The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Innate immunity pathways regulate the nephropathy gene Apolipoprotein L1
Open accessAbstract
Apolipoprotein L1 (APOL1) risk variants greatly elevate the risk of kidney disease in African Americans. Here we report a cohort of patients who developed collapsing focal segmental glomerulosclerosis while receiving therapeutic interferon, all of whom carried the APOL1 high-risk genotype. This finding raised the possibility that interferons and the molecular pattern recognition receptors that stimulate interferon production may contribute to APOL1-associated kidney disease. In cell culture, interferons and toll-like receptor agonists increased APOL1 expression by up to 200-fold, in some cases with the appearance of transcripts not detected under basal conditions. PolyI:C, a double-stranded RNA TLR3 agonist, increased APOL1 expression by upregulating interferons directly or through an interferon-independent, IRF-3 dependent pathway. Using pharmacological inhibitors, shRNA knockdown, and chromatin immunoprecipitation, we found that the interferon-independent TLR3 pathway relied on signaling through TBK1, NF-kB, and Jak kinases, and on binding of IRF1, IRF2, and STAT2 at the APOL1 transcription start site. We also demonstrate that overexpression of the APOL1 risk variants is more injurious to cells than overexpression of the wild-type APOL1 protein. Our study illustrates that anti-viral pathways may be an important inducer of kidney disease in individuals with the APOL1 high-risk genotype and identifies potential targets for prevention or treatment.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors
Kawai, T., & Akira, S. (2010) · Nature Immunology · doi:10.1038/ni.1863 · Cited by 9,304
Association of Trypanolytic ApoL1 Variants with Kidney Disease in African Americans
Genovese, G., Friedman, D. J., Ross, M. D., Lecordier, L., Uzureau, P., Freedman, B. I., Bowden, D. W., Langefeld, C. D., Oleksyk, T. K., Uscinski Knob, A. L., et al. (2010) · Science · doi:10.1126/science.1193032 · Cited by 2,028
Self-citationAPOL1 Genetic Variants in Focal Segmental Glomerulosclerosis and HIV-Associated Nephropathy
Kopp, J. B., Nelson, G. W., Sampath, K., Johnson, R. C., Genovese, G., An, P., Friedman, D., Briggs, W., Dart, R., Korbet, S., et al. (2011) · Journal of the American Society of Nephrology · doi:10.1681/asn.2011040388 · Cited by 855
Self-citationPeroxisomes Are Signaling Platforms for Antiviral Innate Immunity
Dixit, E., Boulant, S., Zhang, Y., Lee, A. S. Y., Odendall, C., Shum, B., Hacohen, N., Chen, Z. J., Whelan, S. P., Fransen, M., et al. (2010) · Cell · doi:10.1016/j.cell.2010.04.018 · Cited by 817
ENCODE Data in the UCSC Genome Browser: year 5 update
Rosenbloom, K. R., Sloan, C. A., Malladi, V. S., Dreszer, T. R., Learned, K., Kirkup, V. M., Wong, M. C., Maddren, M., Fang, R., Heitner, S. G., et al. (2012) · Nucleic Acids Research · doi:10.1093/nar/gks1172 · Cited by 766
Tzur, S., Rosset, S., Shemer, R., Yudkovsky, G., Selig, S., Tarekegn, A., Bekele, E., Bradman, N., Wasser, W. G., Behar, D. M., et al. (2010) · Human Genetics · doi:10.1007/s00439-010-0861-0 · Cited by 653
A Physical and Regulatory Map of Host-Influenza Interactions Reveals Pathways in H1N1 Infection
Shapira, S. D., Gat-Viks, I., Shum, B. O. V., Dricot, A., de Grace, M. M., Wu, L., Gupta, P. B., Hao, T., Silver, S. J., Root, D. E., et al. (2009) · Cell · doi:10.1016/j.cell.2009.12.018 · Cited by 635
Apolipoprotein L-I is the trypanosome lytic factor of human serum
Vanhamme, L., Paturiaux-Hanocq, F., Poelvoorde, P., Nolan, D. P., Lins, L., Van Den Abbeele, J., Pays, A., Tebabi, P., Van Xong, H., Jacquet, A., et al. (2003) · Nature · doi:10.1038/nature01461 · Cited by 500
Reilly, S. M., Chiang, S.-H., Decker, S. J., Chang, L., Uhm, M., Larsen, M. J., Rubin, J. R., Mowers, J., White, N. M., Hochberg, I., et al. (2013) · Nature Medicine · doi:10.1038/nm.3082 · Cited by 433
Clark, K., Plater, L., Peggie, M., & Cohen, P. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.000414 · Cited by 385
Cited by
Focal Segmental Glomerulosclerosis
Rosenberg, A. Z., & Kopp, J. B. (2017) · Clinical Journal of the American Society of Nephrology · doi:10.2215/cjn.05960616 · Cited by 562
Self-citationTransgenic expression of human APOL1 risk variants in podocytes induces kidney disease in mice
Beckerman, P., Bi-Karchin, J., Park, A. S. D., Qiu, C., Dummer, P. D., Soomro, I., Boustany-Kari, C. M., Pullen, S. S., Miner, J. H., Hu, C.-A. A., et al. (2017) · Nature Medicine · doi:10.1038/nm.4287 · Cited by 344
Self-citationCross-validation of SARS-CoV-2 responses in kidney organoids and clinical populations
Helms, L., Marchiano, S., Stanaway, I. B., Hsiang, T.-Y., Juliar, B. A., Saini, S., Zhao, Y. T., Khanna, A., Menon, R., Alakwaa, F., et al. (2021) · JCI Insight · doi:10.1172/jci.insight.154882 · Cited by 47
Metadata
- Authors
- Nichols, B., Jog, P., Lee, J. H., Blackler, D., Wilmot, M., D'Agati, V., Markowitz, G., Kopp, J. B., Alper, S. L., Pollak, M. R., & Friedman, D. J.
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 87
- Issue
- 2
- Pages
- 332-342
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2092001580
- Cited by
- 355
- References
- 30
- FWCI
- 18.31
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Innate immunity pathways regulate the nephropathy gene Apolipoprotein L1. https://app.cochat.ai/papers/10.1038/ki.2014.270
- The paper
- Nichols, B., Jog, P., Lee, J. H., Blackler, D., Wilmot, M., D'Agati, V., Markowitz, G., Kopp, J. B., Alper, S. L., Pollak, M. R., & Friedman, D. J. (2015). Innate immunity pathways regulate the nephropathy gene Apolipoprotein L1. Kidney International. https://doi.org/10.1038/ki.2014.270
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
