Ask about this productRelated genes to: STAMBPL1 antibody
- Gene:
- STAMBPL1 NIH gene
- Name:
- STAM binding protein like 1
- Previous symbol:
- -
- Synonyms:
- AMSH-LP, KIAA1373, AMSH-FP, FLJ31524, ALMalpha, bA399O19.2
- Chromosome:
- 10q23.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-25
- Date modifiied:
- 2016-10-05
Related products to: STAMBPL1 antibody
Related articles to: STAMBPL1 antibody
- Gastric cancer (GC) is a highly aggressive malignancy with limited therapeutic options and poor clinical outcomes. Aberrant regulation of the ubiquitin-proteasome system contributes to tumorigenesis by disrupting protein homeostasis and signal transduction. STAMBPL1, a JAMM family deubiquitinase (DUB) implicated in several cancers, remains poorly characterized in GC, and its mechanistic relevance to disease progression warrants investigation. - Source: PubMed
Publication date: 2025/11/27
Tang XiaochengQiu JunChen ChunyuZhang JiaweiTan RongchangLi WeiyaoHuang JintuanChen HaoYang Zuli - Gastric cancer (GC) continues to pose a significant global health burden, necessitating a thorough understanding of the molecular mechanisms driving its progression. This study aimed to investigate the regulatory role of SMAD3 in modulating Sestrin2 ubiquitination stability and its implications in GC cell behaviors. - Source: PubMed
Publication date: 2025/08/01
Zhang NingZhao NaZhang HainanYao LeSi Hongtao - In the clinic, anti-tumor angiogenesis is commonly employed for treating recurrent, metastatic, drug-resistant triple-negative, and advanced breast cancer. Our previous research revealed that the deubiquitinase STAMBPL1 enhances the stability of MKP-1, thereby promoting cisplatin resistance in breast cancer. In this study, we discovered that STAMBPL1 could upregulate the expression of the hypoxia-inducible factor HIF1α in breast cancer cells. Therefore, we investigated whether STAMBPL1 promotes tumor angiogenesis. We demonstrated that STAMBPL1 increased transcription in a non-enzymatic manner, thereby activating the HIF1α/VEGFA signaling pathway to facilitate triple-negative breast cancer angiogenesis. Through RNA-seq analysis, we identified the transcription factor GRHL3 as a downstream target of STAMBPL1 that is responsible for mediating transcription. Furthermore, we discovered that STAMBPL1 regulates transcription by interacting with the transcription factor FOXO1. These findings shed light on the role and mechanism of STAMBPL1 in the pathogenesis of breast cancer, offering novel targets and avenues for the treatment of triple-negative and advanced breast cancer. - Source: PubMed
Publication date: 2025/04/10
Fang HuanLiang HuichunYang ChuanyuJiang DeweiLuo QianmeiCao Wen-MingZhang HuifengChen Ceshi - Abnormal antioxidant capacity in cancer cells is intimately linked to tumor aggressiveness. Modulating oxidative stress status and inhibiting ferroptosis represents a novel anticancer therapeutic strategy. STAM Binding Protein Like 1 (STAMBPL1), a deubiquitinase, is implicated in various malignancies, yet its function in inhibiting ferroptosis and therapeutic potential for cholangiocarcinoma (CCA) remains unexplored. - Source: PubMed
Publication date: 2024/12/04
Wang ZhihuaiZhang YinjieShen YuhangZhu ChunfuQin XihuGao Yuan - Kidney renal clear cell carcinoma (KIRC) is recognized as an immunogenic tumor, and immunotherapy is incorporated into its treatment landscape for decades. The acquisition of a tumor mesenchymal phenotype through epithelial-to-mesenchymal transition (EMT) is associated with immune evasion and can contribute to immunotherapy resistance. Here, the involvement of STAM Binding Protein Like 1 (STAMBPL1) is reported in the development of mesenchymal and immune evasion phenotypes in KIRC cells. Mechanistically, STAMBPL1 elevated protein abundance and surface accumulation of TAM Receptor AXL through diminishing the TRIM21-mediated K63-linked ubiquitination and subsequent lysosomal degradation of AXL, thereby enhancing the expression of mesenchymal genes while suppressing chemokines CXCL9/10 and HLA/B/C. In addition, STAMBPL1 enhanced PD-L1 transcription via facilitating nuclear translocation of p65, and knockdown (KD) of STAMBPL1 augmented antitumor effects of PD-1 blockade. Furthermore, STAMBPL1 silencing and the tyrosine kinase inhibitor (TKI) sunitinib also exhibited a synergistic effect on the suppression of KIRC. Collectively, targeting the STAMBPL1/TRIM21/AXL axis can decrease mesenchymal phenotype and potentiate anti-tumor efficacy of cancer therapy. - Source: PubMed
Publication date: 2024/11/11
Huang ShiyuQin XukeFu ShujieHu JunchengJiang ZhengyuHu MinZhang BanghuaLiu JiachenChen YujieWang MinghuiLiu XiuhengChen ZhiyuanWang Lei