VPS72 antibody - N-terminal region (ARP33348_P050)
- Known as:
- VPS72 (anti-) - N-terminal region (ARP33348_P050)
- Catalog number:
- arp33348_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- VPS72 antibody - N-terminal region (ARP33348_P050)
Related genes to: VPS72 antibody - N-terminal region (ARP33348_P050)
- Gene:
- VPS72 NIH gene
- Name:
- vacuolar protein sorting 72 homolog
- Previous symbol:
- TCFL1
- Synonyms:
- YL-1, YL1, Swc2
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-08
- Date modifiied:
- 2016-10-05
Related products to: VPS72 antibody - N-terminal region (ARP33348_P050)
Related articles to: VPS72 antibody - N-terminal region (ARP33348_P050)
- Recently, a high-frequency gain of the human-specific NOTCH2NL gene was found in anaplastic thyroid cancer, yet its amplification status in other cancers is still unknown. In our study, we discovered that NOTCH2NLA, a paralog of the NOTCH2NL gene, exhibited a recurrent genetic alteration (101/1071) in breast cancer (BRCA), with amplification being the primary alteration type (100/1071). Furthermore, BRCA patients with NOTCH2NLA amplification had a significantly worse prognosis in terms of disease-specific survival (DSS), disease-free interval (DFI), and progression-free interval (PFI). Weight correlation network analysis (WGCNA) showed that PRCC and VPS72 genes were the hub genes in co-expression network of NOTCH2NLA amplification in the BRCA cohort. Moreover, Gene Set Enrichment Analysis (GSEA) indicated that NOTCH2NLA amplification was involved in the regulation of multiple signaling pathways such as cell cycle, ribosome biogenesis, and the Notch signaling pathway. Finally, we found that cell cycle inhibitors such as Flavopirdol, AT-7519, and PHA-793,887 were more sensitive for cells with NOTCH2NLA amplification, whereas MEK inhibitors were just on the contrary. In vitro experiments demonstrated that overexpression of NOTCH2NLA in breast cancer cells promoted cell growth and enhanced sensitivity to AT-7519 treatment. Collectively, our findings suggest that NOTCH2NLA amplification may be a new prognostic marker of BRCA and cell cycle inhibitors were more suitable for therapy on BRCA patients with NOTCH2NLA amplification. - Source: PubMed
Publication date: 2026/05/21
Wang YuchuanSang YeDou QianyiChen MengkeTang QinLin BoHu Guanghui - To develop and validate a demethylation-driven gene signature for predicting HCC prognosis, immune microenvironment features, and therapeutic vulnerabilities. We integrated transcriptomic data from TCGA-LIHC (n = 346 tumors) and GEO-GSE112790 (n = 183 tumors) with a curated list of 3,743 demethylation-related genes (DRGs). Tumor-associated DRGs were identified via differential expression analysis and WGCNA. A prognostic six-gene signature was derived using univariate Cox and LASSO regression, and a risk score model was constructed by multivariate Cox analysis. Patients were stratified into high- and low-risk groups. Model performance was evaluated using Kaplan-Meier and time-dependent ROC analyses. Immune infiltration was assessed by ssGSEA, somatic mutations were profiled, and drug sensitivity was predicted via the GDSC database. G6PD expression was validated using immunohistochemistry. A six-gene prognostic signature (CEP41, SUB1, CDC20, G6PD, VPS72, SPINDOC) was established. The risk score significantly stratified patients into high- and low-risk groups with distinct overall survival (p < 0.001). The model showed strong predictive accuracy with AUCs ≥ 0.70 at 1, 3, and 5 years. High-risk patients exhibited enrichment in cell cycle, DNA repair, and metabolic pathways, along with an immunosuppressive microenvironment marked by regulatory T cells and myeloid-derived suppressor cells. Somatic mutation analysis revealed differential TP53 mutation frequencies between risk groups. Drug sensitivity prediction indicated that high-risk patients may respond better to agents such as Tozasertib and Navitoclax. IHC confirmed significant upregulation of G6PD in HCC tissues, supporting its role in metabolic reprogramming. This study establishes a robust, demethylation-driven six-gene signature that effectively stratifies HCC patients into distinct prognostic groups. The model integrates multi-omic insights into tumor biology and therapeutic vulnerability, providing a clinically actionable framework for personalized risk assessment and treatment planning in hepatocellular carcinoma. - Source: PubMed
Publication date: 2026/02/26
Wang ZhengweiShi LeiLi YongjianLiu SikaiShi Wanyin - Rhesus macaques (Macaca mulatta) are the most common non-human primates living in captivity. The use of rhesus macaques as model objects is determined, first of all, by their phylogenetic and physiological closeness to humans, and, as a consequence, the possibility of extrapolating the obtained results to humans. Currently, it is known that a number of biochemical changes occur under various physiological conditions, including at the transcriptomic level. The real-time polymerase chain reaction is a widely used universal method for gene expression analysis. Carrying out such studies always requires a preliminary selection of "housekeeping genes" (HKGs) - genes necessary for the implementation of basic functions in the cell and stably expressed in different cell types and under different conditions. At present, there are only two systematic studies on the search for HKGs in the rhesus macaque brain, and therefore in this work a search and systematization of HKGs for this species were carried out. As a result, two panels of promising HKGs for M. mulatta were formed: an extended panel, consisting of 56 genes, and a small panel, consisting of 8 genes: ARHGDIA, CYB5R1, NDUFA7, RRAGA, TTC1, UBA6, VPS72, and YWHAH. Both panels of potential HKGs do not have pseudogenes in macaques or humans, are characterized by stable and sufficient expression in the brain of rhesus macaques and can be used to analyze expression not only in the brain but also in peripheral blood. However, it should be noted that the data have not been experimentally verified and require verification in laboratory conditions. - Source: PubMed
Shulskaya M VAlieva A KhKumakov I RShadrina M ISlominsky P A - The histone variant H2A.Z resides within active gene promoters, but how it influences chromatin state and nucleosome stability remains poorly understood. Here, we probe two H2A.Z binding proteins with seemingly opposing function: VPS72, an SRCAP subunit that aids in H2A.Z deposition, and ANP32E, a histone chaperone which is thought to remove H2A.Z. Using functional genomics and biochemical assays, we show that VPS72 and ANP32E co-occupy active promoters yet function antagonistically. VPS72 promotes H2A.Z incorporation, acetylation, BRG1 recruitment, and transcription, whereas ANP32E constrains these features by stabilizing nucleosomes. Loss of ANP32E increases VPS72 binding, chromatin accessibility, and transcription, while co-depletion of VPS72 reverses these effects. Reconstitution assays show that ANP32E promotes nucleosome assembly and prevents DNA unwrapping, providing a mechanistic basis for function. Our results support a model where promoter accessibility arises from antagonistic and cooperative actions, revealing a general paradigm in which counterbalancing factors govern gene regulatory potential. - Source: PubMed
Publication date: 2026/01/30
Murphy PatrickHua ShanReger NoahSokolova VladyslavaHuang KaiLiehHaseley MaryClaireParker MystieCasler KarliTan DongyanWagner Eric - VPS72, primarily located in the nucleus, may play a role in hepatocellular carcinoma (HCC) progression. More research is required to assess if VPS72 mRNA or protein levels, along with clinical parameters, can diagnose or predict HCC and affect its progression through immune cell infiltration regulation. - Source: PubMed
Publication date: 2026/01/24
Huang ManxianWan XiaobingWu JuanChen HongSun ChangliZhang LimingLiu Min