ABHD4
- Known as:
- ABHD4
- Catalog number:
- 000941A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABHD4
Related genes to: ABHD4
- 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
Related articles to: ABHD4
- Cardiolipin (CL) is a unique dimeric phospholipid essential for mitochondrial integrity and stress signaling. While most CL is present in the inner mitochondrial membranes (IMM), CL can be exposed to the outer mitochondrial membrane (OMM) under specific physiological and pathological conditions; however, the mechanisms regulating its metabolism at the OMM are poorly defined. Based on its striking structural similarity to Cld1p, a yeast CL hydrolase, we hypothesized that α/β-hydrolase domain-containing protein 4 (ABHD4) functions as a mammalian CL hydrolase. We identified two isoforms of mouse ABHD4 arising from alternative splicing: ABHD4-1 localizes to lipid droplets, whereas ABHD4-2 selectively targets mitochondria and is enriched in oxidative tissues. We demonstrate that ABHD4 selectively hydrolyzes CL in vitro, producing monolysocardiolipin (MLCL) and dilysocardiolipin (DLCL). Site-directed mutagenesis identified catalytic serine residues as essential for enzymatic activity in ABHD4 and its Drosophila homolog, Pummelig. In contrast to Cld1p, which resides in the IMM, topological analyses indicate that ABHD4-2 and Pummelig-2 localize to the cytosolic face of the OMM, a conserved orientation that suggests a function distinct from classic acyl chain remodeling of CL. In brown adipocytes, ABHD4-2 overexpression reduces mitochondrial membrane potential in an activity-dependent manner. In silico analyses further reveal conservation of the catalytic triad across yeast, insect, and mammalian orthologs, supporting an evolutionarily conserved role for this enzyme family in CL metabolism. Together, these findings identify ABHD4-2 as an OMM-localized phospholipase with preferential CL hydrolase activity and define an isoform-specific pathway linking CL metabolism to mitochondrial stress responses. - Source: PubMed
Publication date: 2026/08/06
Narayanasamy RajaSanders Matthew AZhang HuameiMoreno-Torres MartaRamseyer Vanesa DWei Hong-GuangFærgeman Nils JKelly Christopher VGranneman James G - 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