MDM2 pSer186/Ser188 antibody Ab
- Known as:
- MDM2 pSer186/Ser188 (anti-) Antibody
- Catalog number:
- 1488082
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- MDM2 pSer186/Ser188 antibody
Related genes to: MDM2 pSer186/Ser188 antibody Ab
- Gene:
- MDM2 NIH gene
- Name:
- MDM2 proto-oncogene
- Previous symbol:
- -
- Synonyms:
- HDM2, MGC5370
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-10
- Date modifiied:
- 2017-12-01
Related products to: MDM2 pSer186/Ser188 antibody Ab
Related articles to: MDM2 pSer186/Ser188 antibody Ab
- Synaptic function and plasticity depend on the precise control of protein abundance and turnover, governed by the balance of synthesis and degradation. This review examines the regulatory mechanisms that maintain synaptic protein stability, focusing on the Ubiquitin-Proteasome System (UPS), autophagy-lysosomal pathways, and related proteolytic systems. We detail how key enzymes, including E3 ligases such as Nedd4-1, Mdm2, and Parkin, and deubiquitinating enzymes like USP46 and USP8, dynamically regulate the degradation of critical synaptic components from AMPA and NMDA receptors to scaffolds like PSD-95 and SHANK3. We further explore how autophagy, including chaperone-mediated and activity-dependent forms, contributes to synaptic remodeling and quality control. Crucially, dysfunction of synaptic degradation pathways is a common thread in neurodevelopmental and neurodegenerative disorders. We summarize evidence linking proteostatic malfunction to the pathogenesis of Alzheimer's disease (through impaired clearance of Aβ and tau), Parkinson's disease (via α-synuclein turnover), epilepsy, autism spectrum disorder, and ischemic injury. The review highlights how genetic mutations in degradation machinery or their synaptic targets converge to disrupt synaptic integrity and neural circuit function. By integrating findings from basic neurobiology and disease models, this review underscores the central importance of synaptic proteostasis and aims to identify critical regulatory molecules that retain potentials for diagnostic biomarkers and therapeutic targets for neurological disease. - Source: PubMed
Publication date: 2026/04/29
Li YuanyuanHou Xiao-YuTao Yanmei - Retroperitoneal liposarcoma (RPL) presents a distinct "high-risk" disease spectrum, in which the phenotypic transition from well-differentiated liposarcoma (WDLPS) to dedifferentiated liposarcoma (DDLPS) constitutes a critical biological event leading to treatment failure and patient mortality. This review provides a systematic summary of the clinical features and multi-omics mechanisms underlying this transition. Clinically, this process is characterized by time-dependent malignant progression over approximately 7-8 years. Biologically, it reflects a layered evolutionary process involving a shared genomic trunk defined by MDM2 proto-oncogene (MDM2) and cyclin-dependent kinase 4 (CDK4), secondary driver events such as JUN proto-oncogene, AP-1 transcription factor subunit (JUN), and GLI family zinc finger 1 (GLI1), as well as progressive epigenetic locking. Recent single-cell multi-omics studies have further revealed that hypoxia and immunosuppressive pressure within the tumor microenvironment (TME) play pivotal roles in phenotypic plasticity through the selection of tumor adipocyte stem cells (tumor ASCs) with stem-like features. On the basis of this genome-epigenome-microenvironment coupling model, we discuss novel therapeutic strategies including induced redifferentiation, metabolic targeting, and microenvironment remodeling, thereby providing a theoretical foundation for interrupting the malignant progression of RPL. - Source: PubMed
Publication date: 2026/04/29
Zhuang AoboWang XuelingCheng YingxueZhang ChenheLiu HuajieLi RunchunWan YunyanZeng WeiWu TingLi Wengang - Testis-specific protease 50 (TSP50), a tumor-associated antigen with minimal expression in normal tissues, emerges as a promising therapeutic target. In this study, we report its aberrant overexpression and proliferation-promoting role in skin cutaneous melanoma (SKCM). Using a TSP50 promoter-driven luciferase reporter system, we identified etoposide-an FDA-approved topoisomerase II (TOP2) inhibitor-as a potent suppressor of TSP50 transcription. Etoposide can effectively reduces the activity of TSP50 promoter, thereby inhibiting its mRNA and protein expression. Functionally, etoposide markedly inhibits SKCM cells proliferation and triggers ferroptosis, with these effects mediated by TSP50 downregulation. In xenograft models, etoposide treatment significantly attenuated tumor growth with favorable safety profiles. Mechanistically, etoposide stabilizes p53 by weakening the MDM2-p53 interaction while enhancing MDM2-TOP2α binding. CUT&Tag and RT-qPCR revealed that p53 binds to a specific region (-200 to -249 bp) of TSP50 promotor, leading to transcriptional repression. Our findings delineate a novel TOP2α/MDM2/p53/TSP50 axis in SKCM and propose etoposide as a precision therapy for TSP50-overexpressing melanomas. - Source: PubMed
Publication date: 2026/04/28
Yang ShuoGao DenghuiLi MingyueZhang BoyuWei JinliangLi XiaoliLi JiaweiGao FengSun LuguoYu ChunleiZheng LihuaSong ZhenboYang XiaoguangBao YongliHuang Yanxin - Gastrodia elata Blume (G. elata) is a valuable traditional Chinese medicine (TCM) that has been widely used in China. We systematically reviewed tonic and life-extending records in ancient medical literature, as well as the life-prolonging and senescence-delaying effects identified in modern pharmacological research, to provide a theoretical basis for the clinical application and product development of G. elata in tonification and anti-aging. Scientific databases, including CNKI (Chinese literature) and PubMed, were searched to gather relevant literature on the anti-aging effects of G. elata. The targets of the main chemical components of G. elata were predicted and collected through a database, and the intersection of compound targets and disease targets was identified. Protein-protein interaction network analysis, Gene Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to explore the potential mechanisms underlying the anti-aging effects of G. elata. The record of G. elata demonstrates a definitive life-extending effect. Modern pharmacological studies have confirmed that it prolongs the lifespan of short-lived animals and slows the aging processes of the brain, skin, bone, and skeletal muscle in animals. Network pharmacology analysis identified 15 common targets shared between candidate target genes of G. elata and anti-aging target genes. TP53, ESR1, EP300, SIRT1, STAT3, CCND1, HDAC2, MDM2, PPARG, TNF, and HSP90AA1 were identified as core genes in the protein-protein interaction (PPI) network analysis. KEGG enrichment analysis indicated that the anti-aging mechanisms of G. elata may be associated with chemical receptor activation, insulin resistance, the citric acid cycle, the PPAR signaling pathway, the glucagon signaling pathway, and the thyroid hormone signaling pathway. This article summarizes previous studies and modern research on the anti-aging effects of G. elata, suggesting that it holds significant potential for clinical applications in anti-aging. - Source: PubMed
Publication date: 2026/04/20
Wang RuoyingXin ChenranLiu WencongCheng ZhiqiangZhu HongyanHan Jihong - Cytogenetics analysis of adipocytic tumours revealed varieties of chromosomal translocations beyond MDM2 amplification, so, this report aimed to identify these translocations and recognise the altered genes with their fusion partners. - Source: PubMed
Atta I SShafek S IAbdel-Hamid M