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Showing 13 to 24 of 33 entries
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L-Arginine Ameliorates Defective Autophagy in GM2 Gangliosidoses by mTOR Modulation.

Cells

Castejón-Vega B, Rubio A, Pérez-Pulido AJ, Quiles JL, Lane JD, Fernández-Domínguez B, Cachón-González MB, Martín-Ruiz C, Sanz A, Cox TM, Alcocer-Gómez E, Cordero MD.
PMID: 34831346
Cells. 2021 Nov 11;10(11). doi: 10.3390/cells10113122.

AIMS: Tay-Sachs and Sandhoff diseases (GM2 gangliosidosis) are autosomal recessive disorders of lysosomal function that cause progressive neurodegeneration in infants and young children. Impaired hydrolysis catalysed by β-hexosaminidase A (HexA) leads to the accumulation of GM2 ganglioside in neuronal...

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Castejón-Vega B, Rubio A, Pérez-Pulido AJ, et al. L-Arginine Ameliorates Defective Autophagy in GM2 Gangliosidoses by mTOR Modulation. Cells. 2021;10(11)doi: 10.3390/cells10113122.
Castejón-Vega, B., Rubio, A., Pérez-Pulido, A. J., Quiles, J. L., Lane, J. D., Fernández-Domínguez, B., Cachón-González, M. B., Martín-Ruiz, C., Sanz, A., Cox, T. M., Alcocer-Gómez, E., & Cordero, M. D. (2021). L-Arginine Ameliorates Defective Autophagy in GM2 Gangliosidoses by mTOR Modulation. Cells, 10(11), . https://doi.org/10.3390/cells10113122
Castejón-Vega, Beatriz, et al. "L-Arginine Ameliorates Defective Autophagy in GM2 Gangliosidoses by mTOR Modulation." Cells vol. 10,11 (2021). doi: https://doi.org/10.3390/cells10113122
Castejón-Vega B, Rubio A, Pérez-Pulido AJ, Quiles JL, Lane JD, Fernández-Domínguez B, Cachón-González MB, Martín-Ruiz C, Sanz A, Cox TM, Alcocer-Gómez E, Cordero MD. L-Arginine Ameliorates Defective Autophagy in GM2 Gangliosidoses by mTOR Modulation. Cells. 2021 Nov 11;10(11). doi: 10.3390/cells10113122. PMID: 34831346; PMCID: PMC8619250.
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Late onset Sandhoff disease presenting with lower motor neuron disease and stuttering.

Neuromuscular disorders : NMD

Alonso-Pérez J, Casasús A, Gimenez-Muñoz Á, Duff J, Rojas-Garcia R, Illa I, Straub V, Töpf A, Díaz-Manera J.
PMID: 34210542
Neuromuscul Disord. 2021 Aug;31(8):769-772. doi: 10.1016/j.nmd.2021.04.011. Epub 2021 May 27.

Defects in the HEXB gene which encodes the β-subunit of β-hexosaminidase A and B enzymes, cause a GM2 gangliosidosis, also known as Sandhoff disease, which is a rare lysosomal storage disorder. The most common form of the disease lead...

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Alonso-Pérez J, Casasús A, Gimenez-Muñoz Á, et al. Late onset Sandhoff disease presenting with lower motor neuron disease and stuttering. Neuromuscul Disord. 2021;31(8):769-772doi: 10.1016/j.nmd.2021.04.011.
Alonso-Pérez, J., Casasús, A., Gimenez-Muñoz, �. �., Duff, J., Rojas-Garcia, R., Illa, I., Straub, V., Töpf, A., & Díaz-Manera, J. (2021). Late onset Sandhoff disease presenting with lower motor neuron disease and stuttering. Neuromuscular disorders : NMD, 31(8), 769-772. https://doi.org/10.1016/j.nmd.2021.04.011
Alonso-Pérez, Jorge, et al. "Late onset Sandhoff disease presenting with lower motor neuron disease and stuttering." Neuromuscular disorders : NMD vol. 31,8 (2021): 769-772. doi: https://doi.org/10.1016/j.nmd.2021.04.011
Alonso-Pérez J, Casasús A, Gimenez-Muñoz Á, Duff J, Rojas-Garcia R, Illa I, Straub V, Töpf A, Díaz-Manera J. Late onset Sandhoff disease presenting with lower motor neuron disease and stuttering. Neuromuscul Disord. 2021 Aug;31(8):769-772. doi: 10.1016/j.nmd.2021.04.011. Epub 2021 May 27. PMID: 34210542.
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Urine proteomics analysis of patients with neuronal ceroid lipofuscinoses.

