Jeremy Nathans

Jeremy Nathans
Born (1958-07-31) July 31, 1958 (age 68)
New York City U.S.
EducationMIT (B.S.), Stanford University (M.D., Ph.D.)
Known forOpsin genes and colour vision, the mechanisms underlying red–green colour blindness, trichromatic mouse models, Brn3/POU4F transcription factors, Wnt receptor discovery, planar cell polarity, Norrin/Frizzled4 signaling, retinal disease genetics, and CNS vascular biology.
AwardsWorld Laureate Association Prize in Life Science or Medicine (2024); Nemmers Prize in Medical Science (2022); Benjamin Franklin Medal in the Life Science (2020); Helen Keller Prize in Vision Research (2019); member, National Academy of Medicine (2011); Edward Scolnick Prize in Neuroscience (2009); Champalimaud Award for Vision Research (2008); member, National Academy of Sciences (1996)
Scientific career
FieldsMolecular biology and genetics; neuroscience; ophthalmology
WorkplacesJohns Hopkins University
David Hogness
Websitenathanslab.mbg.jhmi.edu

Jeremy Nathans (born July 31, 1958) is a professor of molecular biology and genetics at the Johns Hopkins University School of Medicine. From 1988 to 2026, he was an investigator of the Howard Hughes Medical Institute. He is a member of the National Academy of Sciences and the National Academy of Medicine.

Nathans is known for isolating and characterising the opsin genes that encode the human short-wave (blue), medium-wave (green), and long-wave (red) color vision receptors, work that revealed the molecular genetic basis for trichromatic color vision and for inherited variation in red-green color vision. His subsequent research identified the molecular mechanisms of blue cone monochromacy and tritanopia (loss of short-wave sensitivity), the locus control region that governs mutually exclusive cone opsin expression, and the molecular mechanisms of several inherited retinal diseases, including Stargardt disease and vitelliform macular dystrophy. His laboratory also discovered the Frizzled family of Wnt receptors and the Norrin/Frizzled4 signaling pathway, which functions as an essential regulator of the blood-retina barrier. This work has led to a clinical-stage drug candidate for diabetic macular edema.

As of 2026, Nathans’ published work has been cited more than 47,000 times on Google Scholar, with an h-index of 108.

Personal life

Nathans was born on July 31, 1958, in New York City. He is married to Thanh Huynh. They have two children, Riva (born 1988) and Rosalie (born 1994).

Education

Nathans received a B.S. in Life Sciences and a B.S. in Chemistry from the Massachusetts Institute of Technology in 1979. He earned a Ph.D. in Biochemistry from Stanford University School of Medicine in 1985, working in the laboratory of David Hogness, and an M.D. from Stanford in 1987. He was a postdoctoral fellow at Genentech with Axel Ullrich in 1987.

Career

Nathans joined the Johns Hopkins University School of Medicine in 1988 as an Assistant Professor. He has been a Full Professor in the Departments of Molecular Biology and Genetics, Neuroscience, and Ophthalmology since 1996, and he was an HHMI Investigator from 1988 to 2026 From 2019 to 2023, Nathans served as Interim Director of the Department of Molecular Biology and Genetics at Johns Hopkins. He has held the Samuel Theobald Professorship in Ophthalmology at the Wilmer Eye Institute since 2015.

Research

Color vision and opsin genes

As an MD-PhD student at Stanford Medical School, Nathans isolated and sequenced the human genes encoding the short-wave (blue), medium-wave (green), and long-wave (red) cone opsins, the protein components (opsins) of the light receptors in the human retina that mediate trichromatic color vision. This work revealed the first sequences of genes coding for G-protein-coupled receptors (GPCRs) and the first sequences of eukaryotic sensory receptors. GPCRs are the targets of a large fraction of approved drugs, and this work had broad significance for structural biology and pharmacology beyond vision research.

Nathans showed that the middle- and long-wavelength opsin genes sit in a head-to-tail tandem array on the X chromosome. He further showed that meiotic recombination between these highly similar genes produces hybrid genes and copy-number changes, which is the molecular mechanism underlying the common variations in red-green color vision that are colloquially referred to as “color blindness”. Nathans and postdoctoral fellow Charles Weitz showed that autosomal dominant tritanopia (loss of short-wave sensitivity) is caused by amino acid substitution mutations in the short-wave opsin gene. Nathans and graduate student Shannath Merbs produced the human cone pigments in transfected cells and determined the absorbance spectra of the normal versions of each pigment and the common variants underlying anomalous red-green color vision. Variant long- and medium-wave cone pigment absorbance spectra were also measured in the living human eye using a psychophysical color matching test.

