Ask about this productRelated genes to: POLDIP3 antibody
- Gene:
- POLDIP3 NIH gene
- Name:
- DNA polymerase delta interacting protein 3
- Previous symbol:
- -
- Synonyms:
- PDIP46, KIAA1649, SKAR, PDIP3
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-27
- Date modifiied:
- 2017-07-26
Related products to: POLDIP3 antibody
Related articles to: POLDIP3 antibody
- Esophageal cancer (ESCA) is a prevalent malignancy with high morbidity and mortality. It has been demonstrated that lactylation, a novel post-translational modification, is linked to tumor progression and immunity. The objective of this study was to look into the potential role of lactylation-related genes in the prognosis and immune microenvironment of ESCA. - Source: PubMed
Publication date: 2025/08/26
Xie LimingYang QiuxingZhao WenjingLan GuangzhiTai Guomei - Glioblastoma multiforme, one of the most malignant types of brain tumor, heavily relies on glycolytic pathways and is significantly influenced by immune infiltration and its surrounding microenvironment. Growing evidence implies that increase in glycolysis can lead to lactate accumulation, which further contributed to histone lactylation, playing a crucial role in tumor development, maintenance, and therapeutic response. This study explores the prognostic and therapeutic potential of lactylation-related genes in glioblastoma multiforme. Using single-cell (GSE162631) and bulk transcriptome datasets (TCGA, CGGA, and GSE16011), we identified lactylation-related genes through ssGSEA and WGCNA. Moreover, a machine learning framework, incorporating 10 algorithms and 101 combinations, was used to establish an eight-gene lactylation-related signature (POLDIP3, MMP14, MDK, KDELR2, GSTK1, DEDD2, CD151, and BRI3) with robust predictive accuracy for patient survival. A nomogram with lactylation-related signature integration was developed as a quantitative prognostic instrument for clinical use. Moreover, patients classified by lactylation-related signature risk scores showed distinct immune status, tumor mutation burden, immunotherapy response, and drug sensitivity. The expression of those lactylation-related genes was further validated by quantitative PCR and functional experiment in normal and GBM cell lines. Overall, this study establishes a lactylation-related signature with significant potential for glioblastoma multiforme prognostic prediction, targeted prevention, and individualized therapy. - Source: PubMed
Publication date: 2025/05/23
Wen WenjieChen JiongxueDeng FuyinGuo DajiZuo YouChen XuewenLi YoujiaLi YiTang Yamei - Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that primarily affects the motor neurons, causing progressive muscle weakness and paralysis. While research has focused on understanding pathological mechanisms in the motor cortex and spinal cord, there is growing evidence that extra-motor brain regions may also play a role in the pathogenesis or progression of ALS. - Source: PubMed
Publication date: 2025/04/25
Grima NatalieSmith Andrew NShepherd Claire EHenden LyndalZaw ThiriCarroll LukeRowe Dominic BKiernan Matthew CBlair Ian PWilliams Kelly L - Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disorder characterized neuropathologically by TDP-43 proteinopathy with loss of TDP-43 nuclear splicing activity and formation of cytoplasmic TDP-43 aggregates. The lack of suitable experimental models of TDP-43 proteinopathy has hampered the discovery of effective therapies. We already showed that chronic and mild oxidative insult by sodium arsenite (ARS) triggered TDP-43 cytoplasmic aggregation and stress granules (SGs) formation in ALS patient-derived fibroblasts and motor neurons differentiated from induced pluripotent stem cells (iPSC-MNs). However, whether this insult induces a reduction of TDP-43 splicing activity in the nucleus, thus recapitulating both gain and loss of function pathomechanisms, still remains to be determined. In this study we first showed that chronic ARS in human neuroblastoma cells triggered TDP-43 cytoplasmic mislocalization, SGs formation and defective splicing of TDP-43 target genes UNC13A and POLDIP3 as functional readouts of TDP-43 proteinopathy. Additionally, a dysregulation of autophagy and senescence markers was observed in this condition. In a preliminary drug screening approach with autophagy-promoting drugs, namely rapamycin, lithium carbonate and metformin, only rapamycin prevented ARS-induced loss of TDP-43 splicing activity. We then demonstrated that, in addition to TDP-43 cytoplasmic aggregation, chronic ARS triggered TDP-43 loss of splicing activity also in ALS patient-derived primary fibroblasts and iPSC-MNs and that rapamycin was beneficial to reduce these TDP-43 pathological features. By switching to a neuro-glial 3D in vitro model, we observed that treatment of ALS iPSC-brain organoids with chronic ARS also induced a defective TDP-43 splicing activity which was prevented by rapamycin. Collectively, we established different human cell models of TDP-43 proteinopathy which recapitulate TDP-43 gain and loss of function, prevented by rapamycin administration. Human neuroblastoma cells and patient-derived fibroblasts and 2D- and 3D-iPSC models exposed to chronic oxidative stress represent therefore suitable in vitro platforms for future drug screening approaches in ALS. - Source: PubMed
Publication date: 2024/11/12
Casiraghi ValeriaSorce Marta NiceSantangelo SerenaInvernizzi SabrinaBossolasco PatriziaLattuada ChiaraBattaglia CristinaVenturin MarcoSilani VincenzoColombrita ClaudiaRatti Antonia - Lactylation has been found to regulate several types of biological processes in cancer. However, there is limited research on lactylation-related genes in predicting the prognosis of ovarian cancer (OC). This study aimed to explore the functional roles of lactylation-related genes in OC. - Source: PubMed
Publication date: 2024/05/29
Yu LeiJing ChunxiaZhuang SulianJi LiweiJiang Li