Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 72

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Current and potential new treatment strategies for creatine deficiency syndromes

Fernandes-Pires, Gabriella, Braissant, Olivier·2022·Molecular Genetics and Metabolism

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.ymgme.2021.12.005

Cites

16 of 16 references verified0 citation errors · 0 not checkable

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.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

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

Show all 16 references

Research works printed but not linked: 116

  1. Wyss, 1992, Mitochondrial creatine kinase: a key enzyme of aerobic energy metabolism, Biochim. Biophys. Acta, 1102, 119, 10.1016/0005-2728(92)90096-K · DOI · Paper page
  2. Wallimann, 2011, The creatine kinase system and pleiotropic effects of creatine, Amino Acids, 40, 1271, 10.1007/s00726-011-0877-3 · DOI · Paper page
  3. Dolder, 2003, Inhibition of the mitochondrial permeability transition by creatine kinase substrates.Requirement for microcompartmentation, J. Biol. Chem., 278, 17760, 10.1074/jbc.M208705200 · DOI · Paper page
  4. Wallimann, 1992, Intracellular compartmentation, structure and function of creatine kinase isoenzymes in tissues with high and fluctuating energy demands: the 'phosphocreatine circuit' for cellular energy homeostasis, Biochem., 281, 21, 10.1042/bj2810021 · DOI · Paper page
  5. Schlattner, 2006, Mitochondrial creatine kinase in human health and disease, Biochim. Biophys. Acta, 1762, 164, 10.1016/j.bbadis.2005.09.004 · DOI · Paper page
  6. Braissant, 2011, Creatine deficiency syndromes and the importance of creatine synthesis in the brain, Amino Acids, 40, 1315, 10.1007/s00726-011-0852-z · DOI · Paper page
  7. Hanna-El-Daher, 2016, Creatine synthesis and exchanges between brain cells: what can be learned from human creatine deficiencies and various experimental models?, Amino Acids, 48, 1877, 10.1007/s00726-016-2189-0 · DOI · Paper page
  8. da Silva, 2009, Creatine synthesis: hepatic metabolism of guanidinoacetate and creatine in the rat in vitro and in vivo, Am. J. Physiol. Endocrinol. Metab., 296, E256, 10.1152/ajpendo.90547.2008 · DOI
  9. Braissant, 2001, Endogenous synthesis and transport of creatine in the rat brain: an in situ hybridization study, Mol. Brain Res., 86, 193, 10.1016/S0169-328X(00)00269-2 · DOI
  10. Baker, 2021, GATM and GAMT synthesize creatine locally throughout the mammalian body and within oligodendrocytes of the brain, Brain Res., 1770, 10.1016/j.brainres.2021.147627 · DOI
  11. Ohtsuki, 2002, The blood-brain barrier creatine transporter is a major pathway for supplying creatine to the brain, J. Cereb. Blood Flow Metab., 22, 1327, 10.1097/01.WCB.0000033966.83623.7D · DOI
  12. Mak, 2009, Immunohistochemical localisation of the creatine transporter in the rat brain, Neuroscience, 163, 571, 10.1016/j.neuroscience.2009.06.065 · DOI
  13. Braissant, 2010, Dissociation of AGAT, GAMT and SLC6A8 in CNS: relevance to creatine deficiency syndromes, Neurobiol. Dis., 37, 423, 10.1016/j.nbd.2009.10.022 · DOI · Paper page
  14. Lowe, 2015, The distribution of the creatine transporter throughout the human brain reveals a spectrum of creatine transporter immunoreactivity, J. Comp. Neurol., 523, 699, 10.1002/cne.23667 · DOI
  15. Joncquel-Chevalier Curt, 2015, Creatine biosynthesis and transport in health and disease, Biochimie, 119, 146, 10.1016/j.biochi.2015.10.022 · DOI · Paper page
  16. Schulze, 2016, Systemic availability of guanidinoacetate affects GABAA receptor function and seizure threshold in GAMT deficient mice, Amino Acids, 48, 2041, 10.1007/s00726-016-2197-0 · DOI
