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DNA methylation in schizophrenia in different patient-derived cell types.

NPJ schizophrenia

Vitale AM, Matigian NA, Cristino AS, Nones K, Ravishankar S, Bellette B, Fan Y, Wood SA, Wolvetang E, Mackay-Sim A.
PMID: 28560252
NPJ Schizophr. 2017 Jan 23;3:6. doi: 10.1038/s41537-016-0006-0. eCollection 2017.

DNA methylation of gene promoter regions represses transcription and is a mechanism via which environmental risk factors could affect cells during development in individuals at risk for schizophrenia. We investigated DNA methylation in patient-derived cells that might shed light...

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Vitale AM, Matigian NA, Cristino AS, et al. DNA methylation in schizophrenia in different patient-derived cell types. NPJ Schizophr. 2017;3:6doi: 10.1038/s41537-016-0006-0.
Vitale, A. M., Matigian, N. A., Cristino, A. S., Nones, K., Ravishankar, S., Bellette, B., Fan, Y., Wood, S. A., Wolvetang, E., & Mackay-Sim, A. (2017). DNA methylation in schizophrenia in different patient-derived cell types. NPJ schizophrenia, 36. https://doi.org/10.1038/s41537-016-0006-0
Vitale, Alejandra M, et al. "DNA methylation in schizophrenia in different patient-derived cell types." NPJ schizophrenia vol. 3 (2017): 6. doi: https://doi.org/10.1038/s41537-016-0006-0
Vitale AM, Matigian NA, Cristino AS, Nones K, Ravishankar S, Bellette B, Fan Y, Wood SA, Wolvetang E, Mackay-Sim A. DNA methylation in schizophrenia in different patient-derived cell types. NPJ Schizophr. 2017 Jan 23;3:6. doi: 10.1038/s41537-016-0006-0. eCollection 2017. PMID: 28560252; PMCID: PMC5441549.
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Generation of a human embryonic stem cell line stably expressing high levels of the fluorescent protein mCherry.

World journal of stem cells

Ovchinnikov DA, Turner JP, Titmarsh DM, Thakar NY, Sin DC, Cooper-White JJ, Wolvetang EJ.
PMID: 22993664
World J Stem Cells. 2012 Jul 26;4(7):71-9. doi: 10.4252/wjsc.v4.i7.71.

AIM: The generation and characterization of a human embryonic stem cell (hESC) line stably expressing red fluorescent mCherry protein.METHODS: Lentiviral transduction of a ubiquitously-expressed human EF-1α promoter driven mCherry transgene was performed in MEL2 hESC. Red fluore-scence was assessed...

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Ovchinnikov DA, Turner JP, Titmarsh DM, et al. Generation of a human embryonic stem cell line stably expressing high levels of the fluorescent protein mCherry. World J Stem Cells. 2012;4(7):71-9doi: 10.4252/wjsc.v4.i7.71.
Ovchinnikov, D. A., Turner, J. P., Titmarsh, D. M., Thakar, N. Y., Sin, D. C., Cooper-White, J. J., & Wolvetang, E. J. (2012). Generation of a human embryonic stem cell line stably expressing high levels of the fluorescent protein mCherry. World journal of stem cells, 4(7), 71-9. https://doi.org/10.4252/wjsc.v4.i7.71
Ovchinnikov, Dmitry A, et al. "Generation of a human embryonic stem cell line stably expressing high levels of the fluorescent protein mCherry." World journal of stem cells vol. 4,7 (2012): 71-9. doi: https://doi.org/10.4252/wjsc.v4.i7.71
Ovchinnikov DA, Turner JP, Titmarsh DM, Thakar NY, Sin DC, Cooper-White JJ, Wolvetang EJ. Generation of a human embryonic stem cell line stably expressing high levels of the fluorescent protein mCherry. World J Stem Cells. 2012 Jul 26;4(7):71-9. doi: 10.4252/wjsc.v4.i7.71. PMID: 22993664; PMCID: PMC3443714.
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Neuronal Lipid Metabolism: Multiple Pathways Driving Functional Outcomes in Health and Disease.

