Ask about this productRelated genes to: ATP8B2 Blocking Peptide
- Gene:
- ATP8B2 NIH gene
- Name:
- ATPase phospholipid transporting 8B2
- Previous symbol:
- -
- Synonyms:
- ATPID, KIAA1137
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-25
- Date modifiied:
- 2016-06-28
Related products to: ATP8B2 Blocking Peptide
Related articles to: ATP8B2 Blocking Peptide
- Mitophagy is essential for cancer formation and invasion, but its role in colorectal cancer (CRC) remains unclear. We obtained sequencing data and mitophagy-related genes (MP-RGs) from public databases. Differential expression analysis and weighted gene coexpression network analysis (WGCNA) identified mitophagy-related differentially expressed genes (DE-MPGs). Mendelian randomization (MR) analysis identified candidate genes with genetically supported causal relevance to CRC. Biomarkers were identified using machine learning, receiver operating characteristic (ROC) analysis and expression studies. Single-cell RNA sequencing (scRNA-seq) analyzed biomarker expression profiles in various CRC cell types. Quantitative PCR (qPCR) validated biomarker expression in clinical CRC samples. 147 DE-MPGs were identified. MR analysis revealed seven genes with potential causal contributions to CRC susceptibility. Three genes, SGCE (IVW: OR = 1.00041, p = 0.011), ATP8B2 (IVW: OR = 0.99920, p = 0.042), and RANGAP1 (IVW: OR = 0.99861, p = 0.002), were selected as biomarkers. Immune microenvironment and checkpoint differences were observed between CRC and controls. Biomarker expression varied among cell types. qPCR showed decreased SGCE and ATP8B2 and increased RANGAP1 in CRC. SGCE, ATP8B2, and RANGAP1 can serve as mitophagy-related biomarkers with genetically supported causal relevance to CRC, providing new insights for CRC diagnosis and therapy. - Source: PubMed
Zhao JingyiKong MengWang SiningCao ZhixinTian Xiangguo - Glaucoma, the leading cause of irreversible blindness worldwide, is characterized by elevated intraocular pressure (IOP) resulting from impaired aqueous humor (AH) outflow through the trabecular meshwork (TM). We demonstrate altered phospholipids (PLs) levels and increased activity of the interconversion enzyme phosphatidylserine decarboxylase (PSD) in the TM of individuals with primary open-angle glaucoma. Elevating PSD alone is sufficient to raise IOP in normotensive mice, whereas depleting PSD restores IOP in glaucomatous mice. Although certain PL classes are generally altered in glaucoma, specific PLs with minor structural variations within those classes exhibit variability in their levels in TM and AH, indicating a potential lipid transport abnormality. We identified a distinct set of ocular lipid species altered in glaucoma, implicating alterations in the levels and functionality of the lipid transporter ATP8B2. This flippase alone, however, does not seem to affect IOP but appears to amplify the effects of PSD. - Source: PubMed
Edwards GeneaKaur RuminderMueller AnnaZiebarth NoëlLee Richard KBhattacharya Sanjoy K - A previous study of 200,000 exome-sequenced UK Biobank participants investigating the association between rare coding variants and BMI had implicated two genes, MC4R and PCSK1, at exome-wide significance. In addition, further 66 genes were significant with an uncorrected p value of <0.001. - Source: PubMed
Publication date: 2025/11/19
Curtis David - Atherosclerosis, a major cause of global mortality, involves the transformation of macrophages into foam cells, which is a key pathological process. This study aims to elucidate the molecular mechanisms that contribute to foam cell formation and the progression of atherosclerosis. - Source: PubMed
Publication date: 2025/05/22
Bu RuiZhao WeihaoLiang Rui - Our study aims to screen and explore the potential molecular mechanisms of atherosclerosis using a comprehensive research approach combining bioinformatics analysis and molecular biology experiments. Bioinformatics analyses were conducted to screen for key genes with significantly differential expression in atherosclerosis. Subsequently, macrophages and foam cells induced from THP-1 cells were utilized to validate the function of these key genes through siRNA knockdown. Molecular biology experiments encompassed reverse transcription polymerase chain reaction (RT-PCR), Western Blotting, immunofluorescence staining, and JC-1 probe detection of mitochondrial membrane potential. ATP8B2, encoding a P4-ATPase, was significantly downregulated in both plaque tissues and circulating macrophages of atherosclerosis patients. This enzyme influences membrane fusion and other dynamic processes by affecting the asymmetric distribution of phospholipids within the bilayer. Knockdown of ATP8B2 expression significantly inhibited autophagic flux in macrophages, manifested by abnormal accumulation of LC3-II and p62 protein levels. Furthermore, downregulation of ATP8B2 expression significantly inhibited the degradation of oxidized low-density lipoprotein (ox-LDL) by macrophages. Simultaneously, reduced ATP8B2 expression led to decreased mitochondrial membrane potential and mitochondrial dysfunction. Our study unveils for the first time the crucial role of ATP8B2 in atherosclerosis, particularly in maintaining autophagic flux, promoting ox-LDL degradation, and sustaining mitochondrial homeostasis. - Source: PubMed
Publication date: 2025/03/28
Miao XiaodongPan RuiChang Fei