  17. De Deyn, 2001, Endogenous guanidino compounds as uremic neurotoxins, Kidney Int. Suppl., 78, S77, 10.1046/j.1523-1755.2001.59780077.x · DOI
  18. Koga, 2005, Brain creatine functions to attenuate acute stress responses through GABAnergic system in chicks, Neuroscience, 132, 65, 10.1016/j.neuroscience.2005.01.004 · DOI
  19. Neu, 2002, Activation of GABA(A) receptors by guanidinoacetate: a novel pathophysiological mechanism, Neurobiol. Dis., 11, 298, 10.1006/nbdi.2002.0547 · DOI
  20. Almeida, 2006, Exocytotic release of creatine in rat brain, Synapse, 60, 118, 10.1002/syn.20280 · DOI
  21. Peral, 2010, Na(+)/Cl(-)/creatine transporter activity and expression in rat brain synaptosomes, Neuroscience, 165, 53, 10.1016/j.neuroscience.2009.10.001 · DOI
  22. Bothwell, 2001, Hypo-osmotic swelling-activated release of organic osmolytes in brain slices: implications for brain oedema in vivo, J. Neurochem., 77, 1632, 10.1046/j.1471-4159.2001.00403.x · DOI
  23. Alfieri, 2006, Creatine as a compatible osmolyte in muscle cells exposed to hypertonic stress, J. Physiol., 576, 391, 10.1113/jphysiol.2006.115006 · DOI
  24. Bothwell, 2002, Swelling-activated taurine and creatine effluxes from rat cortical astrocytes are pharmacologically distinct, J. Membr. Biol., 185, 157, 10.1007/s00232-001-0121-2 · DOI
  25. Braissant, 2019, Longitudinal neurometabolic changes in the hippocampus of a rat model of chronic hepatic encephalopathy, J. Hepatol., 71, 505, 10.1016/j.jhep.2019.05.022 · DOI
  26. Galbraith, 2006, Possible role of creatine concentrations in the brain in regulating appetite and weight, Brain Res., 1101, 85, 10.1016/j.brainres.2006.05.032 · DOI
  27. Wallimann, 2020, Role of creatine and creatine kinase in UCP1-independent adipocyte thermogenesis, Am. J. Physiol. Endocrinol. Metab., 319, E944, 10.1152/ajpendo.00367.2020 · DOI
  28. Rahbani, 2021, Creatine kinase B controls futile creatine cycling in thermogenic fat, Nature, 590, 10.1038/s41586-021-03221-y · DOI
  29. Sun, 2021, Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine, Nature, 593, 580, 10.1038/s41586-021-03533-z · DOI
  30. Ji, 2019, Slc6a8-mediated creatine uptake and accumulation reprogram macrophage polarization via regulating cytokine responses, Immunity, 51, 272, 10.1016/j.immuni.2019.06.007 · DOI
  31. Hall, 2020, Creatine transporter, reduced in colon tissues from patients with inflammatory bowel diseases, regulates energy balance in intestinal epithelial cells, epithelial integrity, and barrier function, Gastroenterology, 159, 984, 10.1053/j.gastro.2020.05.033 · DOI
  32. Harmon, 2021, The application of creatine supplementation in medical rehabilitation, Nutrients, 13, 1825, 10.3390/nu13061825 · DOI
  33. Item, 2001, Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans, Am. J. Hum. Genet., 69, 1127, 10.1086/323765 · DOI · Paper page
  34. Salomons, 2001, X-linked creatine-transporter gene (SLC6A8) defect: a new creatine-deficiency syndrome, Am. J. Hum. Genet., 68, 1497, 10.1086/320595 · DOI · Paper page
  35. van de Kamp, 2011, Clinical features and X-inactivation in females heterozygous for creatine transporter defect, Clin. Genet., 79, 264, 10.1111/j.1399-0004.2010.01460.x · DOI
  36. Rosenberg, 2004, High prevalence of SLC6A8 deficiency in X-linked mental retardation, Am. J. Hum. Genet., 75, 97, 10.1086/422102 · DOI
  37. Clark, 2006, X-linked creatine transporter (SLC6A8) mutations in about 1% of males with mental retardation of unknown etiology, Hum. Genet., 119, 604, 10.1007/s00439-006-0162-9 · DOI
