HAT p300
- Known as:
- HAT p300
- Catalog number:
- NB100-507G
- Product Quantity:
- 0.2 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- HAT p300
Related genes to: HAT p300
- Gene:
- EP300 NIH gene
- Name:
- E1A binding protein p300
- Previous symbol:
- -
- Synonyms:
- p300, KAT3B
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-31
- Date modifiied:
- 2015-09-11
Related products to: HAT p300
Related articles to: HAT p300
- We aim to screen and analyze the ferroptosis inflammation-related hub genes associated with idiopathic pulmonary fibrosis (IPF). The GSE52463 and GSE110147 datasets were obtained from the GEO database and merged. The DEGs were selected by differential analysis and intersected with inflammation-related genes and ferroptosis-related genes to acquire the ferroptosis-related differentially expressed genes (FRDEGs). GO, KEGG, GSEA, and GSVA were performed to investigate the features of FRDEGs. The key module genes were selected by WGCNA and employed to generate the PPI network using Cytoscape. Subsequently, the hub genes were identified using cytoHubba and validated by ROC curves generated by survivalROC. Finally, the correlations of hub genes were analyzed through Spearman and the subtypes of IPF were constructed using ConsensusClusterPlus. A total of 1814 DEGs were screened out and 18 FRDEGs were acquired from the intersection of DEGs, ferroptosis-related genes, and inflammation-related genes. GO and KEGG analysis revealed that FRDEGs were primarily involved in bacterial-origin molecular, response infectious disease, and iron ion transport. GSEA results suggested a predominant association with autoimmune diseases and GSVA identified ten different pathways between PF and control. Through WGCNA, three highly correlated modules were identified and ten key module genes were obtained by intersecting genes in the three modules with FRDEGs. Finally, employing three algorithms within the cytoHubba led to the identification of eight hub genes: CCND1, TP53, STAT3, CTNNB1 CDH1, ESR1, HSP90AA1, and EP300. Eventually, two distinct subtypes of IPF were identified. The present research successfully identified the hub genes associated with ferroptosis and inflammation and their biological effects on IPF. Furthermore, two disease subtypes of IPF were constructed. - Source: PubMed
Publication date: 2024/05/11
Niu ChongyangMeng XiaoyuWang Tan - The symptoms of most neurodegenerative diseases, including Parkinson's disease (PD), usually do not occur until substantial neuronal loss occurs. This makes the process of early diagnosis very challenging. Hence, this research used variant call format (VCF) analysis to detect variants and novel genes that could be used as prognostic indicators in the early diagnosis of prodromal PD. - Source: PubMed
Publication date: 2024/04/29
Badawy Marwa TSalama Aya ASalama Mohamed - To find out the differences in gene characteristics between cervical cancer patients with and without lymph node metastasis, and to provide reference for therapy. - Source: PubMed
Publication date: 2024/04/29
He HaoHe MisiZhou QiTang YingWang JingLi XiuyingZou Dongling - Acute myeloid leukemia (AML) with mixed-lineage leukemia (MLL) gene rearrangements (MLL-r) is an aggressive subtype of blood cancer with dismal prognosis, underscoring the urgent need for novel therapeutic strategies. E1A-binding protein (EP300) and CREB-binding protein (CREBBP) function as essential transcriptional coactivators and acetyltransferases, governing leukemogenesis through diverse mechanisms. Targeting EP300/CREBBP holds great promise for treating leukemia with some certain cytogenetic abnormalities. Here, we demonstrated that EP300 and CREBBP are core epigenetic regulators in the pathogenesis of MLL-r AML through assaying the transposase-accessible chromatin with high-throughput sequencing (ATAC-seq). Knocking-out EP300/CREBBP and inhibitor (A-485) treatment depressed the MLL-r cells proliferation, while the MLL wild-type cells remained uninfluenced. We found that the CDK4/RB/E2F axis was downregulated specifically in MLL-r AML cell after A-485 treatment by RNA-seq, western blot and cut-tag analyses. EP300/CREBBP inhibitor selectively exerted potent anti-leukemia activity through blocking the MLL-r-BET complex binding to H3K27Ac modification on critical genes loci, distinct from global histone acetylation. Collectively, our study identified EP300/CREBBP as a critical epigenetic driver of MLL-r leukemia and validated their therapeutic potential through targeting inhibition, offering a promising avenue for improving clinical outcomes in this aggressive leukemia. - Source: PubMed
Publication date: 2024/05/01
Wu WenqiJiang YananXing DonghuiZhai YixinSun HuimengHe XiangLuo KaipingXu PengpengPan FengDong GuoleiRen GuibingZhao Zhigang - There is a lack of effective drugs to treat the progression and recurrence of chordoma, which is widely resistant to treatment in chemotherapy. The authors investigated the functional and therapeutic relevance of the E1A-binding protein p300 (EP300) in chordoma. - Source: PubMed
Wen LingzhiXie BinLi HuiHuang JunShi YingTao YongguangChen Yuanbing