Frontiers in molecular neuroscience

Tracey TJ, Steyn FJ, Wolvetang EJ, Ngo ST.
PMID: 29410613
Front Mol Neurosci. 2018 Jan 23;11:10. doi: 10.3389/fnmol.2018.00010. eCollection 2018.

Lipids are a fundamental class of organic molecules implicated in a wide range of biological processes related to their structural diversity, and based on this can be broadly classified into five categories; fatty acids, triacylglycerols (TAGs), phospholipids, sterol lipids...

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Tracey TJ, Steyn FJ, Wolvetang EJ, et al. Neuronal Lipid Metabolism: Multiple Pathways Driving Functional Outcomes in Health and Disease. Front Mol Neurosci. 2018;11:10doi: 10.3389/fnmol.2018.00010.
Tracey, T. J., Steyn, F. J., Wolvetang, E. J., & Ngo, S. T. (2018). Neuronal Lipid Metabolism: Multiple Pathways Driving Functional Outcomes in Health and Disease. Frontiers in molecular neuroscience, 1110. https://doi.org/10.3389/fnmol.2018.00010
Tracey, Timothy J, et al. "Neuronal Lipid Metabolism: Multiple Pathways Driving Functional Outcomes in Health and Disease." Frontiers in molecular neuroscience vol. 11 (2018): 10. doi: https://doi.org/10.3389/fnmol.2018.00010
Tracey TJ, Steyn FJ, Wolvetang EJ, Ngo ST. Neuronal Lipid Metabolism: Multiple Pathways Driving Functional Outcomes in Health and Disease. Front Mol Neurosci. 2018 Jan 23;11:10. doi: 10.3389/fnmol.2018.00010. eCollection 2018. PMID: 29410613; PMCID: PMC5787076.
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Modelling ischemia-reperfusion injury (IRI) .

APL bioengineering

Hidalgo A, Glass N, Ovchinnikov D, Yang SK, Zhang X, Mazzone S, Chen C, Wolvetang E, Cooper-White J.
PMID: 31069299
APL Bioeng. 2018 Mar 20;2(2):026102. doi: 10.1063/1.5000746. eCollection 2018 Jun.

Coronary intervention following ST-segment elevation myocardial infarction (STEMI) is the treatment of choice for reducing cardiomyocyte death but paradoxically leads to reperfusion injury. Pharmacological post-conditioning is an attractive approach to minimize Ischemia-Reperfusion Injury (IRI), but candidate drugs identified in...

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Hidalgo A, Glass N, Ovchinnikov D, et al. Modelling ischemia-reperfusion injury (IRI) . APL Bioeng. 2018;2(2):026102doi: 10.1063/1.5000746.
Hidalgo, A., Glass, N., Ovchinnikov, D., Yang, S. K., Zhang, X., Mazzone, S., Chen, C., Wolvetang, E., & Cooper-White, J. (2018). Modelling ischemia-reperfusion injury (IRI) . APL bioengineering, 2(2), 026102. https://doi.org/10.1063/1.5000746
Hidalgo, Alejandro, et al. "Modelling ischemia-reperfusion injury (IRI) ." APL bioengineering vol. 2,2 (2018): 026102. doi: https://doi.org/10.1063/1.5000746
Hidalgo A, Glass N, Ovchinnikov D, Yang SK, Zhang X, Mazzone S, Chen C, Wolvetang E, Cooper-White J. Modelling ischemia-reperfusion injury (IRI) . APL Bioeng. 2018 Mar 20;2(2):026102. doi: 10.1063/1.5000746. eCollection 2018 Jun. PMID: 31069299; PMCID: PMC6481709.
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Inhibition of the cGAS-STING pathway ameliorates the premature senescence hallmarks of Ataxia-Telangiectasia brain organoids.

Aging cell

Aguado J, Chaggar HK, Gómez-Inclán C, Shaker MR, Leeson HC, Mackay-Sim A, Wolvetang EJ.
PMID: 34459078
Aging Cell. 2021 Sep;20(9):e13468. doi: 10.1111/acel.13468. Epub 2021 Aug 30.

