Ask about this productRelated genes to: TPD52 Blocking Peptide
- 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 Blocking Peptide
Related articles to: TPD52 Blocking Peptide
- Venetoclax (VEN) resistance remains a major obstacle to durable responses in acute myeloid leukemia (AML). Although the core circadian regulator brain and muscle ARNT-like protein 1 (BMAL1) has been implicated in AML progression and drug response, its role in acquired VEN resistance remains unclear. In this study, VEN-resistant R-THP1 and R-MOLM13 cells were established, and the role of BMAL1 was evaluated using public datasets, clinical samples, cell experiments, and in vivo xenograft models. BMAL1 was upregulated in relapsed/refractory AML samples and VEN-resistant cells, and high BMAL1 expression was associated with adverse clinical outcomes. BMAL1 knockdown increased VEN sensitivity, promoted apoptosis, and reduced proliferation and clonogenic capacity in resistant cells, whereas BMAL1 overexpression produced the opposite effects in parental cells. Consistently, BMAL1 depletion reduced leukemia burden and enhanced the response to VEN in vivo. Integrated transcriptomic and proteomic analyses identified tumor protein D52 (TPD52) as a downstream candidate associated with BMAL1-mediated VEN resistance. TPD52 was upregulated in resistant AML cells, and its genetic modulation recapitulated the effects of BMAL1 on VEN sensitivity and malignant phenotypes of AML. Co-immunoprecipitation supported an association between BMAL1 and TPD52, while cycloheximide chase assays showed that BMAL1 enhanced TPD52 protein stability. Modulation of BMAL1 or TPD52 also altered p-PI3K and p-AKT without markedly affecting on total PI3K or AKT expression. In conclusion, these findings indicate that BMAL1 contributes to acquired VEN resistance by interacting with and stabilizing TPD52, accompanied by PI3K/AKT activation. BMAL1-TPD52 axis maybe a novel therapeutic target to overcome VEN resistance in AML. - Source: PubMed
Publication date: 2026/09/11
Li SongyangYang YongjieLiu DongmeiHuang MeixiaLi JiayaoDu YinxiaoQin ZifeiLiu XiaomeiHuang NingYang Jing - Tumor protein D52 (TPD52) family proteins are involved in the proliferation, survival and malignant progression of oral squamous cell carcinoma (OSCC). However, their roles in chemoresistance remain incompletely understood. The present study investigated the contribution of TPD52 family proteins to anticancer drug resistance, with particular emphasis on tumor protein D54 (TPD54). OSCC cells were treated with cisplatin, 5‑fluorouracil, or docetaxel (DTX), and the expression of TPD52 family members was examined. Gain‑ and loss‑of‑function analyses were performed to evaluate cell viability, apoptotic responses, cytochrome p450 (P450) and P‑glycoprotein (P‑gp) activities, protein expression, intracellular localization and membrane/cytosol distribution. Anticancer drug treatment increased the expression of TPD52, TPD53 and TPD54. Among these family members, TPD54 showed the strongest association with DTX resistance by attenuating the reduction in cell viability without affecting cell‑cycle progression. TPD54 overexpression attenuated DTX‑associated apoptotic responses and was associated with changes in apoptosis‑, ferroptosis‑, and autophagy‑related marker proteins. TPD54 expression had little effect on the activities of P450 3A4 or P450 1B1 but significantly increased P‑gp activity. Membrane/cytosol fractionation demonstrated increased membrane localization of endogenous P‑gp following TPD54 overexpression, whereas co‑immunoprecipitation and immunocytofluorescence analyses revealed an association and partial co‑localization between TPD54 and P‑gp. These findings suggest that TPD54 contributes to DTX resistance in OSCC cells through modulation of P‑gp localization and activity. The present study identifies TPD54 as a potential contributor to P‑gp‑associated chemoresistance and provides a basis for further investigation of the molecular mechanisms underlying multidrug resistance in OSCC. - Source: PubMed
Publication date: 2026/07/24
Nara MakiMukudai YoshikiWatanabe MasatakaKindaichi NodokaYamada KonomiAbe YuzoShimane ToshikazuShirota TatsuoOhba Seigo - 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
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