Ask about this productRelated genes to: AP1M2 antibody
- Gene:
- AP1M2 NIH gene
- Name:
- adaptor related protein complex 1 subunit mu 2
- Previous symbol:
- -
- Synonyms:
- HSMU1B, mu2, AP1-mu2
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-01
- Date modifiied:
- 2018-05-03
Related products to: AP1M2 antibody
Related articles to: AP1M2 antibody
- Bladder cancer remains one of the most common malignancies of the urinary tract. Although the treatment landscape has expanded rapidly in recent years, gemcitabine still occupies a central position in intravesical treatment for non-muscle-invasive bladder cancer, in perioperative systemic therapy for muscle-invasive disease, and in platinum-based first-line regimens for advanced urothelial carcinoma. Yet the long-term benefit of gemcitabine is frequently curtailed by primary non-response or acquired resistance. In practice, this problem is often recognized only after radiographic progression or clear clinical deterioration has occurred. This review summarizes recent progress in bladder cancer therapy and translational research, with a particular emphasis on the biological basis and hierarchical evolution of gemcitabine resistance. We establish a 3-stage operational model of resistance, distinguishing: (1) early pharmacologic resistance driven by impaired drug uptake/activation or enhanced inactivation; (2) intermediate resistance driven by enhanced DNA damage repair, replication stress tolerance, and pro-survival autophagy signaling; and (3) late adaptive resistance driven by epithelial-mesenchymal transition (EMT), stemness maintenance, metabolic reprogramming, non-coding RNA-mediated epigenetic regulation, inflammatory microenvironmental remodeling, and extracellular vesicle-based intercellular transmission. These layers function as an interactive network, with sequential emergence under treatment pressure and parallel activation in context-dependent clinical settings. We stratify key mechanistic nodes (including the HYAL4-V1/CD44/JAK2-STAT3/CDA axis, AKR1C3, AP1M2-RAD54B, PRPF19-DDB1, AKT/mTOR signaling, Beclin-1-dependent autophagy, the MINCR/ZEB1/PHGDH axis, and IL-6-associated inflammatory states) by their clinical evidence quality and translational readiness, explicitly distinguishing preclinical discovery from clinically validated findings. Critically, most mechanistic findings remain at the preclinical or retrospective validation stage, with no markers yet approved for routine clinical use. Future work must prioritize longitudinal paired clinical samples, standardized analytic assays for dynamic biomarkers, and the integration of functional models (organoids, microfluidic systems), multi-omics technologies (single-cell sequencing, spatial transcriptomics), and liquid-biopsy approaches to translate mechanistic discoveries into clinically actionable predictive tools and therapeutic strategies. - Source: PubMed
Publication date: 2026/05/29
Jin MingCai ZhenzhenBu MingLiu JichengZhang Xiaojie - RING box Protein 1 (Rbx1) is a RING-domain protein that serves as the catalytic core of the SKP1-Cullin1-F-box (SCF) ubiquitin ligase complex. It is implicated in the ubiquitination process during plant self-incompatibility, growth, and abiotic stress responses. Two Arabidopsis Rbx1 homologous genes, designated ClRbx1-1 and ClRbx1-2, were identified in the genome of 'Xiangshui' lemon. Both ClRbx1 genes are highly expressed in pollen, furthermore, their expression was generally upregulated under self-pollination compared to cross-pollination conditions. Additionally, under simulated salt stress, the expression of ClRbx1 in leaves increased overall. The result of yeast two-hybrid showed that ClRbx1-1 could interact with several proteins associated with self-incompatibility and stress-responses, including Cullin1-2, S-RNase, S-RNase, Ubc12, AP1M2, and Peroxidase25. Yeast three-hybrid assays further demonstrated that ClRbx1-1 interacts with both Cullin1-2 and SKP1-6/SKP1-14 to assemble a canonical SCF complex. Notably, Ubc12 is highly expressed in pollen and its expression level is higher under self-pollination than under cross-pollination. This suggests that ClRbx1-1, cooperating with Ubc12, might function to regulate the self-incompatibility response via the RUB (related to ubiquitin) modification pathway. Overexpression of ClRbx1 in Arabidopsis resulted in dwarfism, and significantly improved salt stress tolerance. Overexpression of ClRbx1 in 'Xiangshui' lemon, achieved via Agrobacterium rhizogenes mediated hairy root transformation, led to a significant increase in salt stress tolerance. In summary, this study collectively elucidates the critical functions of ClRbx1 in self-incompatibility and salt stress response in 'Xiangshui' lemon, laying a solid foundation for further dissection of the molecular mechanisms by which the SCF complex mediates self-incompatibility and abiotic stress in plants. - Source: PubMed
Publication date: 2026/04/30
Nai YiLi YuzeZhang YuexingLuo CongYang TianLan MoyingWei JumeiLi MingqingWu WentingPeng LonghuiHuang GuixiangHe XinHua - Ganoderma lucidum has a long-standing history of use as a medicinal mushroom, with its spore oil (GLSO) extracted from broken cell walls using CO2 supercritical extraction. However, there is a notable scarcity of experimental studies on the protective effects and underlying mechanisms of GLSO on immune function impairment. The present study aims to explore the characteristics that GLSO contributes to protecting immune functions in cyclophosphamide-induced immunocompromised mice through a multi-omics analysis approach. GLSO administration significantly improved serum hemolysin levels, macrophage phagocytosis, and NK cell activity in immunosuppressed mice. Metagenomics, metabolomic, and proteomic analyses revealed that the immune protection mediated by GLSO was associated with structural rearrangements within gut microflora and shifts in microbial diversity. Specifically, there was an increase in beneficial microorganisms and a decrease in pathogenic organisms, accompanied by various alterations in metabolites and protein expressions. The identified 5 metabolites (propionic acid, beta-glycyrrhetinic acid, 3-aminosalicylic acid, creatine, and 2-phenylacetamide) and 5 proteins (Slc9a9, Blm, Hk3, AP1M2, and J chain) might serve as potential mediators of GLSO to alleviate immune dysfunction collectively caused by CYP in immunosuppressed mice. - Source: PubMed
Publication date: 2026/03/02
Deng ShuqiWu XiaoxiaoXu WendongWu XuCai HongfeiWang ShengpengLiu JuyanCao Jiliang - Adaptor-related protein complex 1 subunit mu 2 (AP1M2) has been has been shown to be overexpressed in breast cancer tissues. However, whether AP1M2 regulates triple-negative breast cancer (TNBC) progression and chemoresistance is unknown. - Source: PubMed
Publication date: 2026/01/30
Cui RuijieChen HongliZhao XinXu ShengFang Bing - This study was the first to identify the biallelic loss-of-function variant in AP1M2 as the cause of autoinflammatory disease with colitis and aimed to elucidate the pathogenesis of AP1M2 deficiency in mice and humans. - Source: PubMed
Publication date: 2026/03/26
Jin TaijieDai JialinLiu ChenluBai RenkuiEisenberg RachelWang YushaZhang JiahuiYin WeiAllis KatrinaHenderson Lindsay BMorrow MichelleDeuitch Natalie TLee Pui YKastner Daniel LYu XiaominZhou Qing