Ataxia-telangiectasia (A-T) is a genetic disorder caused by the lack of functional ATM kinase. A-T is characterized by chronic inflammation, neurodegeneration and premature ageing features that are associated with increased genome instability, nuclear shape alterations, micronuclei accumulation, neuronal defects...

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Aguado J, Chaggar HK, Gómez-Inclán C, et al. Inhibition of the cGAS-STING pathway ameliorates the premature senescence hallmarks of Ataxia-Telangiectasia brain organoids. Aging Cell. 2021;20(9):e13468doi: 10.1111/acel.13468.
Aguado, J., Chaggar, H. K., Gómez-Inclán, C., Shaker, M. R., Leeson, H. C., Mackay-Sim, A., & Wolvetang, E. J. (2021). Inhibition of the cGAS-STING pathway ameliorates the premature senescence hallmarks of Ataxia-Telangiectasia brain organoids. Aging cell, 20(9), e13468. https://doi.org/10.1111/acel.13468
Aguado, Julio, et al. "Inhibition of the cGAS-STING pathway ameliorates the premature senescence hallmarks of Ataxia-Telangiectasia brain organoids." Aging cell vol. 20,9 (2021): e13468. doi: https://doi.org/10.1111/acel.13468
Aguado J, Chaggar HK, Gómez-Inclán C, Shaker MR, Leeson HC, Mackay-Sim A, Wolvetang EJ. Inhibition of the cGAS-STING pathway ameliorates the premature senescence hallmarks of Ataxia-Telangiectasia brain organoids. Aging Cell. 2021 Sep;20(9):e13468. doi: 10.1111/acel.13468. Epub 2021 Aug 30. PMID: 34459078; PMCID: PMC8441292.
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Identification of on-target mutagenesis during correction of a beta-thalassemia splice mutation in iPS cells with optimised CRISPR/Cas9-double nickase reveals potential safety concerns.

APL bioengineering

Alateeq S, Ovchinnikov D, Tracey T, Whitworth D, Al-Rubaish A, Al-Ali A, Wolvetang E.
PMID: 31069325
APL Bioeng. 2018 Dec 03;2(4):046103. doi: 10.1063/1.5048625. eCollection 2018 Dec.

Precise and accurate gene correction is crucial for enabling iPSC-based therapies, and Cas9-Nickase based approaches are increasingly considered for

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Alateeq S, Ovchinnikov D, Tracey T, et al. Identification of on-target mutagenesis during correction of a beta-thalassemia splice mutation in iPS cells with optimised CRISPR/Cas9-double nickase reveals potential safety concerns. APL Bioeng. 2018;2(4):046103doi: 10.1063/1.5048625.
Alateeq, S., Ovchinnikov, D., Tracey, T., Whitworth, D., Al-Rubaish, A., Al-Ali, A., & Wolvetang, E. (2018). Identification of on-target mutagenesis during correction of a beta-thalassemia splice mutation in iPS cells with optimised CRISPR/Cas9-double nickase reveals potential safety concerns. APL bioengineering, 2(4), 046103. https://doi.org/10.1063/1.5048625
Alateeq, Suad, et al. "Identification of on-target mutagenesis during correction of a beta-thalassemia splice mutation in iPS cells with optimised CRISPR/Cas9-double nickase reveals potential safety concerns." APL bioengineering vol. 2,4 (2018): 046103. doi: https://doi.org/10.1063/1.5048625
Alateeq S, Ovchinnikov D, Tracey T, Whitworth D, Al-Rubaish A, Al-Ali A, Wolvetang E. Identification of on-target mutagenesis during correction of a beta-thalassemia splice mutation in iPS cells with optimised CRISPR/Cas9-double nickase reveals potential safety concerns. APL Bioeng. 2018 Dec 03;2(4):046103. doi: 10.1063/1.5048625. eCollection 2018 Dec. PMID: 31069325; PMCID: PMC6481731.
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Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia.

iScience

Yeo AJ, Chong KL, Gatei M, Zou D, Stewart R, Withey S, Wolvetang E, Parton RG, Brown AD, Kastan MB, Coman D, Lavin MF.
PMID: 33437944
iScience. 2020 Dec 23;24(1):101972. doi: 10.1016/j.isci.2020.101972. eCollection 2021 Jan 22.

