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
- Pseudomonas aeruginosa (P. aeruginosa) keratitis can progress rapidly to vision-threatening disease, even with intensive therapy. Virulence-associated genes are key determinants of ocular-surface pathogenesis. We therefore sought to develop a composite wbp-exo genotyping framework for risk stratification and to guide wbp-dependent, LPS-directed, levofloxacin-polymyxin B (LVX-POL) combination therapy for high-risk corneal infections. - Source: PubMed
Publication date: 2026/08/11
Wei MingdaZhang ZijunZhao XudongXu BolingShi QingquanCheng ZhenXu XizhanWei ZhenyuLu XinxinLi LiLiang Qingfeng - Synapses are thought to be a vulnerable site in hearing loss. One gene required for normal synapse maintenance is Wbp2, which encodes a transcriptional co-activator of oestrogen and progesterone receptors. The Wbp2 mouse mutant allele knocks down transcription to minimal levels and leads to progressive increase in ABR thresholds for high frequencies from 4 weeks onwards in homozygotes. This is accompanied by swelling of nerve terminals below inner hair cells and dysregulation of key post-synaptic proteins. We have used the design of the Wbp2 mutation to investigate whether the synaptic swelling and increase in auditory thresholds can be prevented or reversed by activating the Wbp2 gene either prior to or after the onset of hearing loss, respectively. The influence of a common modifier of auditory function, Cdh23, was also studied by crossing a repaired Cdh23 allele into the Wbp2 colony. We found that activation of Wbp2 at either 4 weeks old or postnatal day 4 failed to halt or prevent the progression of hearing loss in Wbp2 homozygous mutant mice. Surprisingly, correction of the Cdh23 allele in Wbp2 mice completely abolished the auditory phenotype, restoring hearing thresholds to normal up to 26 weeks of age. These findings reveal the difficulty in reversing early-onset synaptic defects and highlight genetic background, including known modifiers like Cdh23, as a critical factor in auditory research. - Source: PubMed
Publication date: 2026/07/25
Kumar RechalPentland Daniel RIngham Neil JLewis Morag AMartelletti ElisaSteel Karen P - 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