  38. Stöckler-Ipsiroglu, 2014, Guanidinoacetate methyltransferase (GAMT) deficiency: outcomes in 48 individuals and recommendations for diagnosis, treatment and monitoring, Mol. Genet. Metab., 111, 16, 10.1016/j.ymgme.2013.10.018 · DOI · Paper page
  39. Lion-François, 2006, High frequency of creatine deficiency syndromes in patients with unexplained mental retardation, Neurology, 67, 1713, 10.1212/01.wnl.0000239153.39710.81 · DOI
  40. Arias, 2007, Creatine transporter deficiency: prevalence among patients with mental retardation and pitfalls in metabolite screening, Clin. Biochem., 40, 1328, 10.1016/j.clinbiochem.2007.07.010 · DOI
  41. Schulze, 2003, Lack of creatine in muscle and brain in an adult with GAMT deficiency, Ann. Neurol., 53, 248, 10.1002/ana.10455 · DOI
  42. Rackayova, 2017, Creatine in the central nervous system: from magnetic resonance spectroscopy to creatine deficiencies, Anal. Biochem., 529, 144, 10.1016/j.ab.2016.11.007 · DOI
  43. Schulze, 1997, Creatine deficiency syndrome caused by guanidinoacetate methyltransferase deficiency: diagnostic tools for a new inborn error of metabolism, J. Pediatr., 131, 626, 10.1016/S0022-3476(97)70075-1 · DOI
  44. Battini, 2002, Creatine depletion in a new case with AGAT deficiency: clinical and genetic study in a large pedigree, Mol. Genet. Metab., 77, 326, 10.1016/S1096-7192(02)00175-0 · DOI
  45. DeGrauw, 2002, Congenital creatine transporter deficiency, Neuropediatrics, 33, 232, 10.1055/s-2002-36743 · DOI
  46. van de Kamp, 2013, New insights into creatine transporter deficiency: the importance of recycling creatine in the brain, J. Inherit. Metab. Dis., 36, 155, 10.1007/s10545-012-9537-3 · DOI
  47. Braissant, 2014, GAMT deficiency: 20 years of a treatable inborn error of metabolism, Mol. Genet. Metabol., 111, 1, 10.1016/j.ymgme.2013.11.002 · DOI
  48. van de Kamp, 2014, X-linked creatine transporter deficiency: clinical aspects and pathophysiology, J. Inherit. Metab. Dis., 37, 715, 10.1007/s10545-014-9713-8 · DOI
  49. Mercimek-Mahmutoglu, 2006, GAMT deficiency: features, treatment, and outcome in an inborn error of creatine synthesis, Neurology, 67, 480, 10.1212/01.wnl.0000234852.43688.bf · DOI
  50. Stromberger, 2003, Clinical characteristics and diagnostic clues in inborn errors of creatine metabolism, J. Inherit. Metab. Dis., 26, 299, 10.1023/A:1024453704800 · DOI
  51. Braissant, 2008, AGAT, GAMT and SLC6A8 distribution in the central nervous system, in relation to creatine deficiency syndromes: a review, J. Inherit. Metab. Dis., 31, 230, 10.1007/s10545-008-0826-9 · DOI
  52. Edison, 2007, Creatine synthesis: production of guanidinoacetate by the rat and human kidney in vivo, Am. J. Physiol. Renal. Physiol., 293, F1799, 10.1152/ajprenal.00356.2007 · DOI
  53. Braissant, 2012, Creatine and guanidinoacetate transport at blood-brain and blood-cerebrospinal fluid barriers, J. Inherit. Metab. Dis., 35, 655, 10.1007/s10545-011-9433-2 · DOI · Paper page
  54. Almeida, 2004, Creatine and guanidinoacetate: diagnostic markers for inborn errors in creatine biosynthesis and transport, Mol. Genet. Metab., 82, 214, 10.1016/j.ymgme.2004.05.001 · DOI
  55. Sijens, 2005, 1H chemical shift imaging of the brain in guanidino methyltransferase deficiency, a creatine deficiency syndrome; guanidinoacetate accumulation in the gray matter, Eur. Radiol., 15, 1923, 10.1007/s00330-005-2670-8 · DOI
  56. Choe, 2013, L-arginine:glycine amidinotransferase deficiency protects from metabolic syndrome, Hum. Mol. Genet., 22, 110, 10.1093/hmg/dds407 · DOI
  57. Levin, 2021, X-linked creatine transporter deficiency results in prolonged QTc and increased sudden death risk in humans and disease model, Genet. Med., 23, 1864, 10.1038/s41436-021-01224-8 · DOI