There is evidence that ATM mutated in ataxia-telangiectasia (A-T) plays a key role in protecting against mitochondrial dysfunction, the mechanism for which remains unresolved. We demonstrate here that ATM-deficient cells are exquisitely sensitive to nutrient deprivation, which can be...

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Yeo AJ, Chong KL, Gatei M, et al. Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia. iScience. 2020;24(1):101972doi: 10.1016/j.isci.2020.101972.
Yeo, A. J., Chong, K. L., Gatei, M., Zou, D., Stewart, R., Withey, S., Wolvetang, E., Parton, R. G., Brown, A. D., Kastan, M. B., Coman, D., & Lavin, M. F. (2021). Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia. iScience, 24(1), 101972. https://doi.org/10.1016/j.isci.2020.101972
Yeo, Abrey J, et al. "Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia." iScience vol. 24,1 (2021): 101972. doi: https://doi.org/10.1016/j.isci.2020.101972
Yeo AJ, Chong KL, Gatei M, Zou D, Stewart R, Withey S, Wolvetang E, Parton RG, Brown AD, Kastan MB, Coman D, Lavin MF. Impaired endoplasmic reticulum-mitochondrial signaling in ataxia-telangiectasia. iScience. 2020 Dec 23;24(1):101972. doi: 10.1016/j.isci.2020.101972. eCollection 2021 Jan 22. PMID: 33437944; PMCID: PMC7788243.
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Klotho inhibits neuronal senescence in human brain organoids.

NPJ aging and mechanisms of disease

Shaker MR, Aguado J, Chaggar HK, Wolvetang EJ.
PMID: 34341344
NPJ Aging Mech Dis. 2021 Aug 02;7(1):18. doi: 10.1038/s41514-021-00070-x.

Aging is a major risk factor for many neurodegenerative diseases. Klotho (KL) is a glycosylated transmembrane protein that is expressed in the choroid plexus and neurons of the brain. KL exerts potent anti-aging effects on multiple cell types in...

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Shaker MR, Aguado J, Chaggar HK, et al. Klotho inhibits neuronal senescence in human brain organoids. NPJ Aging Mech Dis. 2021;7(1):18doi: 10.1038/s41514-021-00070-x.
Shaker, M. R., Aguado, J., Chaggar, H. K., & Wolvetang, E. J. (2021). Klotho inhibits neuronal senescence in human brain organoids. NPJ aging and mechanisms of disease, 7(1), 18. https://doi.org/10.1038/s41514-021-00070-x
Shaker, Mohammed R, et al. "Klotho inhibits neuronal senescence in human brain organoids." NPJ aging and mechanisms of disease vol. 7,1 (2021): 18. doi: https://doi.org/10.1038/s41514-021-00070-x
Shaker MR, Aguado J, Chaggar HK, Wolvetang EJ. Klotho inhibits neuronal senescence in human brain organoids. NPJ Aging Mech Dis. 2021 Aug 02;7(1):18. doi: 10.1038/s41514-021-00070-x. PMID: 34341344; PMCID: PMC8329278.
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Kidney organoids from human iPS cells contain multiple lineages and model human nephrogenesis.

Nature

Takasato M, Er PX, Chiu HS, Maier B, Baillie GJ, Ferguson C, Parton RG, Wolvetang EJ, Roost MS, Lopes SM, Little MH.
PMID: 27120161
Nature. 2016 Aug 11;536(7615):238. doi: 10.1038/nature17982. Epub 2016 Apr 27.

No abstract available.