iScience

Iwan K, Clayton R, Mills P, Csanyi B, Gissen P, Mole SE, Palmer DN, Mills K, Heywood WE.
PMID: 33532713
iScience. 2020 Dec 31;24(2):102020. doi: 10.1016/j.isci.2020.102020. eCollection 2021 Feb 19.

The neuronal ceroid lipofuscinoses (NCL) are a group of 13 rare neurodegenerative disorders characterized by accumulation of cellular storage bodies. There are few therapeutic options, and existing tests do not monitor disease progression and treatment response. However, urine biomarkers...

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Iwan K, Clayton R, Mills P, et al. Urine proteomics analysis of patients with neuronal ceroid lipofuscinoses. iScience. 2020;24(2):102020doi: 10.1016/j.isci.2020.102020.
Iwan, K., Clayton, R., Mills, P., Csanyi, B., Gissen, P., Mole, S. E., Palmer, D. N., Mills, K., & Heywood, W. E. (2021). Urine proteomics analysis of patients with neuronal ceroid lipofuscinoses. iScience, 24(2), 102020. https://doi.org/10.1016/j.isci.2020.102020
Iwan, Katharina, et al. "Urine proteomics analysis of patients with neuronal ceroid lipofuscinoses." iScience vol. 24,2 (2021): 102020. doi: https://doi.org/10.1016/j.isci.2020.102020
Iwan K, Clayton R, Mills P, Csanyi B, Gissen P, Mole SE, Palmer DN, Mills K, Heywood WE. Urine proteomics analysis of patients with neuronal ceroid lipofuscinoses. iScience. 2020 Dec 31;24(2):102020. doi: 10.1016/j.isci.2020.102020. eCollection 2021 Feb 19. PMID: 33532713; PMCID: PMC7822952.
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Hexosaminidase A (HEXA) regulates hepatic sphingolipid and lipoprotein metabolism in mice.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Montgomery MK, Taddese AZ, Bayliss J, Nie S, Williamson NA, Watt MJ.
PMID: 34800307
FASEB J. 2021 Dec;35(12):e22046. doi: 10.1096/fj.202101186R.

Hexosaminidase A (HexA), a heterodimer consisting of HEXA and HEXB, converts the ganglioside sphingolipid GM2 to GM3 by removing a terminal N-acetyl-d-galactosamine. HexA enzyme deficiency in humans leads to GM2 accumulation in cells, particularly in neurons, and is associated...

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Montgomery MK, Taddese AZ, Bayliss J, et al. Hexosaminidase A (HEXA) regulates hepatic sphingolipid and lipoprotein metabolism in mice. FASEB J. 2021;35(12):e22046doi: 10.1096/fj.202101186R.
Montgomery, M. K., Taddese, A. Z., Bayliss, J., Nie, S., Williamson, N. A., & Watt, M. J. (2021). Hexosaminidase A (HEXA) regulates hepatic sphingolipid and lipoprotein metabolism in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 35(12), e22046. https://doi.org/10.1096/fj.202101186R
Montgomery, Magdalene K, et al. "Hexosaminidase A (HEXA) regulates hepatic sphingolipid and lipoprotein metabolism in mice." FASEB journal : official publication of the Federation of American Societies for Experimental Biology vol. 35,12 (2021): e22046. doi: https://doi.org/10.1096/fj.202101186R
Montgomery MK, Taddese AZ, Bayliss J, Nie S, Williamson NA, Watt MJ. Hexosaminidase A (HEXA) regulates hepatic sphingolipid and lipoprotein metabolism in mice. FASEB J. 2021 Dec;35(12):e22046. doi: 10.1096/fj.202101186R. PMID: 34800307.
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Platelet hexosaminidase a enzyme assay effectively detects carriers missed by targeted DNA mutation analysis.