Nathans and graduate student Yanshu Wang discovered a locus control region (LCR) adjacent to the red and green opsin genes. The LCR stochastically activates only one of these two genes per cone cell, explaining the mutually exclusive expression that allows each red or green cone to express only a single opsin.

With Gerald Jacobs and Markus Meister, Nathans genetically engineered mice, which are normally dichromatic, to express a human cone opsin gene. The resulting knock-in mice demonstrated trichromatic color vision, showing that the mammalian brain can extract information from a novel sensory input.

Retinal disease mechanisms

The Nathans laboratory defined the molecular and biochemical basis of several common inherited retinal diseases. Nathans and graduate student Hui Sun showed that the Stargardt disease gene (ABCA4, also known as ABCR) encodes an ATP-dependent transporter protein required for retinoid recycling between photoreceptors and the retinal pigment epithelium.

Nathans and Sun, in collaboration with King-Wai Yau and Takashi Tsunenari, discovered that the bestrophin protein encoded by the vitelliform macular dystrophy (VMD) gene is the founding member of a new family of anion channels and that disease-causing mutations block channel function.

Nathans and postdoctoral fellow Ching-Hwa Sung showed that the most common form of autosomal dominant retinitis pigmentosa is caused by rhodopsin gene mutations that impair protein folding, stability, or transport to the photoreceptor outer segment, leading to apoptotic photoreceptor death.

Transcription factors that control neural development in the visual, auditory, and somatosensory systems

Nathans and postdoctoral fellow Menqing Xiang identified the three members of the BRN3/POUF4 family of transcription factors and showed that they function as essential regulators of dorsal root and trigeminal ganglion neurons (BRN3A/POU4F1), retinal ganglion cells (BRN3B/POU4F2), and inner ear auditory and vestibular hair cells (BRN3C/POU4F3). This work revealed a surprising molecular kinship between these diverse sensory systems. As shown by Nathans’ postdoctoral fellow Tudor Badea, the presence of BRN3B and BRN3C in subsets of retinal ganglion cells and of BRN3A and BRN3C in subsets of dorsal root and trigeminal ganglion neurons further cements these evolutionary relationships.

Wnt signaling and Frizzled receptors

The Nathans laboratory discovered the Frizzled family of cell surface receptors in vertebrates and showed, in a collaboration with the laboratory of Roel Nusse, that Frizzled proteins are the principal receptors for Wnt ligands. The Nathans group has defined the in vivo roles of Frizzled receptors in the central nervous system, skin, heart, and vasculature. A striking conclusion from these experiments was that two of ten Frizzled receptors (FZD3 and FZD6) are devoted to polarity signaling, including the control of hair patterning in the skin and the orientation of sensory structures in inner ear hair cells.

Vascular biology and clinical translation

The Nathans laboratory identified the Norrin/Frizzled4 signaling pathway, which activates the canonical Wnt pathway to control retinal vascular development and maintain the blood-retina barrier (BRB). Disruptions in this pathway are associated with Norrie disease and familial exudative vitreoretinopathy. In vascular endothelial cells in the brain and spinal cord, the same canonical Wnt signal is also communicated via a pair of WNT ligands (WNT7A and WNT7B). Yulian Zhou and Chris Cho, graduate students in the Nathans laboratory, showed that signaling by these two WNT ligands requires a pair of cell surface proteins, RECK and GPR124, in addition to a Frizzled receptor and an LRP5 or LRP6 co-receptor. The Nathans laboratory has shown that, in the context of blood-brain barrier (BBB) development and maintenance, the Norrin and WNT7A/WNT7B systems are partially redundant. Recent work in the Nathans laboratory has focused on the gene expression program for the BBB and the BRB.

Discoveries from the Norrin/Frizzled4/Wnt7a/Wnt7b/Gpr124/Reck signaling work have led to therapeutic development. Restoret (MK-3000, formerly EYE103), an antibody-based Norrin mimic developed by EyeBio (now part of Merck), entered a Phase 2b/3 clinical trial (BRUNELLO) for diabetic macular edema in 2024.

