Ask about this productRelated genes to: APPD antibody
- Gene:
- PLEKHF1 NIH gene
- Name:
- pleckstrin homology and FYVE domain containing 1
- Previous symbol:
- -
- Synonyms:
- APPD, MGC4090, PHAFIN1, ZFYVE15
- Chromosome:
- 19q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-01
- Date modifiied:
- 2016-01-15
Related products to: APPD antibody
Related articles to: APPD antibody
- Hypertension contributes to brain dysfunction through apoptosis, oxidative stress, reduced neuronal connectivity, and neurotransmitter imbalance. Exercise training is a non-pharmacological strategy known to modulate these molecular alterations. This study investigated the effects of high-intensity interval training (HIIT) on transcriptomic changes in the cerebral cortex of spontaneously hypertensive rats (SHR) fed a high-fat diet (HFD). Rats were assigned to either a HIIT intervention group (HIIT-HFD-SHR) or a sedentary control group (HFD-SHR). Cortical RNA was extracted, sequenced using the Illumina NovaSeq 6000 platform, and analyzed with DESeq2. Functional enrichment was conducted using Metascape. RNA-seq identified 1223 differentially expressed genes (DEGs) (adjusted < 0.05), with 51 remaining significant under stringent criteria (adjusted < 0.001, |logFC| > 0.5). Among these, eight key genes were closely associated with the regulation of apoptosis and autophagy, including seven downregulated (, , , , , , ) and one upregulated (). This transcriptomic analysis following HIIT also modulated circadian rhythm, long-term memory processes, and hypoxia response in the hypertensive brain. These findings indicate that HIIT decreases apoptosis and autophagy and improves circadian rhythm, long-term memory, and hypoxia in hypertensive rats' brains. - Source: PubMed
Publication date: 2025/12/27
Sadiq ArslanShah Iqbal AliWu Bor-TsangLin Yi-YuanSu Yi-AnYang Ai-LunLee Shin-Da - Osteosarcoma (OS) is an uncommon malignancy with stagnant survival rates over the past four decades and early-stage metastasis, predominantly affecting children and adolescents. This study identified significant metabolic differences between metastatic and non-metastatic OS samples through bioinformatics analysis, highlighting key processes such as cell proliferation, mitochondrial assembly, and changes in mitochondrial membrane permeability. Among differentially expressed genes, Pleckstrin Homology And FYVE Domain Containing 1 (PLEKHF1) was the most significantly downregulated in metastatic OS samples. Functional experiments demonstrated that PLEKHF1 overexpression in Saos-2 and U2OS cells induced mitochondrial dysfunction, evidenced by increased mtROS levels, decreased mitochondrial membrane potential, and altered cytochrome C distribution. Additionally, PLEKHF1 overexpression inhibited OS cell viability, colony formation, migration, invasion, and epithelial-mesenchymal transition (EMT), while promoting apoptosis. Conversely, knockdown of PLEKHF1 had the opposite effects on Saos-2 and U2OS cells. In vivo, PLEKHF1 overexpression reduced tumor growth and lung metastasis in a mouse model. Conversely, PLEKHF1 knockdown ameliorated Rotenone-induced mitochondrial dysfunction and mitophagy, partially reversing the suppressive effects of Rotenone on OS cell aggressiveness. These findings suggest that PLEKHF1 could serve as an anti-tumor factor by inducing mitochondrial dysfunction, thereby inhibiting OS growth and metastasis. The study highlights the potential of PLEKHF1 as a therapeutic target for managing osteosarcoma, providing valuable insights into the role of mitochondrial dysfunction in OS pathogenesis. - Source: PubMed
Wan JunCai XinyanLiao ZhanLiu YupengLiu QingZhang CanLong Feng - - Source: PubMed
Publication date: 2025/05/27
Yan LifengHou ChenchenLiu JuanWang YiZeng ChenxiYu JunZhou TianyuZhou QingDuan ShengzhongXiong Weining - Osteosarcoma (OS) is the most common bone malignancy in children and adolescents. The 5-year survival rate is only approximately 20% in patients with metastatic and recurrent OS. There is an urgent need to explore novel therapeutic targets to improve the survivorship of OS patients. It has been reported that dysfunction of programmed cell death (PCD) plays an essential role in tumor malignancy. In this study, differentially expressed PCD genes (PCD-DEGs) in OS were identified. Functional enrichment and somatic mutation analysis were performed. Then we established a novel indicator, the cell death index (CDI), to predict therapeutic interventions, immunity responses, and prognosis concerning OS. The expression of PCD genes in osteosarcoma and normal tissues was determined by immunohistochemistry assays. A total of 265 PCD-DEGs were identified in OS, with 141 genes upregulated and 124 genes downregulated. After functional enrichment and somatic mutation analysis, a final PCD-related gene signature, involving the expression levels of CLTCL1, FADS2, and PLEKHF1, demonstrated significant predictive value. A nomogram including clinical characteristics and CDI was developed, which was verified to perform well. Further investigation showed CDI was strongly correlated with immunomodulators, tumor microenvironment, and drug sensitivity in OS. Immunohistochemistry assays illustrated that FADS2, CLTCL1, and PLEKHF1 were suppressed in OS tissues. Further experiments demonstrated that FADS2 inhibits migration and invasion of osteosarcoma cells, while FADS2 induces ferroptosis collaborating with Erastin in osteosarcoma cells. In conclusion, the PCD-related gene signature proposed in this study is a practical prognostic predictor for OS patients, which can make a notable difference in the assessment of clinical outcomes. - Source: PubMed
Publication date: 2025/07/01
Bai GuannanZhao ShaoboChen LushanZhao ManliChen Wenhao - Ankylosing spondylitis (AS) is a chronic autoimmune disease that primarily affects the axial joints. Immune cells play a key role in the pathogenesis of AS. This study integrated bioinformatics methods with experimental validation to explore the role of natural killer (NK) cells in AS. - Source: PubMed
Publication date: 2025/01/24
Chen YulingLi YanXu YuanLv QingYe YuanchunGu Jieruo