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Last update 08 May 2025

TWF1

Last update 08 May 2025

Basic Info

Synonyms

A6, Protein A6, Protein tyrosine kinase 9

+ [6]

Introduction

Actin-binding protein involved in motile and morphological processes. Inhibits actin polymerization, likely by sequestering G-actin. By capping the barbed ends of filaments, it also regulates motility. Seems to play an important role in clathrin-mediated endocytosis and distribution of endocytic organelles (By similarity).

Drugs associated with TWF1

CN116425869

Patent Mining

Target

TWF1

Mechanism-

Active Org.

Beijing Minhai Biological Technology Co., Ltd.

Originator Org.

Beijing Minhai Biological Technology Co., Ltd.

Active Indication

Infectious Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TWF1

100 Translational Medicine associated with TWF1

0 Patents (Medical) associated with TWF1

494

Literatures (Medical) associated with TWF1

01 Jun 2025·Journal of Controlled Release

Hypoxia-responsive oncolytic conjugate triggers type-II immunogenic cell death for enhanced photodynamic immunotherapy

Article

Author: Lin, Jiayi ; Sun, Xin ; Luan, Xin ; Zhang, Xiaokun ; Ren, Maomao ; Liang, Rui ; Wang, Bei ; Kan, Yajie ; Lu, Shengxin ; Wu, Ye ; Chen, Hongzhuan

Immunogenic cell death (ICD) induced by photodynamic therapy (PDT) holds great promise for enhancing anti-tumor immunotherapy; however, its clinical efficacy is often hampered by suboptimal ICD induction and the exacerbation of an immunosuppressive tumor microenvironment (TME) following PDT. Herein, we present a tumor-targeted and hypoxia-responsive peptide-photosensitizer conjugate, A6-dMP-VP, which integrates an oncolytic peptide (dMP) with a CD44-targeting motif (A6), hypoxia-responsive groups, and the photosensitizer verteporfin (VP). Following systemic administration, A6-dMP-VP preferentially accumulates in 4T1 tumors, where the hypoxic TME triggers its response. Remarkably, the combined oncolytic activity and PDT effect of A6-dMP-VP effectively induce type-II ICD via mitochondrial disruption and endoplasmic reticulum stress, leading to robust antigen release. This process significantly enhances dendritic cell maturation and cytotoxic T cell priming, ultimately achieving potent suppression of both primary and metastatic tumors. Our findings establish A6-dMP-VP as a highly effective type-II ICD inducer, offering a novel strategy to overcome the limitations of PDT and advance photodynamic-oncolytic immunotherapy.

28 Mar 2025·Plant Physiology

The transcription factors MYB80 and TEK coordinate callose wall degradation and pollen exine formation in Arabidopsis

Article

Author: Xu, Ping ; Liu, Yaqi ; Xu, Xiaofeng ; Yang, Zhong-Nan ; Yang, Naiying ; Yu, Yahui ; Zhao, Xin ; Qian, Xuexue ; Guo, Yuyi ; Wang, Kaiqi

AbstractPollen development involves cell wall alteration of the male gametophyte, which is critical for plant fertility and requires MYB80 and TRANSPOSABLE ELEMENT SILENCING VIA AT-HOOK (TEK) transcription factors in Arabidopsis (Arabidopsis thaliana). In this study, we found that the myb80 tek double mutant exhibits a compromised degradation of the tetrad callose wall and downregulation of 5 ANTHER-SPECIFIC PROTEIN 6 (A6) genes encoding β-1,3-glucanase. The quintuple mutant of A6 (a6-quint) exhibited delayed callose wall degradation and defective exine structure, and its pollen had a weakened UV resistance. The quadruple mutant of A6 (a6-quad) restored the fertility of rvms-2, a thermosensitive genic male sterile (TGMS) line where the transition from tetrad wall to pollen wall is defective. Transgenic expression of A6 and A6.2 driven by the A9 promoter led to the expression of the 2 genes in the tapetum at earlier anther developmental stages, which caused premature callose wall dissolution and impeded exine formation, indicating the importance of the temporal control of A6s. Furthermore, dual-luciferase and ChIP assay results confirmed the direct regulation of MYB80 and TEK in activating the expression of the above A6s in the tapetum. In conclusion, callose degradation mediated by the MYB80/TEK-A6 pathway is required for the transition from tetrad callose wall to pollen wall.

01 Mar 2025·European Journal of Medicinal Chemistry

Design and synthesis of isatin derivative payloaded peptide-drug conjugate as tubulin inhibitor against colorectal cancer

Article

Author: Zhang, Yongmin ; Li, Yanping ; Wang, Zhaoyang ; Oumata, Nassima ; Xiang, Cen ; Teng, Yuou ; Yu, Peng ; Sun, Guoyang ; Yuan, Mengzhen ; Liu, Zhen ; Wang, Jinjin ; Wang, Ning ; Liu, Futao ; Yu, Jiajia

A series of isatin derivatives which could inhibit colorectal cancer (CRC) were synthesized. Among those compounds, 5B exhibited good inhibitory activity of CRC through the inhibition of tubulin expression, inducing apoptosis, and causing G2/M phase cell cycle arrest pathway, which suggested that 5B could be a potential tubulin inhibitor. Based on that, a novel peptide-drug conjugate (PDC), which employed the CRC cells related receptor CD44 ligand peptide A6 coupling to 5B to accomplish A6-5B. The in vitro and in vivo studies showed that A6-5B could significantly inhibit the tumor growth and metastasis in CRC cells. Mechanistic studies revealed that both 5B and A6-5B exert their antitumor effects by inhibiting tubulin, demonstrating that 5B might play a payload role and A6 could act as a targeting moiety for selective drug delivery to tumor cells.

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TWF1

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