APOL1
- Known as:
- APOL1
- Catalog number:
- Y214068
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- APOL1
Related genes to: APOL1
- Gene:
- APOL1 NIH gene
- Name:
- apolipoprotein L1
- Previous symbol:
- APOL
- Synonyms:
- -
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-03
- Date modifiied:
- 2019-04-23
Related products to: APOL1
Related articles to: APOL1
- End-stage renal disease exhibits a disproportionate prevalence among Black individuals and older adults within the United States and worldwide. A significant genetic contributor to this disparity is the Apolipoprotein L1 (APOL1) gene, found exclusively in populations of African ancestry. We aim to perform a narrative review regarding the current understanding of APOL1 and its complex role in kidney disease pathogenesis. The G1 and G2 APOL1 risk alleles are strongly associated with an elevated risk for non-diabetic chronic kidney disease (CKD), including hypertensive nephropathy, focal segmental glomerulosclerosis, and HIV-associated nephropathy, in individuals who are homozygous or compound heterozygous for these variants. While 10-15% of African Americans carry two APOL1 risk alleles, approximately 80% remain disease-free, suggesting incomplete penetrance and the involvement of additional risk factors. In this condition, renal damage could be induced through different mechanisms such as altered cellular ion transport, mitochondrial dysfunction, and the requirement for additional stressors or "second hits". The increased susceptibility to end-stage renal disease (ESRD) in individuals of African ancestry is influenced by variations in the APOL1 gene. - Source: PubMed
Publication date: 2026/02/28
Szyferman Alanis YaelKleppe SoledadCristiano FabrizioConde-Manotas Juan CCadena-Bonfanti AndrésAroca-Martinez GustavoMusso Carlos G - Genetic testing is increasingly used in the evaluation of kidney transplant (KT) candidates, yet its direct association with transplant-related outcomes remains unclear. This study assessed whether genetic test results are associated with key steps in the KT process. - Source: PubMed
Publication date: 2026/04/17
Caliskan YasarElsurer Afsar RenginAbu Al Rub FadeeRabideau KateDeLonais-Parker AvaTruong DzuyBastani BaharNazzal MustafaRandall HenryVarma ChintalapatiAfsar BarisLentine Krista L - Kidney organoids have emerged as powerful in vitro models for investigating normal kidney physiology, disease development, and drug screening, offering unique advantages over traditional cell culture and animal-based systems. By recapitulating glomerular podocyte-like structures, these models have provided unique opportunities to study the pathophysiology of podocytopathies. While prior reviews have summarized novel applications of kidney organoids to kidney disease research in general, these have largely focused on renal tubular physiology and injury mechanisms, for which a greater body of data currently exists. In this review, however, we solely consider kidney organoid-based studies to date that have modeled diverse forms of podocyte injury. We first discuss investigations of drug-induced podocyte injury via kidney organoids, with consideration of their potential future role as high-throughput platforms for preclinical drug screening. We then examine how organoids have furthered research into the genetics of kidney disease, particularly monogenic forms of focal segmental glomerulosclerosis (FSGS) and collagenopathies, and their potential use to assess variants of uncertain significance and mutation-specific therapeutic responses. We additionally highlight how organoid systems have been employed to model complex glomerular disorders, including APOL1-mediated kidney disease, virus-induced podocyte injury, diabetic nephropathy, and podocyte senescence. We further consider the application of kidney organoids to the study of autoantibody-mediated podocytopathies, an area of emerging research. Finally, we provide an overall critique of the strengths and limitations of kidney organoids models specifically in the context of podocytopathy research, emphasizing unmet research needs and opportunities to enhance their fidelity, maturity, and functional integration as precision medicine tools. - Source: PubMed
Publication date: 2026/04/21
de Cos MarinaZeghal MonaMeliambro Kristin - Living donors of African ancestry have the highest risk of post-donation kidney disease. Apolipoprotein L1 (APOL1) risk variants may contribute to this risk. This study evaluated the effectiveness and implementation of our culturally appropriate APOL1 Testing and Counseling Program to reduce potential donors' decisional conflict for donation. - Source: PubMed
Publication date: 2026/04/20
Gordon Elisa JGacki-Smith JessicaSmith Justin DWicklund CatherineDuquette DebraMuhammad Lutfiyya NDong SiyuanYevugah BrightAnderson GriffinFriedewald JohnGilbert AlexanderTandon DariusBurgess-Bishop JacquelineFox MonicaShuck MarionBinion Phalese ACrawford VeatriceColeman CalmettaHoward JoannAgrawal Akansha - Individuals of African ancestry carrying APOL1 (apolipoprotein L1) high-risk genotypes face a markedly increased risk of kidney failure, yet tools to identify those individuals likely to progress to chronic kidney disease are lacking. Here we profiled plasma proteomes of 851 Penn Medicine BioBank participants of African ancestry (285 males and 566 females) with APOL1 high-risk genotypes and preserved estimated glomerular filtration rate (eGFR) (≥60 ml min 1.73 m). Using elastic net Cox regression adjusted for age, sex, eGFR and albuminuria, we derived a nine-protein APOL1 Proteomic Risk Score (APRS) that predicts a composite outcome of ≥40% eGFR decline, kidney failure or death. APRS achieved a time-dependent area under the receiver operating characteristic curve (tAUC) of 86.5%, outperforming the Kidney Failure Risk Equation (66.1%) and polygenic risk scores, with 10-year event rates of 62.5% versus 3.3% across risk quintiles. External validation in Atherosclerosis Risk in Communities and UK Biobank cohorts confirmed robust accuracy (tAUC 82-85%) and consistent performance across demographic and clinical subgroups. Plasma levels of APRS component proteins correlated with kidney tissue fibrosis and tubular injury pathways, indicating strong biological plausibility. By enabling early and accurate prediction of disease progression in APOL1 high-risk individuals, APRS bridges the gap between genetic susceptibility and clinical translation. This scalable and biologically informed approach provides a precision medicine framework for early intervention and may accelerate development of APOL1-targeted therapies to reduce kidney disease disparities. - Source: PubMed
Publication date: 2026/04/15
Li ChenyuRichards Shola MQuinn GhazalAbedini AminZhu MinyanVerma TanyaMohandes SamerPitts RebeccaBarros VesnaQiu XiaziShin TaehwanLoureiro Joseph JFinkel NancySurapaneni AdityaCoresh JosefGrams Morgan EKarihaloo AnilLi HongzheVerma AnuragRitchie MarylynRader Daniel J Dietrich William FJennings Lori LSusztak Katalin