Ask about this productRelated genes to: PGS1 antibody
- Gene:
- PGS1 NIH gene
- Name:
- phosphatidylglycerophosphate synthase 1
- Previous symbol:
- -
- Synonyms:
- DKFZP762M186
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-15
- Date modifiied:
- 2014-11-19
Related products to: PGS1 antibody
Related articles to: PGS1 antibody
- The hull, composed of the lemma and palea, defines rice grain morphology and influences endosperm filling and quality. However, how palea development affects grain filling and quality remains poorly understood. Here, we identify a rice mutant, palea and grain shrunken 1 (pgs1), which exhibits a markedly reduced palea and elongated sterile lemmas. MutMap-based cloning reveals that PGS1 encodes the MADS-box transcription factor OsMADS15. The pgs1 mutant shows smaller but denser grains with substantially reduced chalkiness, and the expression of several palea identity genes, including G1, OsMADS1, and SL1, is significantly decreased. PGS1 is expressed in multiple floral organs, localizes to the nucleus, and lacks intrinsic transcriptional activation activity. Protein interaction assays show that PGS1 physically interacts with the histone demethylase JMJ706, and JMJ706 knockout lines exhibit floral and grain phenotypes similar to those of pgs1. Together, these results support a functional association between PGS1 and JMJ706 in the regulation of palea development and further suggest that defective palea development affects grain filling and grain quality in rice. - Source: PubMed
Publication date: 2026/04/29
Jin DiYang Chao-YueLiu XiaoLan Jin-SongJiang TaoChen HaoZhang Jia-YingJiang Yu-TongPeng Bo-RanWang Liu-JingHe Guang-HuaWang NanLi Yun-FengZhuang Hui - Renal cell carcinoma (RCC) is characterized by dysregulated lipid metabolism and a high propensity for developing resistance to targeted therapies. Mitophagy is a key process involved in the progression of various cancers, including RCC. Here, using genome-wide CRISPR screening, we identified PRKAB2 as a crucial tumor suppressor in RCC. Reduced PRKAB2 expression correlated with poor prognosis and aggressive clinical features, whereas overexpression of PRKAB2 markedly inhibited RCC cell proliferation, migration, invasion, tumor growth, and metastasis both and . Mechanistically, PRKAB2 overexpression inhibited mitophagy primarily through two distinct mechanisms. First, PRKAB2 enhanced the binding between LRPPRC and PRKN/parkin, competitively reducing PRKN's interaction with PINK1 and thus suppressing ubiquitin-dependent mitophagy. Second, PRKAB2 promoted AMPK phosphorylation, which in turn suppressed SREBF1/SREBP1-mediated transcriptional activation of , leading to decreased CRLS1 expression and reduced synthesis of cardiolipin, a lipid essential for mitophagy. Importantly, PRKAB2 overexpression significantly restored sensitivity to tyrosine kinase inhibitors (TKIs) in sunitinib-resistant RCC cells. Conversely, forced PRKN expression promoted resistance to these drugs, further implicating mitophagy as a key mechanism underlying TKI resistance. Depmap analysis confirmed the association between increased mitophagy and TKI resistance. Overall, our findings identify PRKAB2 as a critical tumor suppressor in RCC, regulating both protein-protein interactions and lipid metabolism to suppress mitophagy. Targeting PRKAB2-associated pathways may provide a promising therapeutic strategy to enhance treatment efficacy and overcome drug resistance in RCC.: ACACA/ACC1: acetyl-CoA carboxylase alpha; AMPK: AMP-activated protein kinase; ATCC: American Type Culture Collection; ATP5F1A: ATP synthase F1 subunit alpha; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; BRCA1: BRCA1 DNA repair associated; Cas: CRISPR-associated; CCCP: carbonyl cyanide m-chlorophenyl hydrazone; ccRCC: clear cell renal cell carcinoma; ChIP: chromatin immunoprecipitation; Co-IP: co-immunoprecipitation; COX4I1: cytochrome c oxidase subunit 4I1; CRISPR: clustered regularly interspaced short palindromic repeats; CRLS1: cardiolipin synthase 1; DNM1L/DRP1: dynamin 1 like; DOX: doxorubicin; FUNDC1: FUN14 domain containing 1; HSPA8: heat shock protein family A (Hsp70) member 8; HSPD1: heat shock protein family D (Hsp60) member 1; GO: gene ontology; IHC: immunohistochemistry; IMM: inner mitochondrial membrane; LDLR: low density lipoprotein receptor; m-SREBF1: mature sterol regulatory element binding transcriptional factor 1; LRPPRC: leucine rich pentatricopeptide repeat containing; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MFN1, mitofusin 1; MFN2: mitofusin 2; MTOR: mechanistic target of rapamycin kinase; OMM: outer mitochondrial membrane; OS: overall survival; PA: phosphatidic acid; PG: phosphatidylglycerol; PGS1: phosphatidylglycerophosphate synthase 1; PINK1: PTEN induced kinase1; PRKAA1/AMPKα1: protein kinase AMP-activated catalytic subunit alpha 1; PRKAA2/AMPKα2: protein kinase AMP-activated catalytic subunit alpha 2; PRKAB1/AMPKβ1: protein kinase AMP-activated catalytic subunit beta 1; PRKAB2/AMPKβ2: protein kinase AMP-activated non-catalytic subunit beta 2; PRKAG1/AMPKγ1: protein kinase AMP-activated non-catalytic subunit gamma 1; PRKN: parkin RBR E3 ubiquitin protein ligase; RCC: renal cell carcinoma; SASA: solvent-accessible surface areas; SUCLG1: succinate-CoA ligase GDP/ADP-forming subunit alpha; TCGA: The Cancer Genome Atlas; TKI: tyrosine kinase inhibitors; UCP1: uncoupling protein 1; ULK1: unc-51 like autophagy activating kinase 1; WCL: whole-cell lysate. - Source: PubMed
