Ask about this productRelated genes to: APOL2 Blocking Peptide
- Gene:
- APOL2 NIH gene
- Name:
- apolipoprotein L2
- Previous symbol:
- -
- Synonyms:
- APOL-II
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-29
- Date modifiied:
- 2015-12-15
Related products to: APOL2 Blocking Peptide
Related articles to: APOL2 Blocking Peptide
- Apolipoproteins L (APOLs) are membrane-associated proteins involved in both resistance to pathogens, such as APOL1-mediated killing of African trypanosomes or APOL3-mediated lysis of intracellular bacteria, and induction of diseases, like APOL1-mediated nephropathy or APOL2-mediated liver fibrosis. Accumulating evidence points to APOLs controlling membrane dynamics linked to immunity. APOL1 and APOL3 are induced by inflammatory signalling and play key roles in the initiation and termination of inflammation by promoting the traffic of Golgi-derived membranes involved in STING activation, as well as mitochondrial membrane fission and fusion involved in auto/mitophagy. APOL2, or murine mAPOL8, is required for profibrotic vesicle exocytosis, whereas mAPOL9 triggers bacterial membrane budding linked to gut immunity control. In dendritic cells, APOL3 or the APOL3-like mAPOL7C promote megapore formation in phagosomal membranes, allowing antigen cross-presentation and apoptosis, both probably linked to cardiolipin solubilization. In adipocytes, mAPOL6 controls inflammation-linked lipid droplets dynamics. Through their membrane-remodeling activities, APOLs participate in the control of infection by bacteria, viruses, and parasites. Thus, natural APOLs mutations represent inborn errors of immunity. - Source: PubMed
Publication date: 2026/03/19
Pays Etienne - Epigenetic modification of the APOL1 gene carrying risk alleles (G1 and G2) may represent a therapeutic strategy for APOL1-related kidney diseases. However, DNA methylation changes associated with APOL1 have not been thoroughly characterized. - Source: PubMed
Publication date: 2026/05/20
Li YangBozack AnneSchlosser PascalRhee Eugene PSurapaneni AdityaWaterhölter AlexRodriguez-Hernandez ZulemaRuggles Kelly VCoresh JosefGrams Morgan E - Homozygosity of two sequence variants within the human gene, called and , in combination with high Apolipoprotein L1 (APOL1) expression levels are linked to a wide spectrum of renal diseases summarized as APOL1-mediated kidney diseases (AMKDs). Previous studies have shown that inflammatory and immunomodulatory triggers are major contributors to elevated APOL1 protein expression. However, little is known about the stability of APOL1 and the role of protein degradation in regulating its intracellular levels. In this study, we systematically investigated these aspects. To investigate degradation dynamics, we used stable HEK293T cell lines with inducible overexpression of GFP-tagged APOL1 vA/G0, its C-terminal risk variants (G1, G2), N-terminal isoforms (vB1, vB3, vC), as well as the deletion mutant (ΔN59), APOL2, and an APOL1–APOL2 chimeric protein (NT-APOL2). Degradation and protein biosynthesis were modified using proteasome inhibitors and cycloheximide, respectively. Treated cells were analyzed using Western blotting, immunofluorescence microscopy and flow cytometry analyses. Moreover, analyses were performed to identify motifs within the APOL1 sequence potentially mediating its degradation. This study shows that APOL1 is subject to remarkably rapid proteasomal degradation, observed for both the APOL1 wildtype (G0) and renal risk variants (RRVs) G1 and G2. Moreover, despite distinct topologies at the intracellular membranes of the APOL1 isoforms, all exhibit rapid protein degradation. In contrast, APOL2 – the closest homolog of APOL1 – demonstrated significantly greater resistance to proteasomal degradation. analyses identified two intrinsically disordered regions (IDRs) present in APOL1 but absent in APOL2, potentially underlying the increased susceptibility to degradation. Notably, APOL1 surface-localized pools were resistant to rapid proteasomal degradation, with no major differences observed between G0 and RRVs. Together our findings suggest that APOL1 stability is highly compartment-specific, with rapid degradation at intracellular pools and pronounced stability at the cell surface. Targeting the stability of APOL1 at the PM represents a promising avenue for the development of novel therapeutic interventions against AMKD. - Source: PubMed
Publication date: 2026/02/16
Höffken VerenaAlvermann LauraNiggemeier DavidBeul KatrinNedvetsky PavelEllinger BernhardAssenmacher DariaGranado DanielPavenstädt HermannWeide Thomas - Psoriasis is a chronic immune-mediated skin disease driven by the interleukin-23/interleukin-17 cytokine axis, yet its immunopathogenesis remains incompletely understood. Housekeeping genes, traditionally considered stably expressed across tissues and cell types, have not been systematically investigated for their role in psoriasis. Here, we aimed to identify psoriasis-associated housekeeping genes and explore their molecular mechanisms and clinical implications. - Source: PubMed
Publication date: 2025/09/01
Tang HaoWang JiachengZhang ShuhaoFeng GuanglongCheng XiangshuMeng XinChen RuiWang JiaqiJiang YongshuaiZhang RuijieLv Wenhua - Radiotherapy is one of the most important adjuvant treatment methods for gastric cancer (GC). However, radioresistance remains a major clinical obstacle. In this study, APOL2 is identified as a key player in promoting non-homologous end joining (NHEJ)-mediated double-strand break (DSB) repair and enhancing radioresistance in GC. Bioinformatics and clinical data revealed that high APOL2 expression is correlated with poor prognosis in GC patients. Functional experiments showed that APOL2 overexpression enhances genomic stability by accelerating DSB repair via the NHEJ pathway, while APOL2 knockout impairs repair capacity. Mechanistically, APOL2 binds to and stabilizes Ku80 by enhancing USP7-mediated deubiquitylation, thereby increasing Ku80 protein levels to promote NHEJ repair, ultimately conferring radioresistance. Moreover, high-throughput screening identified formononetin (FN) as a small molecule capable of disrupting the APOL2-Ku80 interaction, thereby restoring radiosensitivity in GC cells. Our findings underscore the role of APOL2 in mediating radioresistance through Ku80 stabilization and highlight FN as a potential therapeutic agent to counteract radioresistance in GC treatment. - Source: PubMed
Publication date: 2025/09/15
Zu DanBao QimeiHe HanyiZhong YukeDeng MingcongHu YangchanZhang ChunkaiLiang ChenHuang YixingLiu HaidongLi XiaoHe YanhuaLuo GuoyanWu WeixinGuan FenghuiXu ShengfengLiu MinBacolla AlbinoJing JiDu YianTainer John AShi YinYe ZuCheng Xiangdong