WASF1

Last update 08 May 2025

Basic Info

Synonyms

Actin-binding protein WASF1, KIAA0269, Protein WAVE-1

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Introduction

Downstream effector molecule involved in the transmission of signals from tyrosine kinase receptors and small GTPases to the actin cytoskeleton. Promotes formation of actin filaments. Part of the WAVE complex that regulates lamellipodia formation (PubMed:29961568). The WAVE complex regulates actin filament reorganization via its interaction with the Arp2/3 complex (By similarity). As component of the WAVE1 complex, required for BDNF-NTRK2 endocytic trafficking and signaling from early endosomes (By similarity). Also involved in the regulation of mitochondrial dynamics (PubMed:29961568).

100 Clinical Results associated with WASF1

100 Translational Medicine associated with WASF1

0 Patents (Medical) associated with WASF1

588

Literatures (Medical) associated with WASF1

05 May 2025·Journal of Cell Biology

Cell signaling facilitates apical constriction by basolaterally recruiting Arp2/3 via Rac and WAVE

Article

Author: Song, April N. ; Perez, Jadyn M. ; Breiner, Eleanor A. ; Goldstein, Bob ; Medwig-Kinney, Taylor N. ; Zhang, Pu

Apical constriction is a critical cell shape change that drives cell internalization and tissue bending. How precisely localized actomyosin regulators drive apical constriction remains poorly understood. Caenorhabditis elegans gastrulation provides a valuable model to address this question. The Arp2/3 complex is essential in C. elegans gastrulation. To understand how Arp2/3 is locally regulated, we imaged embryos with endogenously tagged Arp2/3 and its nucleation-promoting factors (NPFs). The three NPFs—WAVE, WASP, and WASH—controlled Arp2/3 localization at distinct subcellular locations. We exploited this finding to study distinct populations of Arp2/3 and found that only WAVE depletion caused penetrant gastrulation defects. WAVE localized basolaterally with Arp2/3 and controlled F-actin levels near cell–cell contacts. WAVE and Arp2/3 localization depended on CED-10/Rac. Establishing ectopic cell contacts recruited WAVE and Arp2/3, identifying the contact as a symmetry-breaking cue for localization of these proteins. These results suggest that cell–cell signaling via Rac activates WAVE and Arp2/3 basolaterally and that basolateral Arp2/3 makes an important contribution to apical constriction.

01 Apr 2025·Cell Death & Differentiation

Inhibition of thioredoxin reductase 1 sensitizes glucose-starved glioblastoma cells to disulfidptosis

Article

Author: Gao, Yan ; Tang, Miaolu ; Li, Wei ; Peruggia, Gabrielle ; Qiu, Zhiqiang ; Sallavanti, Jessica ; Sun, Dongxiao ; Kim, Soo Yeon ; Dirks, Kaitlyn

Disulfidptosis is a recently identified form of cell death characterized by the aberrant accumulation of cellular disulfides. This process primarily occurs in glucose-starved cells expressing higher levels of SLC7A11 and has been proposed as a therapeutic strategy for cancers with hyperactive SCL7A11. However, the potential for inducing disulfidptosis through other mechanisms in cancers remains unclear. Here, we found that inhibiting thioredoxin reductase 1 (TrxR1), a key enzyme in the thioredoxin system, induces disulfidptosis in glioblastoma (GBM) cells. TrxR1 expression is elevated in GBM with activated transcriptional coactivator with PDZ-binding motif (TAZ) and correlates with poor prognosis. TrxR1 inhibitors induced GBM cell death that can be rescued by disulfide reducers but not by ROS scavengers or inhibitors of apoptosis, ferroptosis, or necroptosis. Glucose-starved cells, but not those deprived of oxygen or glutamine, increased TrxR1 expression in an NRF2-dependent manner and were more sensitive to TrxR1 inhibition-induced cell death. The dying cells initially exhibited highly dynamic lamellipodia, followed by actin cytoskeleton collapse. This process involved the accumulation of cytosolic peroxisomes and micropinocytic caveolae, as well as small gaps in the plasma membrane. Depletion of the WAVE complex component NCKAP1 partially rescued the cells, whereas Rac inhibition enhanced cell death. In an orthotopic xenograft GBM mouse model, TrxR1 depletion inhibited tumor growth and improved survival. Furthermore, cells undergoing TrxR1 inhibition exhibited features of immunogenic cell death. Therefore, this study suggests the potential of targeting TrxR1 as a therapeutic strategy in GBM.

01 Mar 2025·Cancer Genomics - Proteomics

The WASP/WAVE Protein Family in Breast Cancer and Their Role in the Metastatic Cascade

Review

Author: Yu, Rhiannon Yannan ; Martin, Tracey A ; Jiang, Wen G

The Wiskott-Aldrich syndrome protein (WASP) and the WASP family verprolin-homologous protein (WAVE) family are essential molecules that connect GTPases to the actin cytoskeleton, thereby controlling actin polymerisation through the actin-related protein 2/3 complex. This control is crucial for forming actin-based membrane protrusions necessary for cell migration and invasion. The elevated expression of WASP/WAVE proteins in invasive breast cancer cells highlights their significant role in promoting cell motility and invasion. This review summarises the discovery, structural properties, and activation mechanisms of WASP/WAVE proteins, focuses on the contribution of the WASP/WAVE family to breast cancer invasion and migration, particularly synthesises the results of nearly a decade of research in this field since 2015. By exploring promising therapeutic strategies for breast cancer, including small molecule inhibitors and biological agents, this review stresses the potential for developing anticancer drugs that target the WASP/WAVE family and associated pathways, intending to improve the prognosis for patients with metastatic breast cancer.

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WASF1

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