JIMD reports

Nakagawa S, Zhan J, Sun W, Ferreira JC, Keiles S, Hambuch T, Kammesheidt A, Mark BL, Schneider A, Gross S, Schreiber-Agus N.
PMID: 23430931
JIMD Rep. 2012;6:1-6. doi: 10.1007/8904_2011_120. Epub 2012 Jan 31.

Biochemical testing of hexosaminidase A (HexA) enzyme activity has been available for decades and has the ability to detect almost all Tay-Sachs disease (TSD) carriers, irrespective of ethnic background. This is increasingly important, as the gene pool of those...

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Nakagawa S, Zhan J, Sun W, et al. Platelet hexosaminidase a enzyme assay effectively detects carriers missed by targeted DNA mutation analysis. JIMD Rep. 2012;6:1-6doi: 10.1007/8904_2011_120.
Nakagawa, S., Zhan, J., Sun, W., Ferreira, J. C., Keiles, S., Hambuch, T., Kammesheidt, A., Mark, B. L., Schneider, A., Gross, S., & Schreiber-Agus, N. (2012). Platelet hexosaminidase a enzyme assay effectively detects carriers missed by targeted DNA mutation analysis. JIMD reports, 61-6. https://doi.org/10.1007/8904_2011_120
Nakagawa, Sachiko, et al. "Platelet hexosaminidase a enzyme assay effectively detects carriers missed by targeted DNA mutation analysis." JIMD reports vol. 6 (2012): 1-6. doi: https://doi.org/10.1007/8904_2011_120
Nakagawa S, Zhan J, Sun W, Ferreira JC, Keiles S, Hambuch T, Kammesheidt A, Mark BL, Schneider A, Gross S, Schreiber-Agus N. Platelet hexosaminidase a enzyme assay effectively detects carriers missed by targeted DNA mutation analysis. JIMD Rep. 2012;6:1-6. doi: 10.1007/8904_2011_120. Epub 2012 Jan 31. PMID: 23430931; PMCID: PMC3565630.
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Construction of a hybrid β-hexosaminidase subunit capable of forming stable homodimers that hydrolyze GM2 ganglioside in vivo.

Molecular therapy. Methods & clinical development

Tropak MB, Yonekawa S, Karumuthil-Melethil S, Thompson P, Wakarchuk W, Gray SJ, Walia JS, Mark BL, Mahuran D.
PMID: 26966698
Mol Ther Methods Clin Dev. 2016 Mar 02;3:15057. doi: 10.1038/mtm.2015.57. eCollection 2016.

Tay-Sachs or Sandhoff disease result from mutations in either the evolutionarily related HEXA or HEXB genes encoding respectively, the α- or β-subunits of β-hexosaminidase A (HexA). Of the three Hex isozymes, only HexA can interact with its cofactor, the...

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Tropak MB, Yonekawa S, Karumuthil-Melethil S, et al. Construction of a hybrid β-hexosaminidase subunit capable of forming stable homodimers that hydrolyze GM2 ganglioside in vivo. Mol Ther Methods Clin Dev. 2016;3:15057doi: 10.1038/mtm.2015.57.
Tropak, M. B., Yonekawa, S., Karumuthil-Melethil, S., Thompson, P., Wakarchuk, W., Gray, S. J., Walia, J. S., Mark, B. L., & Mahuran, D. (2016). Construction of a hybrid β-hexosaminidase subunit capable of forming stable homodimers that hydrolyze GM2 ganglioside in vivo. Molecular therapy. Methods & clinical development, 315057. https://doi.org/10.1038/mtm.2015.57
Tropak, Michael B, et al. "Construction of a hybrid β-hexosaminidase subunit capable of forming stable homodimers that hydrolyze GM2 ganglioside in vivo." Molecular therapy. Methods & clinical development vol. 3 (2016): 15057. doi: https://doi.org/10.1038/mtm.2015.57
Tropak MB, Yonekawa S, Karumuthil-Melethil S, Thompson P, Wakarchuk W, Gray SJ, Walia JS, Mark BL, Mahuran D. Construction of a hybrid β-hexosaminidase subunit capable of forming stable homodimers that hydrolyze GM2 ganglioside in vivo. Mol Ther Methods Clin Dev. 2016 Mar 02;3:15057. doi: 10.1038/mtm.2015.57. eCollection 2016. PMID: 26966698; PMCID: PMC4774620.
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Haematopoietic Stem Cell Transplantation Arrests the Progression of Neurodegenerative Disease in Late-Onset Tay-Sachs Disease.