Technology development

The Nathans laboratory has developed diverse research technologies, including ultra-sparse genetically-directed neuronal labeling methods for visualizing cell morphology, dual-colour X-chromosome reporter systems, eye movement testing techniques for assessing central nervous system drug effects in mice, cell-type-specific epigenome analysis methods, and genome-wide approaches for discovering protein-protein interactions.

Lab organization and mentorship

The Nathans laboratory has operated with a mixture of predoctoral and postdoctoral researchers and highly skilled staff scientists.  The latter category included Yanshu Wang, Amir Rattner, Philip Smallwood, John Williams, Jennifer Macke, and Zhongming Li. Former Nathans lab trainees have gone on to faculty or staff scientist positions at Merck, Genentech, GlaxoSmithKline, C4 Therapeutics, SciClone Pharmaceuticals, Meta, the Food and Drug Administration, Janelia Research Campus (HHMI), Massachusetts General Hospital, UCSD, UCLA, the National Eye Institute (NIH), Johns Hopkins Medical School, Harvard Medical School, University of Virginia Medical School, Weill-Cornell Medical School, University of Miami Medical School, Sun Yat-Sen University,  George Washington Medical School, Rutgers University, Columbia University Medical School, Nanjing Normal University, University of Wisconsin Medical School, University of Pennsylvania Medical School, Cincinnati Children’s Hospital, and Nationwide Children's Hospital. The Nathans laboratory is noted for a policy of openly sharing research reagents and materials with the broader scientific community.

Professional service and editorial roles

Nathans has served as a Trustee of The Rockefeller University since 2017. He has been an Editorial Board Member of the Proceedings of the National Academy of Sciences since 1999, served on the Board of Reviewing Editors of eLife from 2012 to 2019, and was an Associate Editor of the Journal of Neuroscience from 1991 to 1996.

Nathans has served on scientific advisory boards for Merck Research Laboratories, Novartis, and Cerevance. He currently serves on the scientific advisory boards for the Foundation Fighting Blindness, Atengen, EyeBiotech (a subsidiary of Merck), and the Harrington Discovery Institute. He serves on award committees for the Lasker Prizes (Albert and Mary Lasker Foundation, 2010 to present) and the Passano Award (2004 to present). Nathans chairs the scientific advisory committee of the Klingenstein Fellowship Awards in Neuroscience, and he is a member of the leadership team of the Life Sciences Research Foundation.

Collected letters, essays, biographical notes, and other writings

A collection of Nathans’ writings on a wide variety of topics, titled “Snapshots of a Life in Science: Letters, Essays, Biographical Notes, and Other Writings (1990-2023)”, is freely available as a pdf on the Nathans laboratory website.

Lectures and other educational materials

Nathans has recorded lectures on the brain and retina, and on creativity in science. He has also recorded lectures on color vision and the blood-brain barrier.

