu ; Cui, Xiaobo ; Bai, Yanping ; Wang, Boqian ; Cui, Yanru ; Bai, Yunfei ; Liu, Xiaoqing ; Li, Xin ; Sun, Hongyang

It was reported that within the head and neck cancer (HNC) cell line CAL21 the epithelial-mesenchymal transition (EMT) and cell proliferation were promoted by Urokinase-Type Plasminogen Activator (PLAU) proteinase through TNFRSF12A. Additionally, in this paper HNC cell lines refer to Fadu and Tu686. A novel PLAU-STAT3 axis was found to be involved in HNC cell line proliferation and metastasis. PLAU expression in HNC samples was upregulated, besides, the elevated expression of PLAU was linked to the lower overall survival (OS) and disease-free survival (DFS). Ectopic PLAU expression promoted cell proliferation and migration, while PLAU knockdown exhibited opposite results. RNA-seq data identified the JAK-STAT signaling pathway, confirmed by western blotting. A recovery assay using S3I-201, a selective inhibitor of signal transducer and activator of transcription 3 (STAT3), indicated that PLAU promoted HNC cell line progression via STAT3 signaling in vitro. The oncogenic role of PLAU in HNC tumor growth in vivo was confirmed using xenograft models. In summary, we identified the tumorigenic PLAU function in the HNC progress. PLAU may represent a potential prognostic biomarker of HNC and the PLAU-STAT3 pathway might be considered a therapeutic target of HNC.

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TWEAKR

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