  58. Carducci, 2002, Guanidinoacetate and creatine plus creatinine assessment in physiologic fluids: an effective diagnostic tool for the biochemical diagnosis of arginine:glycine amidinotransferase and guanidinoacetate methyltransferase deficiencies, Clin. Chem., 48, 1772, 10.1093/clinchem/48.10.1772 · DOI
  59. Stöckler, 1996, Creatine replacement therapy in guanidinoacetate methyltransferase deficiency, a novel inborn error of metabolism, Lancet, 348, 789, 10.1016/S0140-6736(96)04116-5 · DOI · Paper page
  60. Stöckler-Ipsiroglu, 2015, Arginine:glycine amidinotransferase (AGAT) deficiency: clinical features and long term outcomes in 16 patients diagnosed worldwide, Mol. Genet. Metab., 116, 252, 10.1016/j.ymgme.2015.10.003 · DOI
  61. Schulze, 2001, Improving treatment of guanidinoacetate methyltransferase deficiency: reduction of guanidinoacetic acid in body fluids by arginine restriction and ornithine supplementation, Mol. Genet. Metab., 74, 413, 10.1006/mgme.2001.3257 · DOI
  62. Schulze, 2006, Presymptomatic treatment of neonatal guanidinoacetate methyltransferase deficiency, Neurology, 67, 719, 10.1212/01.wnl.0000230152.25203.01 · DOI
  63. Schulze, 2007, Pre-symptomatic treatment of creatine biosynthesis defects, Subcell. Biochem., 46, 167, 10.1007/978-1-4020-6486-9_9 · DOI
  64. Pasquali, 2014, Feasibility of newborn screening for guanidinoacetate methyltransferase (GAMT) deficiency, J. Inherit. Metab. Dis., 37, 231, 10.1007/s10545-013-9662-7 · DOI
  65. Jaggumantri, 2015, Treatment of creatine transporter (SLC6A8) deficiency with oral S-adenosyl methionine as adjunct to L-arginine, glycine, and creatine supplements, Pediatr. Neurol., 53, 360, 10.1016/j.pediatrneurol.2015.05.006 · DOI
  66. Valayannopoulos, 2012, Treatment by oral creatine, L-arginine and L-glycine in six severely affected patients with creatine transporter defect, J. Inherit. Metab. Dis., 35, 151, 10.1007/s10545-011-9358-9 · DOI
  67. van de Kamp, 2012, Long-term follow-up and treatment in nine boys with X-linked creatine transporter defect, J. Inherit. Metab. Dis., 35, 141, 10.1007/s10545-011-9345-1 · DOI · Paper page
  68. Cecil, 2001, Irreversible brain creatine deficiency with elevated serum and urine creatine: a creatine transporter defect?, Ann. Neurol., 49, 401, 10.1002/ana.79 · DOI
  69. Bizzi, 2002, X-linked creatine deficiency syndrome: a novel mutation in creatine transporter gene SLC6A8, Ann. Neurol., 52, 227, 10.1002/ana.10246 · DOI
  70. Póo-Argüelles, 2006, X-linked creatine transporter deficiency in two patients with severe mental retardation and autism, J. Inherit.Metab Dis., 29, 220, 10.1007/s10545-006-0212-4 · DOI
  71. Fons, 2008, Arginine supplementation in four patients with X-linked creatine transporter defect, J. Inherit. Metab. Dis., 31, 724, 10.1007/s10545-008-0902-1 · DOI
  72. Chilosi, 2008, Treatment with L-arginine improves neuropsychological disorders in a child with creatine transporter defect, Neurocase, 14, 151, 10.1080/13554790802060821 · DOI
  73. Wilcken, 2008, Creatine transporter defect: results of 6 months' treatment, J. Inherit. Metab. Dis., 31, 70
  74. Dunbar, 2014, Treatment of X-linked creatine transporter (SLC6A8) deficiency: systematic review of the literature and three new cases, Mol. Genet. Metab., 112, 259, 10.1016/j.ymgme.2014.05.011 · DOI
  75. Bruun, 2018, Treatment outcome of creatine transporter deficiency: international retrospective cohort study, Metab. Brain Dis., 33, 875, 10.1007/s11011-018-0197-3 · DOI
  76. Villar, 2012, Glycine and L-arginine treatment causes hyperhomocysteinemia in cerebral creatine transporter deficiency patients, JIMD Rep., 4, 13
