Ask about this productRelated genes to: UBE2S Blocking Peptide
- Gene:
- UBE2S NIH gene
- Name:
- ubiquitin conjugating enzyme E2 S
- Previous symbol:
- -
- Synonyms:
- E2-EPF
- Chromosome:
- 19q13.43
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-12
- Date modifiied:
- 2016-03-14
Related products to: UBE2S Blocking Peptide
Related articles to: UBE2S Blocking Peptide
- - Source: PubMed
Publication date: 2026/04/24
Yan XiaodongPan ShouqiangZhang JinMao KeleiYu RuihaoXiong YiduoHuang HaixiaZhang Yi - Lung adenocarcinoma (LUAD) is the predominant pathological subtype of non-small cell lung cancer. Its considerable tumor heterogeneity and drug resistance present major clinical obstacles, resulting in unfavorable patient outcomes. Protein palmitoylation is known to be a key factor in tumorigenesis; however, its cell-specific expression patterns and prognostic value in LUAD remain incompletely characterized. - Source: PubMed
Publication date: 2026/04/06
Liu HaixiaoHu YueWang LingyunLi ChanglinLi DongtaoMeng LinghanZheng GuangdaRen JuanxiaShang LuBao Yanju - The turnaround of the tumor suppressor p53 protein, the guardian of the genome, is closely regulated to ensure avoidance of its untimely activation, which could lead to the demise of normal cells. Cancer cells often display mutations in the gene encoding for p53, which interferes with its normal function. The genomic series of colorectal cancer from the Cancer Genome Atlas (TCGA) was interrogated to discover genomic alterations and determine the mRNA expression of enzymes affecting p53 ubiquitination in colorectal cancers with wild-type and mutant . Genomic alterations of p53-regulating E3 ubiquitin ligases were uncommon in colorectal cancers, the most frequent being mutations in . Several p53-regulating E3 ligases were well expressed in subsets of colorectal cancers, two of which, MDM2 and TRIM24, displayed higher mRNA expressions than the normal colorectal epithelia. The former was particularly upregulated in wild-type colorectal cancers, and the latter was upregulated in both wild-type and mutant cancers. Upregulation of TRIM24 in mutant cancers was observed independently of the type of mutations (gain-of-function or other). Among E3 ligases used in proteolysis-targeting chimeras (PROTACs), VHL was upregulated together with its E2-conjugating enzyme UBE2S in colorectal cancers. This survey of p53-targeting ubiquitin ligases provides a roadmap for potential therapeutic strategies working by promoting the destruction of the mutant protein or reactivating its normal function in -mutated colorectal cancers and promoting p53 function by preventing degradation in wild-type cancers. - Source: PubMed
Publication date: 2026/02/26
Voutsadakis Ioannis A - Triple-negative breast cancer (TNBC), particularly the androgen receptor-low (AR-low) subtype, is one of the most aggressive and hard-to-treat forms of BC, characterized by a high index of proliferation, chromosomal instability (CIN), and high prevalence of TP53 mutations. These features fuel therapy resistance, metastases, and poor clinical outcomes. An integrated framework describing the dysregulated molecular networks that support the pathobiology of AR-low TNBC is lacking. Multiple published studies in breast cancer have previously proposed mechanistic links between TP53 loss, AR-low states, and heightened FOXM1-driven G2/M transcriptional programs, potentially via deregulation of E2F activity, chromatin-associated co-regulators (e.g., ATAD2), and disruption of repressive networks involving p53-p21-DREAM and SPDEF. Additional reports suggest that FOXM1-associated circuitry may be reinforced by chromatin regulators such as WDR5 and by mitotic/spindle factors such as ASPM, including through feedback interactions and condensate-associated transcriptional organization. We previously showed that FOXM1, a master regulator transcription factor, is upregulated and is a biomarker of poor prognosis in AR-low TNBC. In this study, we filtered a set of "TNBC core genes" known to promote transcriptional chaos downstream of FoxM1. We identified a set of 15 cell cycle regulators-including mitotic kinesin motors (KIF14, KIF11, KIF4A, KIF2C, and KIF20A), centromeric proteins (CENPA, CENPO, CENPL, CENPF, and OIP5), and regulators of proteolysis (UBE2C, UBE2S, UBE2T, PSMD14, and TUBA1B). These 15 genes, which were ranked highly among genes overexpressed in TNBC featured prominently in gene signatures of chromosomal instability and were also overexpressed among AR-low TNBCs and TP53-mutant breast tumors. We show that expression of each of these 15 genes correlates positively with proliferation markers (Ki67, PCNA, and MCM2) in TNBC, and that the overexpression of this gene set is associated with shorter relapse-free survival and distinct immune/stromal infiltration patterns. In light of prior work, our findings point to a FOXM1-associated 15-gene signature enriched in AR-low TNBC and associated with the high-proliferation and high-CIN phenotypes of this clinically challenging tumor type. This 15-gene set represents an actionable vulnerability with therapeutic potential for AR-low TNBC and provides a framework for rethinking how to manage highly proliferative, genomically unstable BCs. - Source: PubMed
Publication date: 2026/02/14
Rida PadmashreeAndreae RaphaelBikhazi NoahJackson BeneciaWang IvanJinna Nikita - The prognostic heterogeneity of esophageal squamous cell carcinoma (ESCC) necessitates robust biomarkers. Although hypoxia-inducible factor 1 (HIF1) is implicated in ESCC progression, its interplay with ubiquitin-conjugating enzyme E2S (UBE2S) remains uncharacterized. - Source: PubMed
Publication date: 2026/01/28
Ma MingfuLi MengyanLv YuanyuanZhang YahaoPang XuelianMa Yuqing