JIMD reports

Stepien KM, Lum SH, Wraith JE, Hendriksz CJ, Church HJ, Priestman D, Platt FM, Jones S, Jovanovic A, Wynn R.
PMID: 29214523
JIMD Rep. 2018;41:17-23. doi: 10.1007/8904_2017_76. Epub 2017 Dec 07.

Tay-Sachs disease is a rare metabolic disease caused by a deficiency of hexosaminidase A that leads to accumulation of GM2 gangliosides predominantly in neural tissue. Late-onset Tay-Sachs disease variant is associated with a higher level of residual HexA activity....

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Stepien KM, Lum SH, Wraith JE, et al. Haematopoietic Stem Cell Transplantation Arrests the Progression of Neurodegenerative Disease in Late-Onset Tay-Sachs Disease. JIMD Rep. 2017;41:17-23doi: 10.1007/8904_2017_76.
Stepien, K. M., Lum, S. H., Wraith, J. E., Hendriksz, C. J., Church, H. J., Priestman, D., Platt, F. M., Jones, S., Jovanovic, A., & Wynn, R. (2018). Haematopoietic Stem Cell Transplantation Arrests the Progression of Neurodegenerative Disease in Late-Onset Tay-Sachs Disease. JIMD reports, 4117-23. https://doi.org/10.1007/8904_2017_76
Stepien, Karolina M, et al. "Haematopoietic Stem Cell Transplantation Arrests the Progression of Neurodegenerative Disease in Late-Onset Tay-Sachs Disease." JIMD reports vol. 41 (2018): 17-23. doi: https://doi.org/10.1007/8904_2017_76
Stepien KM, Lum SH, Wraith JE, Hendriksz CJ, Church HJ, Priestman D, Platt FM, Jones S, Jovanovic A, Wynn R. Haematopoietic Stem Cell Transplantation Arrests the Progression of Neurodegenerative Disease in Late-Onset Tay-Sachs Disease. JIMD Rep. 2018;41:17-23. doi: 10.1007/8904_2017_76. Epub 2017 Dec 07. PMID: 29214523; PMCID: PMC6122053.
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Accumulated α-synuclein affects the progression of GM2 gangliosidoses.

Experimental neurology

Suzuki K, Yamaguchi A, Yamanaka S, Kanzaki S, Kawashima M, Togo T, Katsuse O, Koumitsu N, Aoki N, Iseki E, Kosaka K, Yamaguchi K, Hashimoto M, Aoki I, Hirayasu Y.
PMID: 27453479
Exp Neurol. 2016 Oct;284:38-49. doi: 10.1016/j.expneurol.2016.07.011. Epub 2016 Jul 21.

The accumulation of α-synuclein (ASyn) has been observed in several lysosomal storage diseases (LSDs) but it remains unclear if ASyn accumulation contributes to LSD pathology. ASyn also accumulates in the neurons of Sandhoff disease (SD) patients and SD model...

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Suzuki K, Yamaguchi A, Yamanaka S, et al. Accumulated α-synuclein affects the progression of GM2 gangliosidoses. Exp Neurol. 2016;284:38-49doi: 10.1016/j.expneurol.2016.07.011.
Suzuki, K., Yamaguchi, A., Yamanaka, S., Kanzaki, S., Kawashima, M., Togo, T., Katsuse, O., Koumitsu, N., Aoki, N., Iseki, E., Kosaka, K., Yamaguchi, K., Hashimoto, M., Aoki, I., & Hirayasu, Y. (2016). Accumulated α-synuclein affects the progression of GM2 gangliosidoses. Experimental neurology, 28438-49. https://doi.org/10.1016/j.expneurol.2016.07.011
Suzuki, Kyoko, et al. "Accumulated α-synuclein affects the progression of GM2 gangliosidoses." Experimental neurology vol. 284 (2016): 38-49. doi: https://doi.org/10.1016/j.expneurol.2016.07.011
Suzuki K, Yamaguchi A, Yamanaka S, Kanzaki S, Kawashima M, Togo T, Katsuse O, Koumitsu N, Aoki N, Iseki E, Kosaka K, Yamaguchi K, Hashimoto M, Aoki I, Hirayasu Y. Accumulated α-synuclein affects the progression of GM2 gangliosidoses. Exp Neurol. 2016 Oct;284:38-49. doi: 10.1016/j.expneurol.2016.07.011. Epub 2016 Jul 21. PMID: 27453479.
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Anti-allergic effects and mechanisms of action of the ethanolic extract of Angelica gigas in dinitrofluorobenzene-induced inflammation models.

