Ask about this productRelated genes to: APOLD1 Blocking Peptide
- Gene:
- APOLD1 NIH gene
- Name:
- apolipoprotein L domain containing 1
- Previous symbol:
- -
- Synonyms:
- FLJ25138, DKFZP434F0318
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-23
- Date modifiied:
- 2016-10-05
Related products to: APOLD1 Blocking Peptide
Related articles to: APOLD1 Blocking Peptide
- The egg laying process of poultry is determined by follicular development. In the present study, hens with lower egg production rates had significantly fewer small white follicles than those with higher rates. In order to investigate the regulatory mechanisms governing the development from white follicles to yellow follicles, transcriptome sequencing was performed on small white follicles (SWFs), small yellow follicles (SYFs) and F6 (the smallest hierarchical follicles) of high-yield laying hens. Pathways enrichment analysis revealed that the vascular endothelial growth factor (VEGF) signaling, peroxisome proliferator-activated receptor (PPAR) signaling, tight junction and gap junction pathways, as well as steroid hormone biosynthesis were involved in follicular development. Compared with the transition from SYFs to F6, the transition from SWFs to SYFs showed more pronounced changes in gene expression profiles. This was validated by Western blot analysis, which revealed significantly upregulated expression of angiogenesis-related proteins (VEGF, VEGFR1, VEGFR2, ANGPT1 and ANGPT2) and downregulated expression of pigment epithelium derived factor (PEDF) in SYFs compared to SWFs. Immunofluorescence staining (IF) confirmed a markedly higher CD31-positive staining area in the theca layer of SYFs than in that of SWFs. Meanwhile, the estradiol (E) and progesterone (P) levels in SYFs increased by 131.6% and 22.2%, respectively, compared to SWFs. At the transcript level, SYFs exhibited upregulation of apolipoprotein D (ApoD), apolipoprotein A1 (APOA1), apolipoprotein L (APOLD1), PPAR and very low-density apolipoprotein (VLDL) mRNA, alongside downregulation of occludin, which was further confirmed by increased VLDLR and PPAR-γ protein abundance and decreased occludin levels. In summary, our results revealed that the SWFs to SYFs transition proceeds with pronounced changes in transcriptional profiles associated with angiogenesis, sex steroid biosynthesis and yolk deposition. The increased steroid hormone production likely enhances the capacity for yolk synthesis. Furthermore, the elevated vascularization in the theca layer of SYFs in coupled with a reduction in tight junctions may facilitate the transport of yolk precursors to access the follicles. - Source: PubMed
Publication date: 2026/05/01
Ma YanfenZhou ShuoMi YulingZhang Caiqiao - Psychedelics such as psilocybin are known for their hallucinogenic properties and have also been reported to produce long-lasting therapeutic effects in depression and possibly also other psychiatric disorders. Several lines of evidence suggest that psilocybin exerts its effects through activation of 5-HT2A receptors located postsynaptically to serotonergic neurons, e.g., in the frontal cortex, parts of the limbic system, including the amygdala and hippocampus, and striatum. The present study was conducted to shed further light on psilocybin-induced changes in gene expression. - Source: PubMed
Publication date: 2026/04/10
Veysi AshkanAtanasovski DanielaArdalan MaryamMotamed NasrinEriksson Elias - Apolipoproteins (APOs) are essentially structural and functional components of lipoproteins, which are composed of 22 members and their effects on certain types of cancer have been studied. However, their roles in endometrial cancer (EC), which is one of the most common malignant tumors in gynecology were unclear and rarely investigated. - Source: PubMed
Publication date: 2026/02/16