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Takasato M, Er PX, Chiu HS, et al. Kidney organoids from human iPS cells contain multiple lineages and model human nephrogenesis. Nature. 2016;536(7615):238doi: 10.1038/nature17982.
Takasato, M., Er, P. X., Chiu, H. S., Maier, B., Baillie, G. J., Ferguson, C., Parton, R. G., Wolvetang, E. J., Roost, M. S., Lopes, S. M., & Little, M. H. (2016). Kidney organoids from human iPS cells contain multiple lineages and model human nephrogenesis. Nature, 536(7615), 238. https://doi.org/10.1038/nature17982
Takasato, Minoru, et al. "Kidney organoids from human iPS cells contain multiple lineages and model human nephrogenesis." Nature vol. 536,7615 (2016): 238. doi: https://doi.org/10.1038/nature17982
Takasato M, Er PX, Chiu HS, Maier B, Baillie GJ, Ferguson C, Parton RG, Wolvetang EJ, Roost MS, Lopes SM, Little MH. Kidney organoids from human iPS cells contain multiple lineages and model human nephrogenesis. Nature. 2016 Aug 11;536(7615):238. doi: 10.1038/nature17982. Epub 2016 Apr 27. PMID: 27120161.
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Expression Pattern of the Aspartyl-tRNA Synthetase DARS in the Human Brain.

Frontiers in molecular neuroscience

Fröhlich D, Suchowerska AK, Voss C, He R, Wolvetang E, von Jonquieres G, Simons C, Fath T, Housley GD, Klugmann M.
PMID: 29615866
Front Mol Neurosci. 2018 Mar 20;11:81. doi: 10.3389/fnmol.2018.00081. eCollection 2018.

Translation of mRNA into protein is an evolutionarily conserved, fundamental process of life. A prerequisite for translation is the accurate charging of tRNAs with their cognate amino acids, a reaction catalyzed by specific aminoacyl-tRNA synthetases. One of these enzymes...

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Fröhlich D, Suchowerska AK, Voss C, et al. Expression Pattern of the Aspartyl-tRNA Synthetase DARS in the Human Brain. Front Mol Neurosci. 2018;11:81doi: 10.3389/fnmol.2018.00081.
Fröhlich, D., Suchowerska, A. K., Voss, C., He, R., Wolvetang, E., von Jonquieres, G., Simons, C., Fath, T., Housley, G. D., & Klugmann, M. (2018). Expression Pattern of the Aspartyl-tRNA Synthetase DARS in the Human Brain. Frontiers in molecular neuroscience, 1181. https://doi.org/10.3389/fnmol.2018.00081
Fröhlich, Dominik, et al. "Expression Pattern of the Aspartyl-tRNA Synthetase DARS in the Human Brain." Frontiers in molecular neuroscience vol. 11 (2018): 81. doi: https://doi.org/10.3389/fnmol.2018.00081
Fröhlich D, Suchowerska AK, Voss C, He R, Wolvetang E, von Jonquieres G, Simons C, Fath T, Housley GD, Klugmann M. Expression Pattern of the Aspartyl-tRNA Synthetase DARS in the Human Brain. Front Mol Neurosci. 2018 Mar 20;11:81. doi: 10.3389/fnmol.2018.00081. eCollection 2018. PMID: 29615866; PMCID: PMC5869200.
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Author Correction: Reprogramming triggers endogenous L1 and Alu retrotransposition in human induced pluripotent stem cells.

Nature communications

Klawitter S, Fuchs NV, Upton KR, Muñoz-Lopez M, Shukla R, Wang J, Garcia-Cañadas M, Lopez-Ruiz C, Gerhardt DJ, Sebe A, Grabundzija I, Merkert S, Gerdes P, Pulgarin JA, Bock A, Held U, Witthuhn A, Haase A, Sarkadi B, Löwer J, Wolvetang EJ, Martin U, Ivics Z, Izsvák Z, Garcia-Perez JL, Faulkner GJ, Schumann GG.
PMID: 30568248
Nat Commun. 2018 Dec 19;9(1):5398. doi: 10.1038/s41467-018-07917-0.

This Article contains an error in the author affiliations. The correct affiliation for author Ruchi Shukla is 'MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road, Edinburgh, EH4 2XU, UK', and is not...

