Ask about this productRelated genes to: VPS28 protein
- Gene:
- VPS28 NIH gene
- Name:
- VPS28 subunit of ESCRT-I
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-13
- Date modifiied:
- 2019-01-31
Related products to: VPS28 protein
Related articles to: VPS28 protein
- Breast cancer (BC) is a highly heterogeneous malignancy and remains the leading cause of cancer-related mortality among women worldwide. Although advances in molecular classification and targeted therapies have improved outcomes for certain subtypes, robust prognostic biomarkers applicable across clinical contexts are still lacking. The CRISPR-Cas9 system offers a powerful platform for identifying cancer cell vulnerabilities and may facilitate the development of clinically relevant prognostic models. - Source: PubMed
Publication date: 2026/05/14
Xiao Wen-TaoHe Jun-YanYang DongXun Yi - During open mitosis, reassembly of the nuclear envelope requires the coordinated recruitment of the ESCRT machinery, initiated by the chromatin-associated factor BAF1 and the nuclear-envelope-associated factor LEM2. Because telomeres are enriched at the reforming envelope, we investigated whether ESCRT factors contribute to telomere integrity. Reduction in the pivotal nuclear ESCRT factor CHMP7 caused DNA damage, heterochromatin disorganization, and telomere defects, including sister telomere associations and telomere free ends. Extending this analysis, we found that additional ESCRT components, including TSG101, VPS28, CHMP4B, and the ESCRT-associated factor AKTIP/Ft1, also contribute to telomere integrity, although with different strengths. Genetic interaction analyses suggest that CHMP7 converges in a common pathway with CHMP4B and AKTIP/Ft1, while it functions in parallel routes to TNKS1, a telomere-specific regulator of the shelterin TRF1. More genetic analyses indicated that BAF1 and LEM2 contribute to safeguarding of telomeres during nuclear envelope reassembly. Because defects in nuclear envelope dynamics and chromatin-membrane coupling are hallmarks of disorders associated with nuclear deformation and fragility, including aging and cancer, our findings contribute a new angle into these conditions and suggest potential targets for selectively modulating telomere maintenance pathways. - Source: PubMed
Publication date: 2026/01/29
Burla RominaLa Torre MattiaMaccaroni KliziaTacconi StefanoDini LucianaSaggio Isabella - Alzheimer's disease (AD) is a global health event with progressive cognitive decline affecting millions of elderly people worldwide. Emerging evidence indicates that sevoflurane may be associated with AD progression. However, the underlying mechanism remains poorly understood. Herein, we explored the potential role of sevoflurane exposure in cognitive ability and the possible mechanisms of action in the early stage of Tg4510 (P301L tau) transgenic mice. - Source: PubMed
He KaiwuZhang ZhijingLi YouzhiXiong WeiXing YanmeiGao WenliKong WeiChen LixinYang XifeiDai Zhongliang - Leishmania donovani (Ld) is the causative agent of visceral leishmaniasis, which results in death if not treated. In mammalian cells, Ld live in vacuolar compartments called Leishmania parasitophorous vacuoles (LdLPVs) that enigmatically divide following parasite replication. We evaluated the role of the endosomal sorting complex required for transport (ESCRT) machinery in the scission of LdLPVs. We found that ESCRT components are constitutively recruited to LdLPVs. We propose that this recruitment depends on the expression of PI(3,4)P2 on LdLPVs. The knockdown (KD) of upstream components of the ESCRT machinery revealed that ALIX, but not TSG101 or VPS28, led to a significant reduction in the parasite burden in infected cultures. Interestingly, LdLPVs in ALIXKDs were more distended and harbored more than 2 parasites. Incorporation of BrdU into Leishmania in THP-1 macrophages revealed that parasite replication was inhibited in ALIXKD due to defective LdLPV scission. These findings establish that non-canonical activation of the ESCRT machinery is required for Leishmania to replicate within macrophages. - Source: PubMed
Publication date: 2025/09/16
Rosero JavierKima Peter E - Cushing's disease is a rare endocrine disorder characterized by excessive endogenous glucocorticoid production, primarily resulting from adrenocorticotropic hormone-secreting pituitary neuroendocrine tumors (ACTH-PitNETs). This study investigated the expression of several genes implicated in the development of ACTH-PitNETs, including EGFR, USP8, CABLES1, USP2, STAM2, VPS28, HDAC2, IL-6, SMARCA4, WEE1, CDKN2A, CCND1, NR4A1, NEUROD1, and RIPK1. The methylation levels of the USP8 and CDKN2A genes were also assessed for insights into their regulatory mechanisms.Formalin-fixed paraffin-embedded pituitary tumor tissue samples from 32 patients diagnosed with ACTH-PitNET and 15 anterior pituitary tissue samples were analyzed. Gene expression was analyzed through quantitative reverse transcription polymerase chain reaction, while methylation was examined through methylation-specific polymerase chain reaction. All data were analyzed with IBM SPSS Statistics 21. The relationships among gene expressions were assessed using principal component analysis.The expression of CABLES1, NR4A1, CCND1, NEUROD1, USP2, and WEE1 differed significantly between the patient and control groups. Additionally, significant correlations were observed between the levels of RIPK1, SMARCA4, and USP2 and pre-operative cortisol levels; WEE1 expression and pre-operative ACTH levels; CDKN2A expression and urinary cortisol levels; CABLES1, NEUROD1, SMARCA4, and STAM2 expression and post-operative cortisol levels at 48 h. CCND1 expression was correlated with adenoma size, while WEE1 expression was linked to remission status. Notably, the CDKN2A gene displayed partial methylation, whereas the USP8 gene was fully unmethylated.The altered expression levels of the USP2, CABLES1, CDKN2A, and WEE1 may be closely associated with the development of ACTH-PitNETs. Notably, WEE1 emerged as a target gene for predicting clinical remission in patients with Cushing's disease. - Source: PubMed
Publication date: 2025/07/30
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