Ask about this productRelated genes to: PTDSS1 Blocking Peptide
- Gene:
- PTDSS1 NIH gene
- Name:
- phosphatidylserine synthase 1
- Previous symbol:
- -
- Synonyms:
- KIAA0024, PSSA, PSS1
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-21
- Date modifiied:
- 2016-10-05
Related products to: PTDSS1 Blocking Peptide
Related articles to: PTDSS1 Blocking Peptide
- PTDSS1 is an emerging oncogenic protein associated with poor survival rates across various cancer types, including esophageal squamous cell carcinoma (ESCC). However, its regulatory mechanisms and therapeutic potential in ESCC remain incompletely understood. Through single-cell RNA sequencing (scRNA-seq) analysis, we identified a PTDSS1-high malignant epithelial subpopulation characterized by resistance to ferroptosis and mitophagy. Our investigations demonstrated that PTDSS1 regulates glutathione (GSH) synthesis and coordinates mitophagy in ESCC cells. Mechanistically, PTDSS1 knockdown promotes interaction between TRIM21 and SLC3A2, leading to diminished SLC3A2 protein expression and subsequent reduction in GSH synthesis. This elevates cellular oxidative stress, thereby triggering PINK1/Parkin mitophagy pathway and ultimately inducing apoptosis and ferroptosis. Furthermore, at the mitochondrial level, the knockdown of PTDSS1 decreases phosphatidylserine (PS) and facilitates mitochondrial fusion protein 2 (MFN2) translocation, providing substrates for mitophagy. Collectively, our findings elucidate a novel mechanism by which PTDSS1 protects ESCC cells from death and offer new perspectives for therapeutic strategies that target PTDSS1 to induce mitophagy and ferroptosis in ESCC. - Source: PubMed
Publication date: 2026/04/23
Zhang XiaoCao ShuruiZhou ChenchenJiang WenWang HongshunHui BingqingDeng XiahengGu Yanhong - Prolificacy is a crucial economic trait in goat production, yet its underlying molecular mechanisms remain incompletely understood due to its polygenic nature. While previous studies have identified several candidate genes, a comprehensive understanding of the local and systemic regulatory networks is lacking. This study aims to dissect the complex molecular basis of high prolificacy in goats through an integrated multi-omics approach. - Source: PubMed
Publication date: 2026/04/06
Jiang FanTao HuChen MengjieShangguan AishaoLv HaimiaoHua ZaidongZhang NianZhang FengXu TianWang WenMa ChengtaoXiong Qi
- Source: PubMed
- Mammalian phosphatidylserine synthase-1 and -2 synthesize phosphatidylserine (PS) by replacing the headgroup of either phosphatidylcholine (PC, PTDSS1) or phosphatidylethanolamine (PE, PTDSS2) with a serine. We determined structures of PTDSS2 from in complex with either PE or serine substrates to resolutions of 2.8-3.2 Å. The structures define substrate binding sites and reveal that the phosphate group of PE is coordinated by two Ca. In addition, we found that PTDSS2 has significant phospholipase D (PLD) activity in the absence of serine, which was not reported previously, and that Ca is required for the PLD activity. These discoveries enrich our knowledge in the mechanism of mammalian PTDSS. - Source: PubMed
Publication date: 2026/02/07
Wang LieZhang ZhenYang HongyuanLaganowsky ArthurZhou Ming - Dysfunction of the neuronal macroautophagy/autophagy-lysosome system is a critical contributor to neuronal death following spinal cord injury (SCI), but the underlying mechanisms remain elusive. Our study demonstrated that SCI induced impaired autophagic flux and lysosomal membrane permeabilization (LMP) in neurons. By combining bulk RNA sequencing with validation experiments, we observed the transient upregulation of the membrane repair factor PI4K2A, which was specifically enriched in lysosomes, after SCI. Crucially, ER-MS and IP-MS analyses revealed an interaction between PI4K2A and the endoplasmic reticulum lipid transfer protein OSBPL6/ORP6. This interaction led to the transport of phosphatidylserine (PS) to damaged lysosomal membranes, promoting LMP repair and subsequently reducing lipid droplet accumulation, which suppressed neuronal death. Furthermore, overexpression of neuronal PI4K2A , through an OSBPL6- and PS-dependent mechanism, reduced LMP-mediated lipid droplet accumulation and increased neuronal survival, thereby improving functional recovery after SCI. Collectively, our findings establish the PI4K2A-OSBPL6/ORP6-PS axis as a novel and essential mechanism for lysosomal membrane repair in neurons. This pathway is crucial for maintaining neuronal lipid homeostasis and represents a promising therapeutic target for reducing neuronal loss and improving functional recovery after central nervous system trauma.: AIF1/IBA1: allograft inflammatory factor 1; Baf A1: bafilomycin A; BMS: Basso Mouse Scale; CNS: central nervous system; co-IP: co-immunoprecipitation; DEGs: differentially expressed genes; DS5: DS55980254; ESCRT: endosomal sorting complex required for transport; GFP: green fluorescent protein; HSPA5/GRP78: heat shock protein family A (HSP70) member 5; HT22: hippocampal neuronal cell line; KEGG: Kyoto Encyclopedia of Genes and Genomes; LD: lipid droplet; LC-MS: liquid chromatography-mass spectrometry; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; LGALS3/GAL3: lectin, galactoside binding, soluble 3; LLOMe: L-leucyl-L-leucine methyl ester; LMP: lysosomal membrane permeabilization; LPC: lysophosphatidylcholine; LPE: lysophosphatidylethanolamine; MFGE8/lactadherin: milk fat globule EGF and factor V/VIII domain containing; MS: mass spectrometry; NAGLU: alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB); NEFH/NF200: neurofilament, heavy polypeptide; OSBPL6/ORP6: oxysterol binding protein-like 6; OSBPL8/ORP8: oxysterol binding protein-like 8; PC: phosphatidylcholine; PLA2G4A/cPLA2: phospholipase A2, group IVA (cytosolic, calcium dependent); PITT: phosphoinositide-initiated membrane tethering and lipid transport; PI4K2A: phosphatidylinositol 4-kinase type 2 alpha; PLS-DA: partial least squares discriminant analysis; PS: phosphatidylserine; PtdIns: phosphatidylinositol; PTDSS1: phosphatidylserine synthase 1; PUFAs: polyunsaturated fatty acids; RBFOX3/NeuN: RNA binding protein, fox-1 homolog (C. elegans) 3; ROS: reactive oxygen species; SCI: spinal cord injury; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TGs: triglycerides. - Source: PubMed
Publication date: 2026/02/04
Zhang HaojieKang YuZhao TianlunHuang DaoqiangHu XuantaoDi JiaweiZhang YilongLu YubaoHuang MudanLi HongYao SenyuLiu BinRong Limin