ABHD7 Blocking Peptide
- Known as:
- ABHD7 Blocking Peptide
- Catalog number:
- 33r-3705
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- ABHD7 Blocking Peptide
Related genes to: ABHD7 Blocking Peptide
- Gene:
- EPHX4 NIH gene
- Name:
- epoxide hydrolase 4
- Previous symbol:
- ABHD7
- Synonyms:
- EPHXRP, FLJ90341, EH4
- Chromosome:
- 1p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-08
- Date modifiied:
- 2019-02-20
Related products to: ABHD7 Blocking Peptide
Related articles to: ABHD7 Blocking Peptide
- Epoxide hydrolases (EHs) constitute a conserved enzyme family that catalyzes the hydrolysis of epoxides into less reactive diols. Beyond their canonical roles in xenobiotic detoxification, EHs have emerged as critical regulators of lipid metabolism, redox balance, and inflammatory signaling. Accumulating evidence implicates EH family members, particularly Ephx1 (microsomal EH) and Ephx2 (soluble EH), in cardiovascular diseases, cancer, neurodegeneration, metabolic disorders, and other pathological conditions. More recently, studies have uncovered specialized functions of Ephx3 and Ephx4, broadening our understanding of EH biology and highlighting their tissue-specific roles in skin homeostasis and lipid signaling. Here, we systematically review the structural features, catalytic mechanisms, and physiological functions of EHs, with an emphasis on their regulatory networks in human diseases. We further discuss advances in genetic, epigenetic, and translational studies that connect EHs to disease susceptibility and progression. Finally, we evaluate the therapeutic potential and challenges of targeting EHs, particularly soluble EH inhibitors, and propose future research directions to bridge basic discoveries with clinical translation. This review aims to provide a comprehensive framework for understanding the multifaceted roles of EHs and to inspire novel strategies for precision medicine. - Source: PubMed
Publication date: 2026/04/28
Tan YadanXu JingjingHuang ZitengWang XiranXing JinshanLi ShengbiaoYi Jingyan - Valine to glutamate substitution at residue 600 of the BRAF oncogene (V600EBRAF mutation) is prevalent in human colorectal cancers with a serrated histopathology and is thought to be a founder mutation. Using a conditional knock-in mouse model we have previously demonstrated that V600EBraf drives crypt hyperplasia in the short term as well as shortened survival linked to increased tumour burden in the long-term. These phenotypes are associated with induction of gene signatures for E2F targets, MYC signalling, G2/M transition, canonical Wnt signalling, and cholesterol biosynthesis. Although these gene signatures are reverted by MEK inhibition, there remains a lack of understanding of the signalling pathways involved, particularly the mechanism of crosstalk between the MAPK and Wnt pathways. Here, we have examined a role for phosphorylation of GSK3αβ isoforms at residues S21/S9. By introducing homozygous knock-in mutations for Gsk3αβS9A/S21A onto the V600EBraf background, we unexpectedly show a marginal effect of these mutations on further increasing crypt proliferation. However, this impact is lost in the long-term as there are no significant differences in mouse survival, tumour burden or tumour grade. Consistently, the Gsk3αβ knock-in mutations do not change the transcriptional programme induced by V600EBraf, except for 3 genes (Ephx4, Eif2b3 Ppp1r13l) whose expression is significantly altered, potentially contributing to the short-term increase in crypt hyperplasia. Overall, our data show that therapeutic strategies targeting GSK3αβ phosphorylation at serines 21/9 are not worthwhile options for V600EBRAF colorectal cancers. - Source: PubMed
Publication date: 2026/03/06
Farahmand PooyehRzasa PaulinaGreen CalebHey FionaGiblett SusanJin HongWest KevinSylvius Nicolas BPritchard Catrin ARufini Alessandro - Colorectal Cancer (CRC) exhibits persistently high incidence and mortality rates worldwide, imposing a substantial socioeconomic burden. Early screening, early diagnosis, and early treatment can significantly improve patients’ survival rates while reducing mortality. However, there remains a lack of effective biomarkers to aid in early screening and diagnosis. As a branch of artificial intelligence, machine learning can automatically analyze large volumes of data, greatly saving human time and resources. The advancement of high-throughput sequencing technology has provided researchers with abundant gene expression data, offering rich data resources for the training and validation of machine learning models. With the development of artificial intelligence, integrating knowledge from bioinformatics, machine learning, molecular biology, and clinical medicine for analysis enables a more comprehensive understanding and exploration of the molecular biological mechanisms underlying CRC. In summary, this project aims to utilize machine learning techniques to screen five CRC signature genes (ABCG2, SCGN, USP2, CLDN1, and EPHX4) from GEO datasets, validate these signature genes using TCGA database, and perform RT-qPCR to detect the relative mRNA expression levels of these genes in CRC. Ultimately, this study seeks to provide novel biomolecular markers for the early diagnosis of CRC. - Source: PubMed
Publication date: 2026/02/22
Chang YuBai MangmangLiu YuBai KaiHu Yunfeng - Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality, necessitating the identification of novel biomarkers for improved prognosis and diagnosis. This study investigates the role of epoxide hydrolase 4 (), a member of the epoxide hydrolase family, in LUAD. Using data sourced from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases, which were subsequently validated by the Gene Expression Omnibus (GEO), we analyzed levels of expression, mutation, and methylation in tumors versus normal tissues. Our findings revealed a significant upregulation of in LUAD tissues compared to normal lung tissues ( < 0.001), correlating with poorer overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI). Furthermore, exhibited considerable diagnostic potential, as demonstrated by an area under the curve (AUC) of 0.854 in a Receiver Operating Characteristic (ROC) analysis. Notably, expression was associated with immune infiltration, specifically Th2 cells, neutrophils, and macrophages, along with immune checkpoint molecules including PD-L1, PD-L2, and TIM-3. Additionally, was involved in pivotal tumor-associated pathways, particularly cell cycle regulation. In conclusion, an elevated expression is indicative of poorer prognosis in LUAD and may play a role in immune evasion and cell cycle dysregulation, highlighting its potential as a promising biomarker for the diagnosis and prognostic prediction of LUAD. - Source: PubMed
Publication date: 2025/05/26
Liu PengzeChen Yutong - Epoxide hydrolase-4 (EPHX4) belongs to the epoxide hydrolase enzyme family, but its biological function remains unclear, especially its potential involvement in the development of pancreatic tumours. This research sought to examine the function of EPHX4 in pancreatic adenocarcinoma (PAAD). - Source: PubMed
Publication date: 2025/04/19
Huang ShaoyangGu DandanXiong Wei