Awards and honors

Teaching recognition

Selected publications

References

  1. 1 2 3 "Jeremy Nathans, MD, PhD | Investigator Emeriti | 1987-2026". www.hhmi.org. Retrieved 10 September 2026.
  2. ↑ "Dr. Jeremy Nathans, MD, PhD". profiles.hopkinsmedicine.org. Archived from the original on 20 November 2025. Retrieved 10 September 2026.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 "Jeremy Nathans – Department of Molecular Biology and Genetics". Retrieved 10 September 2026.
  4. 1 2 3 Nathans, J.; Thomas, D.; Hogness, D. S. (11 April 1986). "Molecular genetics of human color vision: the genes encoding blue, green, and red pigments". Science. 232 (4747). New York, N.Y.: 193–202. Bibcode:1986Sci...232..193N. doi:10.1126/science.2937147. ISSN 0036-8075. PMID 2937147.
  5. 1 2 3 Nathans, J.; Piantanida, T.P.; Eddy, R.L.; Shows, T. B.; Hogness, D.S. (1986). "Molecular genetics of inherited variation in human color vision". Science. 232: 203–210. doi:10.1126/science.3485310. PMID 3485310.
  6. ↑ Nathans, J.; Davenport, C. M.; Maumenee, I. H.; Lewis, R. A.; Hejtmancik, J. F.; Litt, M.; Lovrien, E.; Weleber, R.; Bachynski, B.; Zwas, F. (25 August 1989). "Molecular genetics of human blue cone monochromacy". Science. 245 (4920). New York, N.Y.: 831–838. Bibcode:1989Sci...245..831N. doi:10.1126/science.2788922. ISSN 0036-8075. PMID 2788922.
  7. 1 2 Weitz, C. J.; Went, L. N.; Nathans, J. (August 1992). "Human tritanopia associated with a third amino acid substitution in the blue-sensitive visual pigment". American Journal of Human Genetics. 51 (2): 444–446. ISSN 0002-9297. PMC 1682686. PMID 1386496.
  8. 1 2 Wang, Y.; Macke, J. P.; Merbs, S. L.; Zack, D. J.; Klaunberg, B.; Bennett, J.; Gearhart, J.; Nathans, J. (September 1992). "A locus control region adjacent to the human red and green visual pigment genes". Neuron. 9 (3): 429–440. doi:10.1016/0896-6273(92)90181-c. ISSN 0896-6273. PMID 1524826.
  9. 1 2 Sun, H.; Molday, R. S.; Nathans, J. (19 March 1999). "Retinal stimulates ATP hydrolysis by purified and reconstituted ABCR, the photoreceptor-specific ATP-binding cassette transporter responsible for Stargardt disease". The Journal of Biological Chemistry. 274 (12): 8269–8281. doi:10.1074/jbc.274.12.8269. ISSN 0021-9258. PMID 10075733.
  10. 1 2 Sun, Hui; Tsunenari, Takashi; Yau, King-Wai; Nathans, Jeremy (19 March 2002). "The vitelliform macular dystrophy protein defines a new family of chloride channels". Proceedings of the National Academy of Sciences of the United States of America. 99 (6): 4008–4013. Bibcode:2002PNAS...99.4008S. doi:10.1073/pnas.052692999. ISSN 0027-8424. PMC 122639. PMID 11904445.
  11. 1 2 Xu, Qiang; Wang, Yanshu; Dabdoub, Alain; Smallwood, Philip M.; Williams, John; Woods, Chad; Kelley, Matthew W.; Jiang, Li; Tasman, William; Zhang, Kang; Nathans, Jeremy (19 March 2004). "Vascular development in the retina and inner ear: control by Norrin and Frizzled-4, a high-affinity ligand-receptor pair". Cell. 116 (6): 883–895. doi:10.1016/s0092-8674(04)00216-8. ISSN 0092-8674. PMID 15035989.
  12. 1 2 Wang, Yanshu; Rattner, Amir; Zhou, Yulian; Williams, John; Smallwood, Philip M.; Nathans, Jeremy (7 December 2012). "Norrin/Frizzled4 signaling in retinal vascular development and blood brain barrier plasticity". Cell. 151 (6): 1332–1344. doi:10.1016/j.cell.2012.10.042. ISSN 1097-4172. PMC 3535266. PMID 23217714.
  13. ↑ "Jeremy Nathans". scholar.google.com. Retrieved 10 September 2026.
  14. ↑ Macke, J. P.; Nathans, J. (April 1997). "Individual variation in size of the human red and green visual pigment gene array". Investigative Ophthalmology & Visual Science. 38 (5): 1040–1043. ISSN 0146-0404. PMID 9113000.