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Klawitter S, Fuchs NV, Upton KR, et al. Author Correction: Reprogramming triggers endogenous L1 and Alu retrotransposition in human induced pluripotent stem cells. Nat Commun. 2018;9(1):5398doi: 10.1038/s41467-018-07917-0.
Klawitter, S., Fuchs, N. V., Upton, K. R., Muñoz-Lopez, M., Shukla, R., Wang, J., Garcia-Cañadas, M., Lopez-Ruiz, C., Gerhardt, D. J., Sebe, A., Grabundzija, I., Merkert, S., Gerdes, P., Pulgarin, J. A., Bock, A., Held, U., Witthuhn, A., Haase, A., Sarkadi, B., Löwer, J., Wolvetang, E. J., Martin, U., Ivics, Z., Izsvák, Z., Garcia-Perez, J. L., Faulkner, G. J., & Schumann, G. G. (2018). Author Correction: Reprogramming triggers endogenous L1 and Alu retrotransposition in human induced pluripotent stem cells. Nature communications, 9(1), 5398. https://doi.org/10.1038/s41467-018-07917-0
Klawitter, Sabine, et al. "Author Correction: Reprogramming triggers endogenous L1 and Alu retrotransposition in human induced pluripotent stem cells." Nature communications vol. 9,1 (2018): 5398. doi: https://doi.org/10.1038/s41467-018-07917-0
Klawitter S, Fuchs NV, Upton KR, Muñoz-Lopez M, Shukla R, Wang J, Garcia-Cañadas M, Lopez-Ruiz C, Gerhardt DJ, Sebe A, Grabundzija I, Merkert S, Gerdes P, Pulgarin JA, Bock A, Held U, Witthuhn A, Haase A, Sarkadi B, Löwer J, Wolvetang EJ, Martin U, Ivics Z, Izsvák Z, Garcia-Perez JL, Faulkner GJ, Schumann GG. Author Correction: Reprogramming triggers endogenous L1 and Alu retrotransposition in human induced pluripotent stem cells. Nat Commun. 2018 Dec 19;9(1):5398. doi: 10.1038/s41467-018-07917-0. PMID: 30568248; PMCID: PMC6300592.
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Human iPSC-Derived Cerebellar Neurons from a Patient with Ataxia-Telangiectasia Reveal Disrupted Gene Regulatory Networks.

Frontiers in cellular neuroscience

Nayler SP, Powell JE, Vanichkina DP, Korn O, Wells CA, Kanjhan R, Sun J, Taft RJ, Lavin MF, Wolvetang EJ.
PMID: 29081736
Front Cell Neurosci. 2017 Oct 13;11:321. doi: 10.3389/fncel.2017.00321. eCollection 2017.

Ataxia-telangiectasia (A-T) is a rare genetic disorder caused by loss of function of the ataxia-telangiectasia-mutated kinase and is characterized by a predisposition to cancer, pulmonary disease, immune deficiency and progressive degeneration of the cerebellum. As animal models do not...

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Nayler SP, Powell JE, Vanichkina DP, et al. Human iPSC-Derived Cerebellar Neurons from a Patient with Ataxia-Telangiectasia Reveal Disrupted Gene Regulatory Networks. Front Cell Neurosci. 2017;11:321doi: 10.3389/fncel.2017.00321.
Nayler, S. P., Powell, J. E., Vanichkina, D. P., Korn, O., Wells, C. A., Kanjhan, R., Sun, J., Taft, R. J., Lavin, M. F., & Wolvetang, E. J. (2017). Human iPSC-Derived Cerebellar Neurons from a Patient with Ataxia-Telangiectasia Reveal Disrupted Gene Regulatory Networks. Frontiers in cellular neuroscience, 11321. https://doi.org/10.3389/fncel.2017.00321
Nayler, Sam P, et al. "Human iPSC-Derived Cerebellar Neurons from a Patient with Ataxia-Telangiectasia Reveal Disrupted Gene Regulatory Networks." Frontiers in cellular neuroscience vol. 11 (2017): 321. doi: https://doi.org/10.3389/fncel.2017.00321
Nayler SP, Powell JE, Vanichkina DP, Korn O, Wells CA, Kanjhan R, Sun J, Taft RJ, Lavin MF, Wolvetang EJ. Human iPSC-Derived Cerebellar Neurons from a Patient with Ataxia-Telangiectasia Reveal Disrupted Gene Regulatory Networks. Front Cell Neurosci. 2017 Oct 13;11:321. doi: 10.3389/fncel.2017.00321. eCollection 2017. PMID: 29081736; PMCID: PMC5645492.
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