ABHD4 antibody
- Known as:
- ABHD4 (anti-)
- Catalog number:
- orb101616
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ABHD4 antibody
Related genes to: ABHD4 antibody
- Gene:
- ABHD4 NIH gene
- Name:
- abhydrolase domain containing 4
- Previous symbol:
- -
- Synonyms:
- FLJ12816
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-18
- Date modifiied:
- 2019-03-21
Related products to: ABHD4 antibody
Related articles to: ABHD4 antibody
- Bortezomib, a first-in-class proteasome inhibitor, is widely used to treat multiple myeloma and other hematological malignancies. Despite its therapeutic efficacy, bortezomib causes peripheral neuropathy (PN) in approximately 20-30% of patients, often leading to dose reduction or discontinuation. Preventive or therapeutic approaches to bortezomib-induced PN are currently unavailable, as its precise mechanism remains unclear. In this study, we compared the effects of bortezomib and the second-generation proteasome inhibitor carfilzomib on peripheral nerve cells to identify candidate molecules involved in PN development. Transcriptome profiling of differentiated F11 cells, a hybridoma of a rat embryonic dorsal root ganglion and mouse neuroblastoma cell line N18TG2, revealed that bortezomib selectively upregulated α/β-hydrolase containing domain 4 (Abhd4), whereas carfilzomib did not. This finding was confirmed by quantitative RT-PCR and immunoblotting, which demonstrated consistent increases in Abhd4 mRNA and protein levels following bortezomib treatment. Functional analysis further revealed that Abhd4 overexpression promoted early apoptosis, suggesting a mechanistic link between bortezomib-induced Abhd4 elevation and neuronal vulnerability. Therefore, these results suggest that Abhd4 represents a candidate molecular signature associated with bortezomib-induced PN. Although further in vivo validation is needed, these findings warrant further investigation of Abhd4 as a potential contributor to bortezomib-induced PN. - Source: PubMed
Konishi YusukeOmura TomohiroIjichi TakeshiNishiguchi HirokiHayakawa RyunosukeKitahiro YumiItohara KotaroYamamoto KazuhiroYano Ikuko - Small cell lung cancer (SCLC) is a highly aggressive malignancy with limited therapeutic options. , a member of the lipid-metabolizing enzyme family, has been implicated in various cancers, but its precise role and molecular mechanisms in SCLC remain poorly understood. The aim of this study was to investigate the functional impact of on SCLC progression and to explore its potential links with lipid metabolism and the PI3K/AKT/mTOR signaling pathway. - Source: PubMed
Publication date: 2026/02/26
Chen JingjingYuan ZaixinYin XiWang MengjiaoZhang YanFeng JianXu Liqin - Chemotherapy can compromise the fertility of boys with cancer, yet no standard protocols exist to preserve their reproductive potential. Before puberty, germ cells are almost exclusively spermatogonia that can be the target of anticancer drugs. Doxorubicin (DXO), a widely used anthracycline in pediatric oncology, has been associated with infertility in adulthood, but its immediate effects on prepubertal germ cells remain poorly understood. In the present study, a preclinical rat model of prepubertal DXO exposure was developed to characterize the mechanisms underlying immediate DXO-induced germ cell damage. Six-day-old pups, received a single intraperitoneal injection of DXO (5 mg/kg) and effects were measured after 24 or 48 h. DXO exposure significantly reduced relative testis weight from 24 h and significantly increased apoptosis and germ cell loss at 48 h, while circulating testosterone remained unchanged, suggesting a selective germline effect. RNA-seq was done on GFP-positive germ cells purified at 24 h. Transcriptomic analysis confirmed the enrichment in spermatogonial stem cells (SSCs) in the GFP-sorted population. Moreover, DXO induced 51 differentially expressed genes (49 upregulated, 2 down regulated) that were mostly related the p53-dependant apoptosis pathway. Pro-apoptotic genes (Cdkn1a, Bbc3/Puma, Tp53inp1, Fas) and oxidative stress regulators (Sesn2, Eda2r, Abhd4) were induced, whereas DNA repair genes (Mgmt, Xrcc1, Polh, Gadd45α, …) were not activated. Our data revealed the DXO-induced immediate transcriptomic response after 24 h, leading to germ cell death observed by histology at 48 h. These findings suggest that SSCs respond to DXO by favoring apoptosis and stress regulation, a strategy that may preserve germline integrity and reduce the risk of transmitting genetic damage to the next generation. - Source: PubMed
Publication date: 2026/02/28
Beaud HermanceHug ElisaScott-Boyer Marie-PierRwigemera ArletteTremblay AmélieDroit ArnaudDelbes Géraldine - Colorectal cancer (CRC) is a highly aggressive gastrointestinal malignancy with significant global health consequences. While mitochondrial lipid metabolism genes are known to influence CRC progression, their prognostic relevance remains inadequately explored. - Source: PubMed
Publication date: 2025/11/10
Wang HouZhang KaiWang YueqiuChen MengyunZhang Mingchen - Pediatric obesity is rising globally, and emerging evidence suggests that sleep timing may influence metabolic health through epigenetic mechanisms. This study investigated epigenome-wide DNA methylation patterns associated with bedtime in children and explored their biological relevance. Children aged 6-10 years were classified as early (≤8:30 PM) or late (>8:30 PM) bedtime groups. Saliva-derived DNA was analyzed using the Illumina Infinium MethylationEPIC BeadChip Array, and the Sparse Wrapper Algorithm (SWAG) was applied to identify differentially methylated loci. A total of 1006 CpG sites, representing 571 unique genes, were significantly associated with bedtime ( < 0.001). Significant methylation differences were observed between early and late bedtime groups, with , , , , , , , , , and showing the most consistent variation. Functional enrichment analyses (Gene Ontology, KEGG, and DisGeNET) conducted on the SWAG-identified gene set revealed enrichment in biological processes including peptidyl-lysin demethylation, regulation of sodium ion transport, DNA repair, and lipo-protein particle assembly. Key KEGG pathways included circadian entrainment, neurotransmission (GABAergic, dopaminergic, and glutamatergic), growth hormone synthesis, and insulin secretion. DisGeNET analysis identified associations with neurodevelopmental disorders and cognitive impairment. Cross-comparison with established sleep and obesity gene sets identified ten overlapping genes(, , , , , , , , , and ). These findings suggest that variations in bedtime during childhood may epigenetically modify genes regulating circadian rhythm, metabolism, neuronal connectivity, and stress response, potentially predisposing to later-life developmental, and metabolic challenges. - Source: PubMed
Publication date: 2025/10/31
Richter ErikaPatel PriyadarshniOzdemir Yagmur YNnyaba Ukamaka VMolinari RobertoBabu Jeganathan RGeetha Thangiah