  15. ↑ Merbs, S. L.; Nathans, J. (2 April 1992). "Absorption spectra of human cone pigments". Nature. 356 (6368): 433–435. Bibcode:1992Natur.356..433M. doi:10.1038/356433a0. ISSN 0028-0836. PMID 1557124.
  16. ↑ Merbs, S. L.; Nathans, J. (16 October 1992). "Absorption spectra of the hybrid pigments responsible for anomalous color vision". Science. 258 (5081). New York, N.Y.: 464–466. Bibcode:1992Sci...258..464M. doi:10.1126/science.1411542. ISSN 0036-8075. PMID 1411542.
  17. ↑ Sharpe, L. T.; Stockman, A.; Jägle, H.; Knau, H.; Klausen, G.; Reitner, A.; Nathans, J. (1 December 1998). "Red, green, and red-green hybrid pigments in the human retina: correlations between deduced protein sequences and psychophysically measured spectral sensitivities". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 18 (23): 10053–10069. doi:10.1523/JNEUROSCI.18-23-10053.1998. ISSN 0270-6474. PMC 6793300. PMID 9822760.
  18. ↑ Wang, Y.; Smallwood, P. M.; Cowan, M.; Blesh, D.; Lawler, A.; Nathans, J. (27 April 1999). "Mutually exclusive expression of human red and green visual pigment-reporter transgenes occurs at high frequency in murine cone photoreceptors". Proceedings of the National Academy of Sciences of the United States of America. 96 (9): 5251–5256. Bibcode:1999PNAS...96.5251W. doi:10.1073/pnas.96.9.5251. ISSN 0027-8424. PMC 21850. PMID 10220452.
  19. ↑ Smallwood, Philip M.; Wang, Yanshu; Nathans, Jeremy (22 January 2002). "Role of a locus control region in the mutually exclusive expression of human red and green cone pigment genes". Proceedings of the National Academy of Sciences of the United States of America. 99 (2): 1008–1011. Bibcode:2002PNAS...99.1008S. doi:10.1073/pnas.022629799. ISSN 0027-8424. PMC 117421. PMID 11773636.
  20. ↑ Jacobs, Gerald H.; Williams, Gary A.; Cahill, Hugh; Nathans, Jeremy (23 March 2007). "Emergence of novel color vision in mice engineered to express a human cone photopigment". Science. 315 (5819). New York, N.Y.: 1723–1725. Bibcode:2007Sci...315.1723J. doi:10.1126/science.1138838. ISSN 1095-9203. PMID 17379811.
  21. ↑ Sun, H.; Nathans, J. (September 1997). "Stargardt's ABCR is localized to the disc membrane of retinal rod outer segments". Nature Genetics. 17 (1): 15–16. doi:10.1038/ng0997-15. ISSN 1061-4036. PMID 9288089.
  22. ↑ Sun, H.; Smallwood, P. M.; Nathans, J. (October 2000). "Biochemical defects in ABCR protein variants associated with human retinopathies". Nature Genetics. 26 (2): 242–246. doi:10.1038/79994. ISSN 1061-4036. PMID 11017087.
  23. ↑ Tsunenari, Takashi; Sun, Hui; Williams, John; Cahill, Hugh; Smallwood, Philip; Yau, King-Wai; Nathans, Jeremy (17 October 2003). "Structure-function analysis of the bestrophin family of anion channels". The Journal of Biological Chemistry. 278 (42): 41114–41125. doi:10.1074/jbc.M306150200. ISSN 0021-9258. PMC 2885917. PMID 12907679.
  24. ↑ Sung, C. H.; Schneider, B. G.; Agarwal, N.; Papermaster, D. S.; Nathans, J. (1 October 1991). "Functional heterogeneity of mutant rhodopsins responsible for autosomal dominant retinitis pigmentosa". Proceedings of the National Academy of Sciences of the United States of America. 88 (19): 8840–8844. Bibcode:1991PNAS...88.8840S. doi:10.1073/pnas.88.19.8840. ISSN 0027-8424. PMC 52606. PMID 1924344.
  25. ↑ Portera-Cailliau, Carlos; Sung, Ching-Hwa; Nathans, Jeremy; Adler, Ruben (1994). "Apoptotic photoreceptor cell death in mouse models of retinitis pigmentosa". Proceedings of the National Academy of Sciences of the United States of America. 91 (3): 974–978. doi:10.1073/pnas.91.3.974. PMC 521436. PMID 8302876.