Environmental toxicology and pharmacology

Joo SS, Park D, Shin S, Jeon JH, Kim TK, Choi YJ, Lee SH, Kim JS, Park SK, Hwang BY, Lee DI, Kim YB.
PMID: 21787642
Environ Toxicol Pharmacol. 2010 Sep;30(2):127-33. doi: 10.1016/j.etap.2010.04.007. Epub 2010 May 23.

To confirm the anti-allergic effects of the ethanolic extract of Angelica gigas (EAG), the levels of ear erythema, ear weight, vascular leakage, heamatology, tumor-necrosis factor-α, interleukin-6 and immunoglobulin E from mice sensitized with 2,4-dinitroflurorobenzene were examined. The results showed...

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Joo SS, Park D, Shin S, et al. Anti-allergic effects and mechanisms of action of the ethanolic extract of Angelica gigas in dinitrofluorobenzene-induced inflammation models. Environ Toxicol Pharmacol. 2010;30(2):127-33doi: 10.1016/j.etap.2010.04.007.
Joo, S. S., Park, D., Shin, S., Jeon, J. H., Kim, T. K., Choi, Y. J., Lee, S. H., Kim, J. S., Park, S. K., Hwang, B. Y., Lee, D. I., & Kim, Y. B. (2010). Anti-allergic effects and mechanisms of action of the ethanolic extract of Angelica gigas in dinitrofluorobenzene-induced inflammation models. Environmental toxicology and pharmacology, 30(2), 127-33. https://doi.org/10.1016/j.etap.2010.04.007
Joo, Seong Soo, et al. "Anti-allergic effects and mechanisms of action of the ethanolic extract of Angelica gigas in dinitrofluorobenzene-induced inflammation models." Environmental toxicology and pharmacology vol. 30,2 (2010): 127-33. doi: https://doi.org/10.1016/j.etap.2010.04.007
Joo SS, Park D, Shin S, Jeon JH, Kim TK, Choi YJ, Lee SH, Kim JS, Park SK, Hwang BY, Lee DI, Kim YB. Anti-allergic effects and mechanisms of action of the ethanolic extract of Angelica gigas in dinitrofluorobenzene-induced inflammation models. Environ Toxicol Pharmacol. 2010 Sep;30(2):127-33. doi: 10.1016/j.etap.2010.04.007. Epub 2010 May 23. PMID: 21787642.
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New Approaches to Tay-Sachs Disease Therapy.

Frontiers in physiology

Solovyeva VV, Shaimardanova AA, Chulpanova DS, Kitaeva KV, Chakrabarti L, Rizvanov AA.
PMID: 30524313
Front Physiol. 2018 Nov 20;9:1663. doi: 10.3389/fphys.2018.01663. eCollection 2018.

Tay-Sachs disease belongs to the group of autosomal-recessive lysosomal storage metabolic disorders. This disease is caused by β-hexosaminidase A (HexA) enzyme deficiency due to various mutations in α-subunit gene of this enzyme, resulting in GM2 ganglioside accumulation predominantly in...