Publication date: 2026/02/18
Chen KaileiZhang YuanpengRuan HailongWei ZhihaoWang KeshanCao QiWang QiDong ZiruiWu YilongYang HongmeiLiu LeiLiu YuenanZhang Xiaoping - To investigate the causal relationship between mitochondrial genes and the pathogenesis of carotid plaque (CP), a multiomics-integrated Mendelian randomization (MR) analysis was performed in this study. - Source: PubMed
Publication date: 2025/11/01
Yu ZhuyuanMeng XiangyuanZong ZiyuSong QiHuo YingchaoChen Hao - Cardiolipin (CL), a mitochondria-specific phospholipid, plays a fundamental role in respiratory chain organization and bioenergetic efficiency, yet its contribution to osteogenic differentiation is poorly defined. Here, we used a multimodal approach integrating untargeted LC-MS lipidomics, Raman spectroscopy, fluorescence lifetime imaging microscopy (FLIM), and structural imaging to investigate CL remodeling during human adipose-derived stem cell differentiation. Lipidomics revealed a selective enrichment of highly unsaturated CL species, accompanied by transcriptional upregulation of the cardiolipin biosynthetic and remodeling enzymes CDS1/2, PGS1, CRLS1, TAZ, and HADHA. Lipidomics also revealed a time-dependent increase in membrane-associated lipids including phosphatidylcholine (PC), serine, and phosphatidylinositol (PI). These lipids were implicated in supporting mitochondrial membrane expansion, oxidative phosphorylation, and signaling processes critical for osteoblast maturation. Spatial imaging techniques confirmed cardiolipin accumulation and redistribution in differentiated cells, while Raman-based direct classical least squares (DCLS) analysis provided label-free mapping of lipid species. Gene Ontology (GO) enrichment and protein-protein interaction network analysis further identified biological pathways related to bone remodeling, cardiolipin metabolism, and osteoblast-specific signaling. Fluorescence Lifetime Imaging Microscopy (FLIM) data revealed a metabolic shift from glycolysis to oxidative phosphorylation during differentiation, supported by structural and gene expression evidence. These changes temporally coincided with matrix mineralization and collagen organization, linking CL metabolism to both cellular bioenergetics and extracellular matrix production. Our findings identify cardiolipin remodeling as a metabolic checkpoint in osteogenesis and suggest that targeted modulation of CL pathways may provide new therapeutic strategies for enhancing bone regeneration. - Source: PubMed
Publication date: 2025/12/23
Iftesum MariaGuttula Praveen KumarAgrawal KirtiKundu Subhrajyoti SDas SreyashiDonnarumma FabrizioDevireddy RamGartia Manas Ranjan - The jacaranda ( D. Don.) is a widely cultivated ornamental tree species in urban landscapes, but recent research has highlighted its additional ecological and industrial potential. However, no detailed phenological description has been available for this species. The objective of this study was to establish a standardized phenological scale for D. Don. based on the BBCH coding system and to determine the thermal requirements (growing degree-days, GDD). Thirty-nine secondary stages were used to describe the life cycle of jacaranda in this BBCH scale, distributed across seven principal growth stages (PGSs). Of these thirty-nine secondary stages, five stages correspond to dormancy and sprouting (PGS-0), six stages correspond to leaf development (PGS-1), three correspond to the emergence of the flowering organ (PGS-5), eight correspond to flowering (PGS-6), ten correspond to fruit formation (PGS-7), three correspond to ripening fruit (PGS-8), and four correspond to the beginning of dormancy (PGS-9). Thermal integral analysis indicated that jacaranda requires approximately 3800 accumulated degree-days (GDD) to progress from dormancy to leaf fall. This phenological framework enhances understanding of the growth cycle of D. Don. and provides a useful reference for improving the timing and efficiency of management and phytosanitary treatments in Mediterranean conditions. - Source: PubMed
Publication date: 2025/11/09
Gandía-Ventura IgnacioLópez-Cortés IsabelVelàzquez-Martí Borja