  26. ↑ Sung, C. H.; Makino, C.; Baylor, D.; Nathans, J. (October 1994). "A rhodopsin gene mutation responsible for autosomal dominant retinitis pigmentosa results in a protein that is defective in localization to the photoreceptor outer segment". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 14 (10): 5818–5833. doi:10.1523/JNEUROSCI.14-10-05818.1994. ISSN 0270-6474. PMC 6576989. PMID 7523628.
  27. ↑ Xiang, M.; Zhou, L.; Macke, J. P.; Yoshioka, T.; Hendry, S. H.; Eddy, R. L.; Shows, T. B.; Nathans, J. (July 1995). "The Brn-3 family of POU-domain factors: primary structure, binding specificity, and expression in subsets of retinal ganglion cells and somatosensory neurons". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 15 (7 Pt 1): 4762–4785. doi:10.1523/JNEUROSCI.15-07-04762.1995. ISSN 0270-6474. PMC 6577904. PMID 7623109.
  28. ↑ Gan, L.; Xiang, M.; Zhou, L.; Wagner, D. S.; Klein, W. H.; Nathans, J. (30 April 1996). "POU domain factor Brn-3b is required for the development of a large set of retinal ganglion cells". Proceedings of the National Academy of Sciences of the United States of America. 93 (9): 3920–3925. Bibcode:1996PNAS...93.3920G. doi:10.1073/pnas.93.9.3920. ISSN 0027-8424. PMC 39460. PMID 8632990.
  29. ↑ Xiang, M.; Gan, L.; Zhou, L.; Klein, W. H.; Nathans, J. (15 October 1996). "Targeted deletion of the mouse POU domain gene Brn-3a causes selective loss of neurons in the brainstem and trigeminal ganglion, uncoordinated limb movement, and impaired suckling". Proceedings of the National Academy of Sciences of the United States of America. 93 (21): 11950–11955. Bibcode:1996PNAS...9311950X. doi:10.1073/pnas.93.21.11950. ISSN 0027-8424. PMC 38164. PMID 8876243.
  30. ↑ Xiang, M.; Gan, L.; Li, D.; Chen, Z. Y.; Zhou, L.; O'Malley, B. W.; Klein, W.; Nathans, J. (19 August 1997). "Essential role of POU-domain factor Brn-3c in auditory and vestibular hair cell development". Proceedings of the National Academy of Sciences of the United States of America. 94 (17): 9445–9450. Bibcode:1997PNAS...94.9445X. doi:10.1073/pnas.94.17.9445. ISSN 0027-8424. PMC 23217. PMID 9256502.
  31. ↑ Badea, Tudor C.; Cahill, Hugh; Ecker, Jen; Hattar, Samer; Nathans, Jeremy (26 March 2009). "Distinct roles of transcription factors brn3a and brn3b in controlling the development, morphology, and function of retinal ganglion cells". Neuron. 61 (6): 852–864. doi:10.1016/j.neuron.2009.01.020. ISSN 1097-4199. PMC 2679215. PMID 19323995.
  32. ↑ Badea, Tudor Constantin; Williams, John; Smallwood, Philip; Shi, Melody; Motajo, Oluwaseyi; Nathans, Jeremy (18 January 2012). "Combinatorial expression of Brn3 transcription factors in somatosensory neurons: genetic and morphologic analysis". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 32 (3): 995–1007. doi:10.1523/JNEUROSCI.4755-11.2012. ISSN 1529-2401. PMC 3428801. PMID 22262898.
  33. ↑ Wang, Y.; Macke, J. P.; Abella, B. S.; Andreasson, K.; Worley, P.; Gilbert, D. J.; Copeland, N. G.; Jenkins, N. A.; Nathans, J. (23 February 1996). "A large family of putative transmembrane receptors homologous to the product of the Drosophila tissue polarity gene frizzled". The Journal of Biological Chemistry. 271 (8): 4468–4476. doi:10.1074/jbc.271.8.4468. ISSN 0021-9258. PMID 8626800.
  34. ↑ Bhanot, P.; Brink, M.; Samos, C. H.; Hsieh, J. C.; Wang, Y.; Macke, J. P.; Andrew, D.; Nathans, J.; Nusse, R. (18 July 1996). "A new member of the frizzled family from Drosophila functions as a Wingless receptor". Nature. 382 (6588): 225–230. Bibcode:1996Natur.382..225B. doi:10.1038/382225a0. ISSN 0028-0836. PMID 8717036.