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Solovyeva VV, Shaimardanova AA, Chulpanova DS, et al. New Approaches to Tay-Sachs Disease Therapy. Front Physiol. 2018;9:1663doi: 10.3389/fphys.2018.01663.
Solovyeva, V. V., Shaimardanova, A. A., Chulpanova, D. S., Kitaeva, K. V., Chakrabarti, L., & Rizvanov, A. A. (2018). New Approaches to Tay-Sachs Disease Therapy. Frontiers in physiology, 91663. https://doi.org/10.3389/fphys.2018.01663
Solovyeva, Valeriya V, et al. "New Approaches to Tay-Sachs Disease Therapy." Frontiers in physiology vol. 9 (2018): 1663. doi: https://doi.org/10.3389/fphys.2018.01663
Solovyeva VV, Shaimardanova AA, Chulpanova DS, Kitaeva KV, Chakrabarti L, Rizvanov AA. New Approaches to Tay-Sachs Disease Therapy. Front Physiol. 2018 Nov 20;9:1663. doi: 10.3389/fphys.2018.01663. eCollection 2018. PMID: 30524313; PMCID: PMC6256099.
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Effect of two preservation methods on the viability and enzyme production of a recombinant Komagataella phaffii (Pichia pastoris) strain.

Cryobiology

Alvarado-Fernández AM, Rodríguez-López EA, Espejo-Mojica AJ, Mosquera-Arévalo AR, Alméciga-Díaz CJ, Trespalacios-Rangel AA.
PMID: 34951975
Cryobiology. 2021 Dec 21; doi: 10.1016/j.cryobiol.2021.12.004. Epub 2021 Dec 21.

The methylotrophic yeast Komagataella phaffii, previously known as Pichia pastoris, has been reported as a host for producing human recombinant lysosomal enzymes intended for enzyme replacement therapy. K. phaffii has advantages such as easy genetic handling, rapid growth, cost-effective...

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Alvarado-Fernández AM, Rodríguez-López EA, Espejo-Mojica AJ, et al. Effect of two preservation methods on the viability and enzyme production of a recombinant Komagataella phaffii (Pichia pastoris) strain. Cryobiology. 2021;doi: 10.1016/j.cryobiol.2021.12.004.
Alvarado-Fernández, A. M., Rodríguez-López, E. A., Espejo-Mojica, A. J., Mosquera-Arévalo, A. R., Alméciga-Díaz, C. J., & Trespalacios-Rangel, A. A. (2021). Effect of two preservation methods on the viability and enzyme production of a recombinant Komagataella phaffii (Pichia pastoris) strain. Cryobiology, . https://doi.org/10.1016/j.cryobiol.2021.12.004
Alvarado-Fernández, Angela María, et al. "Effect of two preservation methods on the viability and enzyme production of a recombinant Komagataella phaffii (Pichia pastoris) strain." Cryobiology vol. (2021). doi: https://doi.org/10.1016/j.cryobiol.2021.12.004
Alvarado-Fernández AM, Rodríguez-López EA, Espejo-Mojica AJ, Mosquera-Arévalo AR, Alméciga-Díaz CJ, Trespalacios-Rangel AA. Effect of two preservation methods on the viability and enzyme production of a recombinant Komagataella phaffii (Pichia pastoris) strain. Cryobiology. 2021 Dec 21; doi: 10.1016/j.cryobiol.2021.12.004. Epub 2021 Dec 21. PMID: 34951975.
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The GM2 gangliosidoses: Unlocking the mysteries of pathogenesis and treatment.

Neuroscience letters

Toro C, Zainab M, Tifft CJ.
PMID: 34450229
Neurosci Lett. 2021 Nov 01;764:136195. doi: 10.1016/j.neulet.2021.136195. Epub 2021 Aug 25.

No abstract available.

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Toro C, Zainab M, Tifft CJ. The GM2 gangliosidoses: Unlocking the mysteries of pathogenesis and treatment. Neurosci Lett. 2021;764:136195doi: 10.1016/j.neulet.2021.136195.
Toro, C., Zainab, M., & Tifft, C. J. (2021). The GM2 gangliosidoses: Unlocking the mysteries of pathogenesis and treatment. Neuroscience letters, 764136195. https://doi.org/10.1016/j.neulet.2021.136195
Toro, Camilo, et al. "The GM2 gangliosidoses: Unlocking the mysteries of pathogenesis and treatment." Neuroscience letters vol. 764 (2021): 136195. doi: https://doi.org/10.1016/j.neulet.2021.136195
Toro C, Zainab M, Tifft CJ. The GM2 gangliosidoses: Unlocking the mysteries of pathogenesis and treatment. Neurosci Lett. 2021 Nov 01;764:136195. doi: 10.1016/j.neulet.2021.136195. Epub 2021 Aug 25. PMID: 34450229; PMCID: PMC8572160.
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