WDR12 Antibody (Center)
- Known as:
- WDR12 Antibody (Center)
- Catalog number:
- AP9066c-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- WDR12 Antibody (Center)
Ask about this productRelated genes to: WDR12 Antibody (Center)
- Gene:
- WDR12 NIH gene
- Name:
- WD repeat domain 12
- Previous symbol:
- -
- Synonyms:
- YTM1, FLJ10881
- Chromosome:
- 2q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-09
- Date modifiied:
- 2019-02-18
Related products to: WDR12 Antibody (Center)
Related articles to: WDR12 Antibody (Center)
- Melanoma is the deadliest skin cancer, and despite the success of immune checkpoint blockade, a substantial fraction of patients fail to respond. Tumors can evade cytotoxic lymphocytes by upregulating multiple inhibitory checkpoints. Here we identify WDR12 as a determinant of immunotherapy resistance: WDR12 expression is elevated in nonresponders, and its genetic inhibition increases intratumoral CD8+ T-cell infiltration and enhances cytotoxic function. Mechanistically, WDR12, in cooperation with the chaperonin subunit CCT7, stabilizes the immune checkpoint CD276 (B7-H3) on tumor cells, thereby suppressing T-cell activity and promoting immune escape. To translate these findings, we identify SU14813 as a small-molecule WDR12 inhibitor that binds WDR12 with high specificity, reduces CD276 stability, and relieves CD276-mediated T-cell suppression. In vivo, WDR12 targeting sensitizes tumors to PD-1 blockade, and combined SU14813 and anti-PD-1 therapy produces superior antitumor efficacy. These results define a WDR12-CCT7-CD276 axis that sustains immune resistance in melanoma and nominate WDR12 inhibition with PD-1 blockade as a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/06/27
Pan JieChang RuiminZhang MengDong QianZhang GuanxiongChen XiangChen MingliangLu LixiaLiang XiaoweiGuo YeyeSu Juan - Osteosarcoma (OS) is a common primary malignant bone tumor in children and adolescents. Increasing evidence suggests that immune dysregulation contributes to OS progression, but its tissue-level and systemic features remain incompletely defined. This study aimed to characterize immune-related alterations in OS and identify key immunoregulatory molecules associated with disease progression. - Source: PubMed
Publication date: 2026/05/07
Zhu JichongHuang ChengqianTan Weiming - Osteosarcoma (OS) stands as the predominant malignant primary bone tumor. WDR12 plays a role in diverse biological processes. Nonetheless, the specific function of WDR12 in OS has not been clearly elucidated. Herein, we found that WDR12 is overexpressed and closely associated with poor prognosis of OS. A diagnostic nomogram based on WDR12 and clinical features of OS could effectively predict the overall survival rate of OS patients. Through functional enrichment analysis, multiple potential pathways related to WDR12 expression in tumorigenesis have been identified. Additionally, the expression level of WDR12 is correlated with the tumor immune microenvironment, immune therapy response, and drug treatment response in OS. Importantly, in vitro experiments demonstrated that downregulation of WDR12 significantly inhibited the proliferation and migration abilities of OS cells and in vivo experiments also confirmed that overexpression of WDR12 could promote tumor growth. Hence, WDR12 has the capacity to emerge as a novel prognostic biomarker and therapeutic target for OS. - Source: PubMed
Publication date: 2026/04/08
Zhang ZhimingChen RuiqiLiu ZhongyueLiu BinfengMei LinYin ChiWan LuLi Zhihong - Cognitive SuperAgers (SAs) are individuals aged 80+ with exceptional episodic memory performance for their age, exceeding middle-aged adult norms. This study integrates family- and association-based methods to identify genetic variants associated with SAs in the Midwestern Amish population. - Source: PubMed
Dorfsman DanielPrough Michael BGulyayev AlexCaywood Laura JClouse Jason EHerington Sharlene DSlifer Susan HAdams Larry DLaux Renee ASong Yeunjoo ELynn AudreyFuzzell Sarada LHochstetler Sherri DMiskimen KristyMain Leighanne RWang PingLiu YiningMoore NoelOgrocki PaulaLerner Alan JVance Jeffery MCuccaro Michael LHaines Jonathan LPericak-Vance Margaret AScott William K - Although the use of tyrosine kinase inhibitors (TKIs), such as sunitinib, has led to impressive advancements in the treatment of clear cell renal cell carcinoma (ccRCC), primary or acquired resistance to sunitinib remains elusive. Here, we report that death receptor 5 (DR5) is upregulated in ccRCC tissues and sunitinib-resistant cells, and is associated with poor outcomes and sunitinib resistance. Gain- and loss-of-function experiments revealed that DR5 promotes sunitinib resistance both in vitro and in vivo. Mechanistically, DR5 enhances the activation of NF-κB signalling by reducing the ubiquitin-mediated proteasomal degradation of p65 via competitive binding to the CUL4B-DDB1 E3 ligase complex linker protein WDR12, leading to the transcriptional upregulation of DR5 and BCL2. The positive feedback loop between DR5 and p65 contributes to the upregulation of BCL2 expression, which in turn modulates sunitinib resistance in ccRCC. Notably, targeting the DR5/NF-κB/BCL2 axis sensitizes ccRCC cells to sunitinib both in vitro and in vivo. Clinically, ccRCC patients with high DR5 expression show decreased responsiveness to TKI-based therapy. Collectively, these results highlight the importance of the positive feedback loop involving the DR5/NF-κB axis in sunitinib resistance and provide an effective therapeutic strategy for overcoming resistance. - Source: PubMed
Publication date: 2026/03/23
Tao WenDong YuhaoZuo ShidongWang HanfengLiang QiyangCai TianweiChen XinranWei WenjieZhang ChiTian ShuoWang ChuangLi HongzhaoWang BaojunMa XinHuang QingboShi TaopingHuang YanZhang Xu