  35. ↑ Wang, Yanshu; Chang, Hao; Rattner, Amir; Nathans, Jeremy (2016). "Frizzled Receptors in Development and Disease". Current Topics in Developmental Biology. 117: 113–139. doi:10.1016/bs.ctdb.2015.11.028. ISBN 978-0-12-801382-3. ISSN 1557-8933. PMC 5103317. PMID 26969975.{{cite journal}}: CS1 maint: periodical has ISBN (link)
  36. ↑ Guo, Nini; Hawkins, Charles; Nathans, Jeremy (22 June 2004). "Frizzled6 controls hair patterning in mice". Proceedings of the National Academy of Sciences of the United States of America. 101 (25): 9277–9281. doi:10.1073/pnas.0402802101. ISSN 0027-8424. PMC 438967. PMID 15169958.
  37. ↑ Wang, Yanshu; Badea, Tudor; Nathans, Jeremy (2006). "Order from disorder: Self-organization in mammalian hair patterning". Proceedings of the National Academy of Sciences of the United States of America. 103 (52): 19800–19805. doi:10.1073/pnas.0609712104. ISSN 1471-2202. PMC 1750877. PMID 17172440.
  38. ↑ Wang, Yanshu; Guo, Nini; Nathans, Jeremy (22 February 2006). "The role of Frizzled3 and Frizzled6 in neural tube closure and in the planar polarity of inner-ear sensory hair cells". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 26 (8): 2147–2156. doi:10.1523/JNEUROSCI.4698-05.2005. ISSN 1529-2401. PMC 6674805. PMID 16495441.
  39. ↑ Zhou, Yulian; Wang, Yanshu; Tischfield, Max; Williams, John; Smallwood, Philip M.; Rattner, Amir; Taketo, Makoto M.; Nathans, Jeremy (September 2014). "Canonical WNT signaling components in vascular development and barrier formation". The Journal of Clinical Investigation. 124 (9): 3825–3846. doi:10.1172/JCI76431. ISSN 1558-8238. PMC 4151216. PMID 25083995.
  40. ↑ Zhou, Yulian; Nathans, Jeremy (27 October 2014). "Gpr124 controls CNS angiogenesis and blood-brain barrier integrity by promoting ligand-specific canonical wnt signaling". Developmental Cell. 31 (2): 248–256. doi:10.1016/j.devcel.2014.08.018. ISSN 1878-1551. PMC 4223636. PMID 25373781.
  41. ↑ Cho, Chris; Smallwood, Philip M.; Nathans, Jeremy (30 August 2017). "Reck and Gpr124 Are Essential Receptor Cofactors for Wnt7a/Wnt7b-Specific Signaling in Mammalian CNS Angiogenesis and Blood-Brain Barrier Regulation". Neuron. 95 (5): 1056–1073.e5. doi:10.1016/j.neuron.2017.07.031. ISSN 1097-4199. PMC 5586543. PMID 28803732.
  42. ↑ Wang, Yanshu; Cho, Chris; Williams, John; Smallwood, Philip M.; Zhang, Chi; Junge, Harald J.; Nathans, Jeremy (11 December 2018). "Interplay of the Norrin and Wnt7a/Wnt7b signaling systems in blood-brain barrier and blood-retina barrier development and maintenance". Proceedings of the National Academy of Sciences of the United States of America. 115 (50): E11827–E11836. Bibcode:2018PNAS..11511827W. doi:10.1073/pnas.1813217115. ISSN 1091-6490. PMC 6294914. PMID 30478038.
  43. ↑ Sabbagh, Mark F.; Heng, Jacob S.; Luo, Chongyuan; Castanon, Rosa G.; Nery, Joseph R.; Rattner, Amir; Goff, Loyal A.; Ecker, Joseph R.; Nathans, Jeremy (6 September 2018). "Transcriptional and epigenomic landscapes of CNS and non-CNS vascular endothelial cells". eLife. 7 e36187. doi:10.7554/eLife.36187. ISSN 2050-084X. PMC 6126923. PMID 30188322.
  44. ↑ Wang, Yanshu; Sabbagh, Mark F.; Gu, Xiaowu; Rattner, Amir; Williams, John; Nathans, Jeremy (1 April 2019). "Beta-catenin signaling regulates barrier-specific gene expression in circumventricular organ and ocular vasculatures". eLife. 8 e43257. doi:10.7554/eLife.43257. ISSN 2050-084X. PMC 6443350. PMID 30932813.
