AP1M2
- Known as:
- AP1M2
- Catalog number:
- 001717A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AP1M2
Related genes to: AP1M2
- 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
Related articles to: AP1M2
- Sperm cryodamage is a key factor affecting its post-thaw quality. This study aims to systematically elucidate the molecular response mechanisms of bovine sperm cryodamage by integrating transcriptomic and proteomic analyses. By utilizing the swim-up technique to isolate sperm subpopulations with mild and severe cryodamage, thereby minimizing interference from individual genetic variation. Results demonstrated that mildly damaged sperm exhibited superior motility, structural integrity, and antioxidant capacity, along with less reactive oxygen species accumulation and more active Wnt, mTOR, and Hippo signaling pathways at the transcriptional level. Severely damaged sperm exhibited activation of pathways related to oxidative phosphorylation, thermogenesis, peroxisome, glutathione metabolism, phagocytosis, and DNA repair at the protein level, with ATP5MG, GPX1, XRCC1, and AP1M2 serving as core regulatory factors in these pathways. Additionally, integrated analysis identified eight potential biomarker proteins, including apoptosis-related protein ARL6IP5, anti-apoptotic protein GRINA, adhesion factors CDHR1/LGALS1, DNA repair proteins CUL4B/POLR2E, and core factors RPL14/A1BG in the protein-protein interaction network. Notably, the protein levels of ARL6IP5, CDHR1, and LGALS1 were inconsistent with their gene expression levels. These candidate molecules showed significant correlations with post-thaw sperm quality and were quantitatively validated. The results indicate that mitochondrial energy metabolism, antioxidant and anti-apoptotic defense systems, as well as self-repair and clearance responses, including nucleic acid repair and phagocytosis, represent the molecular response characteristics of sperm cryodamage. These findings complement the molecular mechanisms and regulatory networks of sperm cryodamage, and provide potential targets for evaluating the cryopreservation potential of bull semen and optimizing cryoprotectants. - Source: PubMed
Publication date: 2026/08/01
Song ChengleiJiang QiufeiZhu ChunmaoShi AnNan GuoxiongShen WenjuanZhou JiaminYang ZhuoTuo ZhengjunHan XiaohongTao Jinzhong - Gut homeostasis relies on the tightly controlled balance between intestinal stem cell self-renewal and differentiation. The clathrin adaptor complex AP-1B plays a pivotal role in establishing the polarity of enterocytes as well as in the asymmetric distribution of membrane proteins, including the brush border transporters that govern intestinal absorption. Additionally, AP-1B has been involved in the control of intestinal cell proliferation, which suggests that it may regulate various aspects of gut functional organisation. In this study, we investigated the consequences of conditional mutations of the gene encoding the AP-1B subunit μ1B (Ap1m2) in mouse enteroids. We first showed in this model that Ap1m2 mutations also induce strong polarity defects at the subcellular level in the absorptive enterocytes. Next, we unveiled that AP-1B regulates intestinal cell differentiation at the tissular level, through the commitment of stem/progenitor cells towards the secretory lineage and cell positioning along the crypt-villus axis. Furthermore, we showed that AP-1B inhibition also induces hyperproliferation in enteroids. Notably, we unravelled that, complementary to the Wnt/β-catenin-mediated proliferation described in null mice, AP-1B downregulation triggers a tissue-autonomous, mTOR/YAP-dependent, proliferative pathway. Overall, these results enlighten the pleiotropic roles played by AP-1B in the homeostasis of the gut epithelium. - Source: PubMed
Duclos MaelaBourdais AnneNicolle OphélieHelpiquet AlexandreMichaux GrégoireBidaud-Meynard Aurélien - Bladder cancer (BCa) is a highly prevalent urological malignancy and one of the most frequently occurring cancers worldwide, necessitating the development of diagnostic and therapeutic biomarkers. This study aimed to explore candidate genes that may be involved in the carcinogenesis of BCa. - Source: PubMed
Publication date: 2026/07/18
Sajjadi SanaRamezani AminAlavimanesh SajadAlipoor HojatTakhshid Mohammad Ali - Recognition of infected macrophages by CD4+ T cells is essential to immune protection against (Mtb), the causative agent of tuberculosis (TB). However, not all infected macrophage subsets successfully elicit T cell activation. We recently discovered that M2-like macrophages fail to efficiently activate memory CD4+ T cells when infected with Mtb, yet successfully elicit T cell activation when loaded with peptides, γ-irradiated bacteria, or Mtb whole cell lysate. Since the mechanisms underlying CD4+ T cell evasion by infected M2 but not M1-like macrophages remain underexplored, we sought to determine the genes and pathways unique to Mtb infection of M2-like cells, including alveolar macrophages. RNA sequencing of human macrophages infected with virulent Mtb identified enrichment of IL-10 and type I interferon (IFN) signaling genes, including and , respectively, in infected M2-like monocyte-derived and alveolar macrophages. However, genes involved in MHC-II trafficking, such as , were higher in infected M1-like macrophages. In complementary experiments using fluorescence microscopy and flow cytometry, we observed impaired trafficking of newly synthesized MHC-II to the plasma membrane of Mtb-infected M2-like macrophages despite high total surface MHC-II levels. Neutralization of IL-10 or knockdown of restored MHC-II trafficking to the cell surface among infected M2-like macrophages and significantly enhanced activation of memory CD4+ T cells in an MHC-II-dependent manner. These findings identify coordinated IL-10 and type I IFN signaling as key mechanisms that restrict MHC-II trafficking to the plasma membrane in Mtb-infected M2-like macrophages, thereby limiting antigen presentation and CD4+ T cell activation. We propose that host-directed therapies targeting these pathways in infected alveolar macrophages will facilitate T cell recognition for the prevention or treatment of active TB. - Source: PubMed
Publication date: 2026/07/10
Sandhu Avinaash KGail Daniel PSimmermon Rachel CWebb DemetriaHmiel LauraBark CharlesBryson BryanSilver Richard FCarpenter Stephen - 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