Ask about this productRelated genes to: ABL2 antibody
- Gene:
- ABL2 NIH gene
- Name:
- ABL proto-oncogene 2, non-receptor tyrosine kinase
- Previous symbol:
- ABLL
- Synonyms:
- ARG
- Chromosome:
- 1q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-04-25
Related products to: ABL2 antibody
Related articles to: ABL2 antibody
- Dysfunction of vascular endothelial cells (VECs) is a common feature of both psoriasis and diabetes. Comorbidity of these two conditions increases the risk of diabetic foot ulcer (DFU), yet the shared mechanisms remain unclear. - Source: PubMed
Publication date: 2026/04/13
Xu JiaxinZhang XinZhang TianyuanWang GangLi Qingyang - Chronic obstructive pulmonary disease (COPD) lacks effective early diagnostic biomarkers, and the role of miR-27a-5p in COPD pathogenesis remains unclear. This study aimed to explore its inflammatory regulatory mechanism. - Source: PubMed
Publication date: 2026/05/26
Wang JingfanZhang PingQin Yonggang - Caveolin-1 (CAV1) is a 21 kDa Vesicular Integral-membrane Protein essential for the biogenesis of caveolae, invaginations of the plasma membrane that coordinate membrane trafficking, lipid homeostasis, and signal transduction. CAV1 functions as a scaffolding platform that integrates mechanotransduction, endocytosis, and cellular stress responses, thereby modulating vascular integrity, inflammation, metabolism, and tumorigenesis. To comprehensively understand the phosphorylation landscape of CAV1, global phosphoproteomic datasets and their corresponding experimental metadata were systematically curated and integrated from previously published human cellular studies. The phosphorylation sites with the highest detection frequency across these datasets were considered predominant phosphorylation sites. To assess their functional relevance, phosphosites in other proteins (PsOPs) co-regulated with the predominant CAV1 sites, along with their upstream kinases and high-confidence protein-protein interaction partners, were systematically analyzed. Analysis of global human cellular phosphoproteome datasets revealed that tyrosine 14 (Y14) and serine 37 (S37) of CAV1 are the most frequently detected phosphosites across diverse experimental conditions. Notably, many of the co-regulated proteins obtained were associated with carcinogenesis, apoptosis, and cell cycle regulation, including MET and ERBB2. Our analysis revealed SRC, ABL2, ERBB2, ERBB3, LYN, and TEC as potential upstream kinases of CAV1_Y14, whereas CSNK1E and GRK5 were predicted to regulate CAV1_S37. Considering the challenges associated with site-specific interrogation, we employed a global co-regulation analysis approach to characterize CAV1 phosphorylation dynamics. Our findings reveal that key CAV1 phosphosites modulate oncogenic signaling, cytoskeletal remodeling, and membrane organization, providing novel insights into CAV1-mediated cellular functions and its context-dependent role in tumor progression. - Source: PubMed
Publication date: 2026/05/12
Vaz Chrysilla EspySuresh ManasaDcunha LeonaRaju RajeshKanekar Saptami - F-box only protein 31 (FBXO31) has been implicated in tumorigenesis and development across various human cancers. However, the role of FBXO31 in breast cancer progression remains poorly understood. In this study, we identified FBXO31 as a tumor suppressor in triple-negative breast cancer (TNBC), where it inhibited cell proliferation, migration, and invasion. Furthermore, FBXO31 promoted cystine-glutamate antiporter (xCT)-mediated ferroptosis in TNBC cells. Notably, overexpression of FBXO31 suppressed tumor growth in mice. Mechanistically, ABL-related gene (ABL2) was identified as a novel ubiquitin substrate of FBXO31. FBXO31 specifically interacted with ABL2 and promoted ABL2 ubiquitination and subsequent degradation through its F-box motif. Functionally, ABL2 acted as an oncogenic factor in TNBC cells by promoting cell proliferation, migration, and invasion, while inhibiting xCT-mediated ferroptosis. Rescue experiments showed that FBXO31 inhibited TNBC progression at least partly through down-regulating ABL2 expression. Collectively, our findings reveal a novel molecular mechanism for TNBC progression and provide a potential therapeutic strategy for its treatment. - Source: PubMed
Publication date: 2026/04/15
Zhang YuhaoLuo JingjingXu QingZeng XianzhenWang XinyuXu HuiPan XueshanCao TongHuang HuaMa Jia - Protein kinases dysregulation is implicated in various cancer-related processes; however, its clinical utility and biological significance in head and neck squamous cell carcinoma (HNSCC) remain incompletely understood. This study aimed to establish a novel prognostic signature using kinase-related genes (KRGs) for prognostic and therapeutic prediction in HNSCC. - Source: PubMed
Publication date: 2026/05/05
Zhang YangLv PinCao GuangruiQi NaYu MiaoWu Yaping