PTPLAD1 Blocking Peptide
- Known as:
- PTPLAD1 Blocking Peptide
- Catalog number:
- 33r-9968
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- PTPLAD1 Blocking Peptide
Related genes to: PTPLAD1 Blocking Peptide
- Gene:
- HACD3 NIH gene
- Name:
- 3-hydroxyacyl-CoA dehydratase 3
- Previous symbol:
- PTPLAD1
- Synonyms:
- B-ind1, HSPC121
- Chromosome:
- 15q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-11
- Date modifiied:
- 2016-01-15
Related products to: PTPLAD1 Blocking Peptide
Related articles to: PTPLAD1 Blocking Peptide
- Lung adenocarcinoma (LUAD) is one of the most commonly seen non-small cell lung cancer (NSCLC). Recent progress has highlighted cyclin-dependent kinase (CDK) inhibitors for treating diverse cancers including NSCLC. However, acquired resistance of CDK inhibitors has prompted the exploration of druggable regulatory or compensatory pathways in cell cycle as alternative or combination therapies of CDK inhibitors. - Source: PubMed
Publication date: 2026/03/27
Meng YuZhang ZiyiJia KunWang WeiWang HongxiaHu ZhihuangLiu Jia - HACD3 is from the very long-chain fatty acid dehydratase family and exhibits only mild activity while producing long-chain fatty acids. Numerous studies have uncovered an association of HACD3 with the advancement of diverse cancers. The current study attempts to delve into the potential role of HACD3 in initiating and enhancing lung cancer. - Source: PubMed
Publication date: 2025/08/15
Wang XiaoyingLiang HuijunDu QindanLi YingZhao Yong - Variable splicing (AS) plays important roles in tumor progression. However, the role of the AS factor RBM17 in the progression of hepatocellular carcinoma (HCC) has not yet been elucidated. We used label-free proteomics, single-cell sequencing (scRNA-seq), high throughput sequencing, flow cytometry (FCM), liquid Chromatography-tandem mass spectrometry (LC‒MS/MS), multiparametric immunofluorescence (mIF) and chromatin immunoprecipitation (Chip), to explore the relationship between RBM17 regulation of HCC cell lipid metabolism and the immune microenvironment. Our findings revealed that RBM17 is significantly overexpressed in HCC tissue and is positively correlated with poor prognosis. We found a positive correlation between RBM17 expression and M2 macrophage infiltration. Mechanistically, RBM17 promotes M2 macrophage infiltration by inducing taurocholic acid (T-CA) production, which is achieved through enhancing exon exclusion of CSAD precursor mRNA. Additionally, RBM17 modulates fatty acid metabolism and CD8 T cell infiltration by regulating exon skipping in HACD3 precursor mRNA. Furthermore, RUNX1 activates RBM17 expression and regulates downstream CSAD/T-CA and HACD3/FFA signaling. Importantly, targeting RBM17 can prevent HCC progression, suggesting its potential as a therapeutic target for HCC. Our findings provide new insights into the mechanisms underlying immune cell infiltration and metabolism in HCC and identify RBM17 as a promising therapeutic target. - Source: PubMed
Publication date: 2025/07/23
Wang ZengbinLiu JiayuLai YitingZhong QingSu QianWu LinqingWang ZhihongFang Zhuting - The transcriptional regulation of metabolic genes is crucial for maintaining metabolic homeostasis under cellular stress conditions. Transcription factor 7-like 2 (TCF7l2 or TCF4) is associated with type 2 diabetes (T2D) and functions as a transcription factor for various gluconeogenic genes. T2D often coexists with metabolic dysfunction-associated steatotic liver disease (MASLD) due to common underlying mechanisms and shared risk factors such as insulin resistance and obesity. This study demonstrates the transcriptional regulation of one of the important fatty acid chain elongases implicated in T2D, HACD3 (encoded by gene), under palmitic acid (PA)-induced stress conditions. We observed that TCF7l2 is associated with histone H3K4me3-binder protein TCF19 and is corecruited to the promoter of . Upon PA treatment, the TCF19-TCF7l2 complex dissociates from the lipid chain elongase gene due to the reduced level of H3K4me3 enrichment, leading to activation. Remarkably, gene expression analysis from the PA-injected mice and NAFLD patients indicates an anticorrelation whereby reduced TCF7l2 expression enhances HACD3-mediated chain elongation and triglyceride production, thereby promoting the development of MASLD. Our findings delineate that the epigenetic mechanism of activation of lipid chain elongase genes mediated by TCF7l2 in concert with TCF19 has important implications in metabolic disorders. - Source: PubMed
Publication date: 2025/04/02
Mondal AtanuNandi SandhikSingh VipinChakraborty ArnabBanerjee IndrakshiSen SabyasachiGadad Shrikanth SRoy SiddharthaKamat Siddhesh SDas Chandrima - - Source: PubMed
Publication date: 2024/12/27
Wang XiaoyingDu QindanChen JiayaoWang RongZhao YongLiu SihuiChen Yong Q