  77. Adriano, 2011, Searching for a therapy of creatine transporter deficiency: some effects of creatine ethyl ester in brain slices in vitro, Neuroscience, 199, 386, 10.1016/j.neuroscience.2011.09.018 · DOI
  78. Adriano, 2017, Creatine salts provide neuroprotection even after partial impairment of the creatine transporter, Neuroscience, 340, 299, 10.1016/j.neuroscience.2016.02.038 · DOI
  79. Garbati, 2014, Effects of amide creatine derivatives in brain hippocampal slices, and their possible usefulness for curing creatine transporter deficiency, Neurochem. Res., 39, 37, 10.1007/s11064-013-1188-8 · DOI
  80. Lunardi, 2006, The creatine transporter mediates the uptake of creatine by brain tissue, but not the uptake of two creatine-derived compounds, Neuroscience, 142, 991, 10.1016/j.neuroscience.2006.06.058 · DOI
  81. Perasso, 2009, In vivo neuroprotection by a creatine-derived compound: phosphocreatine-mg-complex acetate, Brain Res., 1285, 158, 10.1016/j.brainres.2009.06.009 · DOI
  82. Burov, 2011, Creatinyl amino acids-new hybrid compounds with neuroprotective activity, J. Pept. Sci., 17, 620, 10.1002/psc.1379 · DOI
  83. Cacciante, 2020, Cyclocreatine treatment ameliorates the cognitive, autistic and epileptic phenotype in a mouse model of creatine transporter deficiency, Sci. Rep., 10, 18361, 10.1038/s41598-020-75436-4 · DOI
  84. Fons, 2010, Response to creatine analogs in fibroblasts and patients with creatine transporter deficiency, Mol. Genet. Metab., 99, 296, 10.1016/j.ymgme.2009.10.186 · DOI
  85. Schjelderup, 2021, Treatment experience in two adults with creatinfe transporter deficiency, Mol. Genet. Metab. Rep., 27
  86. Trotier-Faurion, 2015, Dodecyl creatine ester and lipid nanocapsule: a double strategy for the treatment of creatine transporter deficiency, Nanomedicine (Lond), 10, 185, 10.2217/nnm.13.205 · DOI
  87. Ullio-Gamboa, 2019, Dodecyl creatine ester-loaded nanoemulsion as a promising therapy for creatine transporter deficiency, Nanomedicine (Lond.), 14, 1579, 10.2217/nnm-2019-0059 · DOI
  88. Braakman, 2011, Protein folding and modification in the mammalian endoplasmic reticulum, Annu. Rev. Biochem., 80, 71, 10.1146/annurev-biochem-062209-093836 · DOI · Paper page
  89. Leidenheimer, 2014, Pharmacological chaperoning: a primer on mechanism and pharmacology, Pharmacol. Res., 83, 10, 10.1016/j.phrs.2014.01.005 · DOI
  90. El-Kasaby, 2019, Rescue by 4-phenylbutyrate of several misfolded creatine transporter-1 variants linked to the creatine transporter deficiency syndrome, Neuropharmacology, 161, 10.1016/j.neuropharm.2019.03.015 · DOI
  91. Farr, 2020, The creatine transporter unfolded: a knotty premise in the cerebral creatine deficiency syndrome, Front. Synaptic Neurosci., 12, 10.3389/fnsyn.2020.588954 · DOI
  92. Teschemacher, 2005, Targeting specific neuronal populations using adeno- and lentiviral vectors: applications for imaging and studies of cell function, Exp. Physiol., 90, 61, 10.1113/expphysiol.2004.028191 · DOI
  93. Bourdenx, 2014, Systemic gene delivery to the central nervous system using adeno-associated virus, Front. Mol. Neurosci., 7, 50, 10.3389/fnmol.2014.00050 · DOI
  94. Artusi, 2018, Herpes simplex virus vectors for gene transfer to the central nervous system, Diseases, 6, 10.3390/diseases6030074 · DOI
  95. Ingusci, 2019, Gene therapy tools for brain diseases, Front. Pharmacol., 10, 724, 10.3389/fphar.2019.00724 · DOI · Paper page
  96. Lentz, 2012, Viral vectors for gene delivery to the central nervous system, Neurobiol. Dis., 48, 179, 10.1016/j.nbd.2011.09.014 · DOI · Paper page
