HBUCE1 Antibody
- Known as:
- HBUCE1 Antibody
- Catalog number:
- XW-8020
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- HBUCE1 Antibody
Related genes to: HBUCE1 Antibody
- Gene:
- UBE2D4 NIH gene
- Name:
- ubiquitin conjugating enzyme E2 D4 (putative)
- Previous symbol:
- -
- Synonyms:
- HBUCE1
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-02
- Date modifiied:
- 2017-05-22
Related products to: HBUCE1 Antibody
Related articles to: HBUCE1 Antibody
- Osteosarcoma (OS), the most prevalent primary malignant bone tumor with a dismal prognosis, exhibits significant heterogeneity in programmed cell death (PCD) pathways, but its subtype-specific functional mechanisms remain poorly characterized. This study integrated PCD-related gene signatures to delineate molecular subtypes in OS via consensus clustering, successfully defining four distinct subtypes with divergent prognostic outcomes and immune microenvironments. Differential expression, functional enrichment, and protein-protein interaction (PPI) network analyses revealed subtype-specific PCD pathway associations (e.g., lysosome-dependent cell death, apoptosis, pyroptosis and anoikis), while comparative immune profiling and clinical characterization further refined subgroup identities. A robust prognostic risk model incorporating five pivotal genes (, , , , and ) and metastasis status demonstrated superior predictive performance in both training and external validation cohorts. These findings not only elucidate the functional architecture of PCD across OS molecular subtypes but also establish a clinically actionable model for precision risk stratification and tailored therapeutic strategies. - Source: PubMed
Publication date: 2026/04/11
Zou XinyiRu Yuanfang - The UBE2D family plays essential roles in protein degradation and cell cycle regulation and has been implicated in cancer. However, the specific function of UBE2D4 in glioma and its clinical and biological significance remain unclear. This study aimed to investigate the expression pattern, regulatory mechanism, and functional role of UBE2D4 in glioma progression. - Source: PubMed
Publication date: 2026/02/17
Liu DianZhang KeqinXiao XiangLiu JieYou Jia - Cadmium (Cd) is a toxic environmental heavy metal that exerts harmful effects on multiple tissues, including the kidney, liver, lung, and bone, and is also associated with the development of anemia. However, the precise molecular mechanisms underlying Cd-induced toxicity remain incompletely understood. In this paper, we review the recent molecular mechanisms of Cd-induced toxicity and its modification, with a particular emphasis on our recent findings. Using a combination of DNA microarray analysis, protein-DNA binding assays, and siRNA-mediated gene silencing, we identified several transcription factors, YY1, FOXF1, ARNT, and MEF2A, as novel molecular targets of Cd. The downregulation of their downstream genes, including , , , and , was directly associated with the expression of cytotoxicity. In addition, PPARδ plays a pivotal role in modulating cellular susceptibility to Cd-induced renal toxicity, potentially by regulating apoptosis-related signaling pathways. In addition to apoptosis pathways, Cd toxicity through ROS generation, ferroptosis and pyroptosis were summarized. Furthermore, it has been revealed that Cd suppresses the expression of iron transport-related genes in duodenal epithelial cells leading to impaired intestinal iron absorption as well as decreased hepatic iron levels. These findings provide a mechanistic basis for Cd-induced iron deficiency anemia, implicating disrupted iron homeostasis as a contributing factor. - Source: PubMed
Publication date: 2025/08/04
Lee Jin-YongTokumoto MakiSatoh Masahiko - Acrylamide (ACR) is a by-product of the Maillard reaction, which occurs when food reacts at high temperatures. Occupational exposure is a risk factor for chronic ACR toxicity. ACR may cause neurotoxicity and depressive symptoms with high concentration in the blood; however, the underlying mechanism remains unknown. We showed the rats developed neurotoxic symptoms after being fed with ACR for 28 days, such as reduced activity and hind limb muscle weakness. We investigated whether ACR exposure causes gene expression differences by blood RNA sequencing and analyzed the differential expression of depressive symptoms-associated genes. The result indicated that IFN-γ the key regulator of neurotoxicity and depressive symptoms was induced by ACR. ACR induced the ubiquitin-mediated proteolysis pathway and JAK/STAT pathways gene expression. ACR upregulated the expression of IFN-γ, inducing neuroinflammation and neurotoxicity. ACR also upregulated the expression of JAK2, STAT1, PI3K, AKT, IκBα, UBE2D4, NF-κB, TNF-α, and iNOS in rat brain tissues and Neuro-2a cells. Thus, IFN-γ induction by ACR may induce depressive symptoms, and the ubiquitin-mediated proteolysis pathway and JAK/STAT pathways may involve in ACR neurotoxicity and depressive symptoms. - Source: PubMed
Publication date: 2023/12/28
Chen Yng-TayLin Tzu-JungHung Chia-Yu - Cuproptosis induction is seen as a promising alternative for immunotherapies and targeted therapies in breast cancer. The objective of this research was to examine the prognostic and biological importance of cuproptosis-related genes (CRGs) in lung adenocarcinoma (LUAD). - Source: PubMed
Publication date: 2023/10/22
Liu TingtingWei Jianshe