Ask about this productRelated genes to: WBP2 antibody
- Gene:
- WBP2 NIH gene
- Name:
- WW domain binding protein 2
- Previous symbol:
- -
- Synonyms:
- WBP-2, GRAMD6
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2016-04-05
Related products to: WBP2 antibody
Related articles to: WBP2 antibody
- Impaired proteostasis is a cellular hallmark of aging, and the ubiquitin-proteasome system is a fundamental driver of proteostasis. As an E3 ubiquitin ligase, WW-domain containing protein 1 (WWP1) expression and activity are tightly regulated in cells, while its deregulation has been described in cancer, in neurodegenerative diseases, and in heart failure. However, the protein-protein interaction network of WWP1 is understudied, particularly in the heart. Here, we conducted a yeast-two hybrid (Y2H) screen of a human heart library and identified 21 putative WWP1 interactors, including 12 whose expression and potential function in the heart were previously unappreciated. Central in the identified protein-protein interaction network was WBP2 (WW domain binding protein 2), an oncogenic transcriptional co-activator. Utilizing immunofluorescence and proximity ligation assays, it was confirmed that endogenous WWP1 can co-localize and interact with WBP2 in human heart tissue, and, using the Y2H system, we showed that this interaction is dependent upon the associations between WW domains 1 and 3 from WWP1 and PY domains 2 and 3 of WBP2. In total, these data serve as a launching pad to identify broader protein networks regulated by WWP1 and the regions of interaction which might be targetable to reduce hallmarks of cellular aging. - Source: PubMed
Publication date: 2026/04/17
Arnold Meaghan EWright YmaniGrantham Natalie KPittman Douglas LMatesic Lydia E - Conventional treatment strategies and immunotherapy yield low response rates in head and neck squamous cell carcinoma (HNSCC). This study aimed to explore the potential of immunosuppressive receptor leukocyte immunoglobulin-like receptor subfamily B member 1 (LILRB1) for developing effective immunotherapies for HNSCC. - Source: PubMed
Chen ShuaiWu QiuwanGu ShuoZhou YiCai MingquanWu JunhuaHe JingHe JingjingLin JuliHong ZhicongZhang BinghuangLuo Xianyang - Breast cancer treatment has advanced substantially with the development of targeted and multimodal strategies, yet tumor heterogeneity and therapeutic resistance continue to limit long-term outcomes. This review provides a concise and critical overview of established and emerging targeted therapies, with emphasis on resistance mechanisms, innovations in drug delivery, and integrative therapeutic approaches. Established modalities, including endocrine therapy, HER2-directed antibody and antibody-drug conjugate therapies, and chemotherapy, are summarized alongside key subtype-specific challenges. Emerging targets such as PARP, CDK4/6, WBP2, and Trop2, as well as metabolic and tumor-microenvironment-oriented strategies, are evaluated for their potential to overcome resistance. Advances in immunotherapy, including checkpoint inhibitors, bispecific antibodies, and CAR-T cell therapies, are examined with attention to mechanistic rationale and limitations across breast cancer subtypes. Progress in nanotechnology-based delivery systems, exosome-mediated transport, and multimodal predictive frameworks, including miRNA regulatory networks, is further assessed for its relevance to personalized treatment. Overall, this review synthesizes current molecular insights and therapeutic innovations to inform the development of more effective and durable targeted treatments for breast cancer. - Source: PubMed
Publication date: 2026/01/07
Wu WenningHe YufengZhang Chunxiang - Metformin is an antidiabetic drug that has been tested widely as an anti-cancer agent. However, data from clinical trials have been mixed. Evidence for metformin's efficacy in HER2+ breast cancer exists. Hence, we evaluated whether WBP2, a HER2-coamplified gene, can regulate the response of HER2+ breast cancer to metformin. Identification of biomarkers for predicting metformin response has implications in repurposing metformin for precision oncology. The effect of WBP2 on breast cancer response to metformin was studied using in vitro and mouse models. The mechanism of WBP2 on metformin-induced AMPK activation was elucidated, and its co-expression with p-AMPK was examined in clinical specimens using IHC. RNA-seq analyses were performed to elucidate WBP2's mechanism in energy metabolism. WBP2 inhibited the metformin response of HER2+ breast cancer in vitro and in vivo. These effects were concomitant with WBP2-mediated repression of metformin-induced AMPK activation and mTOR inhibition in HER2+ breast cancer cells, a lower AMP:ATP ratio state, and enhanced glycolytic capacity and mitochondria respiration. Analysis of HER2-positive breast cancer samples supports the negative correlation between WBP2 expression and activated AMPK observed in vitro. RNA-seq analysis revealed the potential mechanism of WBP2 in regulating ATP production processes and preferential effect of WBP2 on metformin response in HER2+ breast cancer. This study reported a novel role of WBP2 in cancer metabolism and energetics that contributes new insights into the molecular etiology of cancer. WBP2 may be a biomarker for patient stratification, paving the way towards repurposing metformin for precision oncology. - Source: PubMed
Publication date: 2026/02/23
Lin HexianKang Shin-AeXie FeiLim Yvonne XinyiSeah Sock HongSabbaghian AmirLu Ssu-YiChew Ting GangDeng Lih-WenWang ShuTai E-ShyongLim Yoon Pin - One of the main factors contributing to aging is reactive oxygen species (ROS), which are produced by dysfunctional mitochondria. Reducing ROS generation is considered an essential treatment for senescence, but no effective treatment has been developed yet. In this study, vitisin B, a tetramer of resveratrol, was found to be an efficient reagent that reduces mitochondrial ROS generation after screening phenylpropanoids (PPs), metabolites produced to overcome ROS-mediated stress in plants. Vitisin B induced mitochondrial functional recovery by activating mitophagy and removing dysfunctional mitochondria. Mitochondrial functional recovery by vitisin B decreased mitochondrial ROS, a by-product generated from dysfunctional mitochondria. In addition, ROS reduction by vitisin B restored senescence-associated phenotypes. RNA sequencing identified WBP2 N-Terminal Like (WBP2NL) as a gene essential for vitisin B-mediated senescence rejuvenation. Knockdown of WBP2NL exhibited effects similar to those of vitisin B, reducing mitochondrial ROS generation and consequently reversing senescence-associated phenotypes. This study elucidates a novel mechanism by which vitisin B reverses senescence by lowering mitochondrial ROS generation. This discovery opens the way to new therapeutic options to control aging by modulating mitochondrial ROS production. - Source: PubMed
Publication date: 2026/01/21
Yoon Jee HeeLee Yun HaengOh SekyungLee Kyeong SeonPark Ji HoLee Yoo JinSo ByeonghyeonKim DuyeolKim MinseonKwon Hyung WookByun YoungjooLee Ki YongPark Joon Tae