  45. ↑ Li, Zhongming; Rattner, Amir; Wang, Yanshu; Smallwood, Philip M.; Sabbagh, Mark; Mannion, Brandon J.; Pennacchio, Len A.; Nathans, Jeremy (2026). "Enhancers that direct gene expression to central nervous system vascular endothelial cells in vivo". Neuron. 114 (10): 1736–1750. doi:10.1016/j.neuron.2026.03.002. PMID 41916278.
  46. ↑ "Merck and EyeBio Announce Initiation of Phase 2b/3 Clinical Trial for Restoret™ for the Treatment of Diabetic Macular Edema". Merck.com. Retrieved 11 September 2026.
  47. ↑ Badea, Tudor Constantin; Nathans, Jeremy (20 December 2004). "Quantitative analysis of neuronal morphologies in the mouse retina visualized by using a genetically directed reporter". The Journal of Comparative Neurology. 480 (4): 331–351. doi:10.1002/cne.20304. ISSN 0021-9967. PMID 15558785.
  48. ↑ Wu, Hao; Luo, Junjie; Yu, Huimin; Rattner, Amir; Mo, Alisa; Wang, Yanshu; Smallwood, Philip M.; Erlanger, Bracha; Wheelan, Sarah J.; Nathans, Jeremy (8 January 2014). "Cellular resolution maps of X chromosome inactivation: implications for neural development, function, and disease". Neuron. 81 (1): 103–119. doi:10.1016/j.neuron.2013.10.051. ISSN 1097-4199. PMC 3950970. PMID 24411735.
  49. ↑ Cahill, Hugh; Rattner, Amir; Nathans, Jeremy (September 2011). "Preclinical assessment of CNS drug action using eye movements in mice". The Journal of Clinical Investigation. 121 (9): 3528–3541. doi:10.1172/JCI45557. ISSN 1558-8238. PMC 3163951. PMID 21821912.
  50. ↑ Mo, Alisa; Mukamel, Eran A.; Davis, Fred P.; Luo, Chongyuan; Henry, Gilbert L.; Picard, Serge; Urich, Mark A.; Nery, Joseph R.; Sejnowski, Terrence J.; Lister, Ryan; Eddy, Sean R.; Ecker, Joseph R.; Nathans, Jeremy (17 June 2015). "Epigenomic Signatures of Neuronal Diversity in the Mammalian Brain". Neuron. 86 (6): 1369–1384. doi:10.1016/j.neuron.2015.05.018. ISSN 1097-4199. PMC 4499463. PMID 26087164.
  51. ↑ Peng, Xi; Emiliani, Francesco; Smallwood, Philip M.; Rattner, Amir; Lei, Hong; Sabbagh, Mark F.; Nathans, Jeremy (22 October 2018). "Affinity capture of polyribosomes followed by RNAseq (ACAPseq), a discovery platform for protein-protein interactions". eLife. 7 e40982. doi:10.7554/eLife.40982. ISSN 2050-084X. PMC 6197854. PMID 30345971.
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  53. ↑ "You searched for jeremy Nathans • iBiology". iBiology. Retrieved 2026-09-11.
  54. ↑ Howard Hughes Medical Institute (HHMI) (24 November 2015). "The Evolution of Human Color Vision," Jeremy Nathans. Retrieved 11 September 2026 – via YouTube.
  55. ↑ Columbia University's Zuckerman Institute (17 December 2020). Jeremy Nathans - Molecular genetic studies of CNS vascular development and disease. Retrieved 11 September 2026 – via YouTube.
  56. ↑ Nathan Dennies / (20 May 2026). "Jeremy Nathans honored at Johns Hopkins School of Medicine Four Doctors Awards". The Hub. Retrieved 11 September 2026.
  57. ↑ "Groundbreaking Molecular Neuroscientist to Receive 2022 Nemmers Prize in Medical Science". News Center. Northwestern University. 14 April 2022. Retrieved 11 September 2026.
  58. ↑ "Jeremy Nathans". The Franklin Institute. 25 January 2020. Retrieved 11 September 2026.
  59. ↑ "Drs. King-Wai Yau and Jeremy Nathans Awarded The Hellen Keller Prize". neuroscience.jhu.edu. Retrieved 11 September 2026.
  60. ↑ "AlumniAwards13". Alumni Association. Retrieved 11 September 2026.
  61. ↑ "Jeremy Nathans - NAM". nam.edu. Retrieved 11 September 2026.
  62. ↑ "McGovern awards Scolnick Prize to HHMI investigator Nathans". MIT News | Massachusetts Institute of Technology. 23 April 2009. Retrieved 11 September 2026.
  63. ↑ "2008: Nathans & Yau | Champalimaud Foundation". fchampalimaud.org. Retrieved 11 September 2026.
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