Ask about this productRelated genes to: PLD2 antibody
- Gene:
- PLD2 NIH gene
- Name:
- phospholipase D2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-21
- Date modifiied:
- 2016-10-05
Related products to: PLD2 antibody
Related articles to: PLD2 antibody
- Progression through the cell cycle requires coordinated regulation of transcription, chromatin state, and cellular metabolism. While metabolic enzymes are known to localize the nucleus and influence chromatin states, how nuclear metabolism itself oscillates during the cell cycle remains unexplored. Here, we combine a customized FUCCI-3 reporter with chromatome mass spectrometry and high-throughput imaging to systematically resolve nuclear and chromatin-associated metabolic changes across cell cycle phases. We identify phosphatidylinositol metabolism as a nuclear pathway that oscillates with the cell cycle, with PIP5K1A, PLCD3, and PLD2 showing phase-specific nuclear and chromatin dynamics. Nuclear PIP2 levels redistribute within the nucleus depending on cell cycle stage. Downregulation of PIP5K1A reduces nuclear PIP2 levels, whereas nuclear enrichment of PIP5K1A increases PIP2 abundance in the nucleus and nucleolus, functionally linking PIP5K1A nuclear localization to nuclear PIP2 synthesis. Moreover, perturbation of nuclear PIP2 synthesis alters chromatin methylation, with a pronounced impact on H4K20 monomethylation. Together, our results reveal that nuclear phosphatidylinositol metabolism is cell cycle regulated and functionally linked to chromatin methylation, establishing nuclear lipid metabolism as a previously unrecognized layer of cell cycle control. - Source: PubMed
Publication date: 2026/04/21
Gañez-Zapater AntoniKourtis SavvasElbæk Camilla ReiterEspinar LorenaToro-Márquez CarolinaColl-Manzano AlbertSmiriglia AlfredoGarcía-López LauraWiegand LauraGuirola MariaFontaine FrédéricMorandi AndreaMüller André CSdelci Sara - - Source: PubMed
Publication date: 2026/03/06
Wang QingzhuTong YannaDing YuchuanWeiss AlexanderFayyaz Aminah IGeng Xiaokun - The rise in electronic waste from the electronics industry has increased environmental and health risks. Pollutants like tris(2-chloroethyl) phosphate (TCEP) and lead (Pb) are particularly concerning for their harmful effects on aquatic life and human health. In the current study, zebrafish were exposed to Pb (190 μg/L) and TCEP (350, 3500, 35000 μg/L) from 4 to 120 hours post-fertilization. Mortality, hatching rate, spinal curvature, and spontaneous movement were observed. qRT-PCR was used to detect neurodevelopmental gene expression. Neurotransmitter levels (serotonin, dopamine, acetylcholine) were measured by ELISA, Pb absorption by ICP-MS, and metabolic changes by metabolomics. Our results indicated that lower doses of TCEP and Pb had no significant effect on spinal curvature or movement. However, high-dose TCEP (35000 μg/L) combined with Pb (190 μg/L) significantly increased spinal curvature (P < 0.001), inhibited movement (P < 0.05), decreased body length (P < 0.01), and reduced heart rate (P < 0.01). Gene expression related to spinal and neurodevelopment was downregulated (P < 0.05), and 5-HT levels increased (P < 0.05). The combined effect of Pb and TCEP was synergistic. Metabolomics showed differential metabolites in lipid pathways, with significant increases in pld1 and pld2 gene expression (P < 0.05). In conclusion, High-dose TCEP combined with Pb exposure synergistically affects early zebrafish development, particularly the spine and nervous system, potentially through glycerophospholipid metabolism and the phospholipase D signaling pathway. - Source: PubMed
Publication date: 2026/02/17
Zhang XiaoshunSong ShanshanJi QiuyiXiang YangXu YongjieZou FeiMeng Xiaojing - The retinal pigment epithelium (RPE) performs key roles in preserving retinal integrity and must continuously manage oxidative stress (OS). We previously demonstrated that the canonical phospholipase D isoforms, PLD1 and PLD2, mediate the RPE inflammatory response triggered by inflammatory injury. This study explores the mechanisms of modulation of OS mediated by PLD inhibition in RPE cells exposed to high glucose (HG) levels. ARPE-19, D407 and the novel human RPE cell line ABC were cultured under HG (33 mM) or normal glucose (NG, 5.5 mM) conditions. To inhibit PLD1, PLD2, and NADPH oxidase (NOX), VU0359595 (PLD1i), VU0285655-1 (PLD2i), and diphenyleneiodonium chloride (DPI) were used, respectively. HG exposure significantly increased reactive oxygen species (ROS) levels and reduced mitochondrial membrane potential (MMP) in ARPE-19 and D407 cells. These effects were prevented by PLD1i and PLD2i in an Nrf-2 and cyclooxygenase-2 -independent manner. In ARPE-19 cells, DPI prevented OS induced by HG as well as the stress triggered by the combination of phosphatidic acid + diacylglycerol, bioactive lipids generated through the PLD pathway-. Similarly, HG elevated ROS levels in ABC cells, and this increase was prevented by PLD1i and DPI. RNAseq analysis showed differential expression of NOX family members (NOX1,2 and 4 and DUOX1 and 2) in ARPE-19 and ABC cells. Our results demonstrate that PLDs inhibition prevent HG-induced OS in RPE cells, possibly by reducing NOX activity. The PLD pathway constitutes a novel pharmacological target to simultaneously mitigate OS and the inflammatory response, two hallmarks of retinal degenerative diseases. - Source: PubMed
Publication date: 2026/01/28
Echevarría María STenconi Paula EBermúdez VicenteCalandria Jorgelina MBazan Nicolas GMateos Melina V - Biphasic molecular adaptations in pyramidal neurons (PNs) projecting from prelimbic (PL) cortex to the nucleus accumbens (NAc) (PL→NAc PNs) are hallmarks of early withdrawal vs. later abstinence from cocaine. However, whether biphasic electrophysiological changes accompany these molecular adaptations is unknown. Here we investigated sex-specific, physiological neuroadaptations in Drd1 (PL)- and Drd2 (PL)-expressing PL→NAc PNs 2 hr or 7 days after cessation of cocaine self administration. Drd1- and Drd2-Cre transgenic male and female rats with virally labeled PL→NAc neurons were trained to self administer cocaine followed by two hours of withdrawal or one week of forced abstinence with or without a cue-induced cocaine- seeking test. Intrinsic excitability was increased selectively in PL→NAc PNs of males, but not females, after 2 hr of withdrawal and 7d of abstinence that was normalized by cue-induced relapse. Increased sEPSC frequency (measure of presynaptic glutamate release) in PL→NAc PNs and decreased AMPA/NMDA ratio (measurement of excitatory synaptic strength) in PL→NAc PNs in males, not females, was present during early withdrawal but normalized as abstinence progressed. In females, not males, an increased AMPA/NMDA ratio occurred after 7d of abstinence that was normalized by cue-induced relapse to cocaine seeking. In contrast to findings in heroin-abstinent rats, PKA inhibition using Rp-cAMPs had no effect on augmented intrinsic excitability of PL→NAc PNs after 7d abstinence. However, RP-cAMPs reversed cocaine-augmented AMPA/NMDA ratio exclusively in PL→NAc PNs of females. These data reveal that cocaine abstinence-induced physiological neuroadaptations in PL→NAc PNs are normalized by cue-induced cocaine seeking in a sex-specific manner. - Source: PubMed
Publication date: 2025/10/03
Kokane Saurabh SRay Chevin MCrow Ayteria DOtis James MMcGinty Jacqueline F