Zhou LinaWang RenchengDu GuiqiangWu YupengLi HuiHe YinyanYe ZhikangXiang Jiangdong - Renal cell carcinoma (RCC) is a common and deadly urological cancer, for which there are no robust prognostic biomarkers or personalized treatment strategies. Paraptosis, a distinct form of regulated cell death marked by cytoplasmic vacuolization, is being increasingly recognized for its roles in tumorigenesis and therapy responses, yet its functional implications in RCC remain poorly defined. Transcriptomic profiles and corresponding clinical metadata from the TCGA-KIRC and GSE33371 datasets were systematically analyzed to characterize the paraptosis-related gene (PaRG) expression profile in renal cell carcinoma (RCC). Patients were categorized into two subtypes via consensus clustering, 574 overlapping differentially expressed genes (DEGs) were identified, and a four-gene (COL7A1, RNASE2, SLC10A2, and APOLD1) prognostic signature was constructed using LASSO and multivariate Cox regression. We analyzed the signature's associations with tumor microenvironment (TME) features, cancer stem cell (CSC) indices, and tumor mutation burden (TMB), and validated the expression of the signature genes in RCC cell lines via qRT-PCR and Western blot. The four-gene signature showed robust prognostic performance (1-, 3-, and 5-year AUC: 0.751, 0.735, and 0.733 in the total cohort; 0.735, 0.731, and 0.767 in the training cohort), with high-risk patients having significantly poorer overall survival than the low-risk group. The low-risk group exhibited higher Stromal, Immune, and ESTIMATE scores (enriched immune/stromal infiltration), while the high-risk group had elevated CSC content and TMB, and the signature correlated with differential sensitivity to multiple chemotherapeutics. Both qRT-PCR and Western blot confirmed upregulation of COL7A1 and RNASE2 and downregulation of SLC10A2 and APOLD1 in RCC cell lines. Our study establishes a paraptosis-based two-subtype classification and four-gene prognostic signature for RCC that can reliably predicting patient survival, delineate TME characteristics, and guide personalized therapy, with COL7A1 emerging as a potential therapeutic target for advancing our understanding of paraptosis in RCC pathogenesis and optimizing treatment. - Source: PubMed
Publication date: 2026/02/23
Qin MengyuanChen MeitingGan YulingFeng XiangqianHuang PingMeng FeifeiYang Yufang - The mammalian Apolipoprotein-L families (APOLs) contain several isoforms of membrane-interacting proteins, some of which are involved in the control of membrane dynamics (traffic, fission and fusion). Specifically, human APOL1 and APOL3 appear to control membrane remodeling linked to pathogen infection. Through its association with Non-Muscular Myosin-2A (NM2A), APOL1 controls Golgi-derived trafficking of vesicles carrying the lipid scramblase Autophagy-9A (ATG9A). These vesicles deliver APOL3 together with phosphatidylinositol-4-kinase-B (PI4KB) and activated Stimulator of Interferon Genes (STING) to mitochondrion-endoplasmic reticulum (ER) contact sites (MERCSs) for the induction and completion of mitophagy and apoptosis. Through direct interactions with PI4KB and PI4KB activity controllers (Neuronal Calcium Sensor-1, or NCS1, Calneuron-1, or CALN1, and ADP-Ribosylation Factor-1, or ARF1), APOL3 controls PI(4)P synthesis. PI(4)P is required for different processes linked to infection-induced inflammation: (i) STING activation at the Golgi and subsequent lysosomal degradation for inflammation termination; (ii) mitochondrion fission at MERCSs for induction of mitophagy and apoptosis; and (iii) phagolysosome formation for antigen processing. In addition, APOL3 governs mitophagosome fusion with endolysosomes for mitophagy completion, and the APOL3-like murine APOL7C is involved in phagosome permeabilization linked to antigen cross-presentation in dendritic cells. Similarly, APOL3 can induce the fusion of intracellular bacterial membranes, and a role in membrane fusion can also be proposed for endothelial APOLd1 and adipocyte mAPOL6, which promote angiogenesis and adipogenesis, respectively, under inflammatory conditions. Thus, different APOL isoforms play distinct roles in membrane remodeling associated with inflammation. - Source: PubMed
Publication date: 2024/12/20
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