  97. Chtarto, 2013, An adeno-associated virus-based intracellular sensor of pathological nuclear factor-kappaB activation for disease-inducible gene transfer, PLoS One, 8, 10.1371/journal.pone.0053156 · DOI
  98. Atchison, 1965, Adenovirus-associated defective virus particles, Science, 149, 754, 10.1126/science.149.3685.754 · DOI · Paper page
  99. Kantor, 2014, Chapter three - methods for gene transfer to the central nervous system, 125, 10.1016/B978-0-12-800149-3.00003-2 · DOI · Paper page
  100. Bourdenx, 2014, Systemic gene delivery to the central nervous system using adeno-associated virus, Front. Mol. Neurosci., 7, 50, 10.3389/fnmol.2014.00050 · DOI
  101. Duque, 2009, Intravenous administration of self-complementary AAV9 enables transgene delivery to adult motor neurons, Mol.Ther., 17, 1187, 10.1038/mt.2009.71 · DOI · Paper page
  102. 2020, High-dose AAV gene therapy deaths, Nat. Biotechnol., 38
  103. Bevan, 2011, Systemic gene delivery in large species for targeting spinal cord, brain, and peripheral tissues for pediatric disorders, Mol. Ther., 19, 1971, 10.1038/mt.2011.157 · DOI · Paper page
  104. Federici, 2012, Robust spinal motor neuron transduction following intrathecal delivery of AAV9 in pigs, Gene Ther., 19, 852, 10.1038/gt.2011.130 · DOI
  105. Wang, 2014, Widespread spinal cord transduction by intrathecal injection of rAAV delivers efficacious RNAi therapy for amyotrophic lateral sclerosis, Hum. Mol. Genet., 23, 668, 10.1093/hmg/ddt454 · DOI
  106. Samaranch, 2012, 23, 382
  107. Ruzo, 2012, Correction of pathological accumulation of glycosaminoglycans in central nervous system and peripheral tissues of MPSIIIA mice through systemic AAV9 gene transfer, Hum. Gene Ther., 23, 1237, 10.1089/hum.2012.029 · DOI
  108. Keeler, 2019, Systemic delivery of AAVB1-GAA clears glycogen and prolongs survival in a mouse model of pompe disease, Hum. Gene Ther., 30, 57, 10.1089/hum.2018.016 · DOI
  109. Aurore, 2020, AAV9-mediated expression of SMN restricted to neurons does not rescue the spinal muscular atrophy phenotype in mice, Mol. Ther., 28, 1887, 10.1016/j.ymthe.2020.05.011 · DOI
  110. Lan, 2021, Challenges in adeno-associated virus-based treatment of central nervous system diseases through systemic injection, Life Sci., 270
  111. Mendell, 2017, 377, 1713
  112. Salomons, 2003, X-linked creatine transporter defect: an overview, J. Inherit. Metab. Dis., 26, 309, 10.1023/A:1024405821638 · DOI
  113. Walker, 1976, Creatine biosynthesis during embryonic development. False feedback suppression of liver amidinotransferase by N-acetimidoylsarcosine and 1-carboxymethyl-2-iminoimidazolidine (cyclocreatine), Biochemistry, 15, 2519, 10.1021/bi00657a004 · DOI
  114. Takeda, 1992, Biosynthesis of guanidinoacetic acid in isolated renal tubules, Eur. J. Clin. Chem. Clin. Biochem., 30, 325
  115. Braissant, 2008, Ammonium alters creatine transport and synthesis in a 3D-culture of developing brain cells, resulting in secondary cerebral creatine deficiency, Eur. J. Neurosci., 27, 1673, 10.1111/j.1460-9568.2008.06126.x · DOI
  116. Hanna-El-Daher, 2015, Mild guanidinoacetate increase under partial guanidinoacetate methyltransferase deficiency strongly affects brain cell development, Neurobiol. Dis., 79, 14, 10.1016/j.nbd.2015.03.029 · DOI

Cited by

Metadata

Authors
Fernandes-Pires, G., & Braissant, O.
Venue
Molecular Genetics and Metabolism
Publisher
Elsevier BV
Published
2022-01
Volume
135
Issue
1
Pages
15-26
ISSN
1096-7192
Cited by
72
References
16
Language
en
Licence
Funders
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (31003A-175778)

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

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.