Ask about this productRelated genes to: TPD52 antibody
- Gene:
- TPD52 NIH gene
- Name:
- tumor protein D52
- Previous symbol:
- -
- Synonyms:
- D52, hD52, N8L
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-30
- Date modifiied:
- 2015-08-26
Related products to: TPD52 antibody
Related articles to: TPD52 antibody
- Aldosterone-producing adenomas (APA) are a major cause of primary aldosteronism. While gene mutations in APA trigger aldosterone overproduction via calcium signaling, their precise regulatory mechanisms remain unclear. Our prior proteomic analysis identified significant upregulation of tumor protein D52 (TPD52), an oncogene protein implicated in cancer progression, in APA. This study investigates the role of TPD52 in regulating aldosterone synthesis and its molecular mechanism. - Source: PubMed
Publication date: 2026/05/01
Xie LingMa LinqiangKang BingChen ZhihaoQi ShuangxinDu ManmanLi JiayuLi JunlongHe YifanXu YongHuang WeiGao RufeiHu JinboYang ShuminLi QifuPeng Chuan - Lynch syndrome, historically known as hereditary nonpolyposis colorectal cancer, is caused by germline mutations in the DNA mismatch repair (MMR) genes, , and . While the genetic changes associated with Lynch Syndrome have previously been characterized, there have not been studies of the associated proteomic alterations, in part because of the limited availability of primary samples and the absence of model systems. In this study, the first large-scale tissue proteomic assessment of Lynch Syndrome samples as well as three other subtypes of colorectal cancer was completed with specimens from the Ohio Colorectal Cancer Prevention Initiative. The cohort contained three groups of microsatellite unstable (MSI-high) CRC patients (Lynch syndrome, double somatic MMR mutation, and MLH1 hypermethylation) and a group of microsatellite stable (MSS) CRC patients. A total of 122 tumor and complimentary normal mucosa samples from 61 patients were evaluated using label-free bottom-up proteomic analysis. Hierarchical clustering analysis of the global proteome showed that the MSS group was significantly different than the three MSI-high groups. Of the 1,084 proteins found to be dysregulated across all four colorectal cancer subtypes, there were age at diagnosis associated shifts in proteins correlated with tumor proliferation and immune regulation for the Lynch syndrome and Double Somatic samples. The proteins TPD52, GMDS, and DSP showed increased protein abundance correlated with older age at diagnosis. In addition, the Lynch syndrome samples showed substantial sex-based differences in immune and inflammatory pathways, for example, downregulation of ZG16, DIS3, and WDR43. This study fills a critical gap as the first proteomic characterization of Lynch syndrome samples to date. Data are available via ProteomeXchange with identifier PXD073693. - Source: PubMed
Publication date: 2026/01/29
Tobias FernandoSekera Emily RXiong XingzhaoFang FeiHampel HeatherPearlman RachelLiu XiaowenSun LiangliangHummon Amanda B - Age-related macular degeneration (AMD), particularly its non-neovascular (dry) form, is a progressive retinal disorder that causes central vision loss and substantial impairment in daily life. Inflammation and immune dysregulation are recognized as core drivers of AMD, yet the contribution of PANoptosis, a form of programmed cell death that integrates pyroptosis, apoptosis, and necroptosis, remains unclear. In this study, we integrated human single-cell transcriptomic and bulk microarray datasets from the retina and retinal pigment epithelium-choroid to characterize PANoptosis-related transcriptional changes in dry AMD. Dimensionality reduction, cell-type annotation, and PANoptosis gene-set scoring revealed a distinct PANoptosis signature enriched in AMD, with particularly strong activation in myeloid populations. By combining differential expression analysis with machine learning-based feature selection, we identified four PANoptosis-related genes (PON2, BNIP3, EPHB6, and TPD52) that robustly distinguished AMD from control samples and were associated with an altered immune microenvironment. Genetic instrument analysis further suggested a positive association between TPD52 expression and AMD risk. At the cellular level, our data highlighted macrophages, especially pro-inflammatory M1-like macrophages, as key coordinators of PANoptosis-related pathways in dry AMD. To validate these findings in vivo, we used a sodium iodate-induced mouse model of dry AMD and observed significant dysregulation of PON2, BNIP3, EPHB6, and TPD52 in the retina by RT-qPCR, consistent with the human transcriptomic results and supporting their involvement in retinal degeneration and inflammation. Together, these findings implicate PANoptosis as an important and previously underappreciated component of dry AMD pathophysiology, define a four-gene PANoptosis-related signature with diagnostic potential, and suggest new molecular targets for therapeutic intervention. - Source: PubMed
Publication date: 2026/02/13
Li JiamingMa YirongHu MiaoZhang QianWang AnqiTang QiuyuGuo QinshangHuang Binglin - There is growing evidence that dysregulation of vesicle-mediated intracellular trafficking pathways leads to the development of various diseases, including cancer. Cancer exploits the intracellular trafficking pathways to modulate the protein flow, alter cell surface protein expression, and drive the hallmarks of cancer progression, such as sustained proliferation signaling and evading immune surveillance. As such, there is increasing interest in understanding the proteins that regulate these processes to better understand cancer biology and to identify novel ways to hinder disease progression. A group of small proteins, known as the Tumor Protein D52 (TPD52)-like family, has been identified and is increasingly recognized for its roles in intracellular trafficking within cancer cells. This family consists of four members: TPD52, TPD53, TPD54, and TPD55. Herein, we review the current literature on the TPD52-like family in cancer and detail the current known cellular functions (e.g., intracellular trafficking roles, lipid biogenesis, cell proliferation, and cell cycle regulation). Overexpression of family members, notably TPD52 and TPD54, has been heavily implicated in tumorigenic roles such as cell migration, invasion, proliferation, and protein-protein interactions. Additionally, there is mounting evidence that this family also has isoform-specific and/or tissue-specific functions, which is of clinical interest. A better understanding of the mechanistic actions of this protein family holds the promise of identifying novel therapeutic targets that exploit the broader multi-target nature of intracellular trafficking regulators to disrupt oncogenic processes. - Source: PubMed
Publication date: 2026/01/28
Dorward Emma LOrtiz MichaelWeekley Claire MMyo Min Kay KDuijf Pascal H GBarreto S GeorgeParker Michael WBonder Claudine S - Myasthenia gravis (MG) is a chronic autoimmune neuromuscular junction disorder mediated by autoantibodies. Existing diagnostic methods mainly rely on serum antibody detection and electrophysiological testing, which are limited by invasiveness and suboptimal sensitivity and specificity. This study aimed to identify potential urinary biomarkers for noninvasive MG diagnosis using proteomics. - Source: PubMed
Publication date: 2026/01/09
Yang JingYang XiZhu Zhen-KunShen LiangSan Shi-GeXiao LianchenYe FanWang Chun-HuaMeng Kun