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Folic acid supplementation in pregnancy and implications in health and disease

Journal of biomedical science, 2014-08, Vol.21 (1), p.77-77, Article 77

2014

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Increasing maternal or post-weaning folic acid alters gene expression and moderately changes behavior in the offspring

PloS one, 2014-07, Vol.9 (7), p.e101674

2014

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DNA Methylation Profiling at Single-Base Resolution Reveals Gestational Folic Acid Supplementation Influences the Epigenome of Mouse Offspring Cerebellum

Frontiers in neuroscience, 2016-05, Vol.10, p.168-168

2016

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Lifestyle, pregnancy and epigenetic effects

Epigenomics, 2015-02, Vol.7 (1), p.85-102

2015

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Glyoxalase I polymorphism rs2736654 causing the Ala111Glu substitution modulates enzyme activity-implications for autism

Autism research, 2011-08, Vol.4 (4), p.262-270

2011

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Proteomic studies identified a single nucleotide polymorphism in glyoxalase I as autism susceptibility factor

American journal of medical genetics, 2004-11, Vol.131A (1), p.11-17

2004

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Microarray analysis reveals higher gestational folic Acid alters expression of genes in the cerebellum of mice offspring-a pilot study

Brain sciences, 2015-01, Vol.5 (1), p.14-31

2015

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A critical tryptophan and Ca2+ in activation and catalysis of TPPI, the enzyme deficient in classic late-infantile neuronal ceroid lipofuscinosis

PloS one, 2010-08, Vol.5 (8), p.e11929

2010

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Diagnosis of late-infantile neuronal ceroid lipofuscinosis using dried blood spot-based assay for TPPI enzyme activity: TPPI diagnostic assay from DBS

Clinica chimica acta, 2020-08, Vol.507, p.62-68

2020

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High Gestational Folic Acid Supplementation Alters Expression of Imprinted and Candidate Autism Susceptibility Genes in a sex-Specific Manner in Mouse Offspring

Journal of molecular neuroscience, 2016-02, Vol.58 (2), p.277-286

2016

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Folic acid supplementation dysregulates gene expression in lymphoblastoid cells – Implications in nutrition

Biochemical and biophysical research communications, 2011-09, Vol.412 (4), p.688-692

2011

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Targeted Disruption of the Cln3 Gene Provides a Mouse Model for Batten Disease

Neurobiology of disease, 1999-10, Vol.6 (5), p.321-334

1999

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4 Biochemistry of neuronal ceroid lipofuscinoses

Advances in Genetics, 2001, Vol.45, p.93-106

2001

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Differential Expression of Small Heat Shock Protein 27 (Hsp27) in Ataxia telangiectasia Brains

Neurochemical research, 2009-09, Vol.34 (9), p.1658-1667

2009

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Purification and Characterization of Bovine Brain Lysosomal Pepstatin‐Insensitive Proteinase, the Gene Product Deficient in the Human Late‐Infantile Neuronal Ceroid Lipofuscinosis

Journal of neurochemistry, 2000-01, Vol.74 (1), p.287-294

2000

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Proteomic approach for the elucidation of biological defects in autism

Journal of autism and developmental disorders, 2001-12, Vol.31 (6), p.557-560

2001

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Diagnosis of late-infantile neuronal ceroid lipofuscinosis using dried blood spot-based assay for TPPI enzyme activity

Clinica chimica acta, 2020-08, Vol.507, p.62-68

2020

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FPGA – realization of digital PWM controller using Q-format-based signal processing

Journal of vibration and control, 2015-04, Vol.21 (5), p.938-948

2015

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Increased brain lysosomal pepstatin-insensitive proteinase activity in patients with neurodegenerative diseases

Neuroscience letters, 1999-04, Vol.264 (1), p.157-160

1999

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Specific substrate for CLN2 proteaseltripeptidylpeptidaseI assay

European journal of paediatric neurology, 2001, Vol.5, p.63-68

2001

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Targeted Disruption of the Cln3 Gene Provides a Mouse Model for Batten Disease

Neurobiology of disease, 2000-04, Vol.7 (2), p.127

2000

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A Critical Tryptophan and Ca.sup.2+ in Activation and Catalysis of TPPI, the Enzyme Deficient in Classic Late-Infantile Neuronal Ceroid Lipofuscinosis

PloS one, 2010-08, Vol.5 (8), p.e11929

2010

Volltextzugriff (PDF)

Proteomic approach for the elucidation of biological defects in autism : Current investigations in autism brain tissue research

Journal of autism and developmental disorders, 2001, Vol.31 (6), p.557-560

2001

Volltextzugriff (PDF)

Receptor Interactions of [beta]-N-Oxalyl-L-[alpha],[beta]-Diaminopropionic Acid, the Lathyrus sativus Putative Excitotoxin, with Synaptic Membranes

Neurochemical research, 1998-09, Vol.23 (9), p.1191

1998

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Receptor interactions of β-N-oxalyl-L-α, β-diaminopropionic acid, the Lathyrus sativus putative excitotoxin, with synaptic membranes

Neurochemical research, 1998-09, Vol.23 (9), p.1191-1196

1998

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Folic acid supplementation in pregnancy and implications in health and disease

Increasing maternal or post-weaning folic acid alters gene expression and moderately changes behavior in the offspring

DNA Methylation Profiling at Single-Base Resolution Reveals Gestational Folic Acid Supplementation Influences the Epigenome of Mouse Offspring Cerebellum

Lifestyle, pregnancy and epigenetic effects

Glyoxalase I polymorphism rs2736654 causing the Ala111Glu substitution modulates enzyme activity-implications for autism

Proteomic studies identified a single nucleotide polymorphism in glyoxalase I as autism susceptibility factor

Microarray analysis reveals higher gestational folic Acid alters expression of genes in the cerebellum of mice offspring-a pilot study

A critical tryptophan and Ca2+ in activation and catalysis of TPPI, the enzyme deficient in classic late-infantile neuronal ceroid lipofuscinosis

Diagnosis of late-infantile neuronal ceroid lipofuscinosis using dried blood spot-based assay for TPPI enzyme activity: TPPI diagnostic assay from DBS

High Gestational Folic Acid Supplementation Alters Expression of Imprinted and Candidate Autism Susceptibility Genes in a sex-Specific Manner in Mouse Offspring

Folic acid supplementation dysregulates gene expression in lymphoblastoid cells – Implications in nutrition

Targeted Disruption of the Cln3 Gene Provides a Mouse Model for Batten Disease

4 Biochemistry of neuronal ceroid lipofuscinoses

Differential Expression of Small Heat Shock Protein 27 (Hsp27) in Ataxia telangiectasia Brains

Purification and Characterization of Bovine Brain Lysosomal Pepstatin‐Insensitive Proteinase, the Gene Product Deficient in the Human Late‐Infantile Neuronal Ceroid Lipofuscinosis

Proteomic approach for the elucidation of biological defects in autism

Diagnosis of late-infantile neuronal ceroid lipofuscinosis using dried blood spot-based assay for TPPI enzyme activity

FPGA – realization of digital PWM controller using Q-format-based signal processing

Increased brain lysosomal pepstatin-insensitive proteinase activity in patients with neurodegenerative diseases

Specific substrate for CLN2 proteaseltripeptidylpeptidaseI assay

Targeted Disruption of the Cln3 Gene Provides a Mouse Model for Batten Disease

A Critical Tryptophan and Ca.sup.2+ in Activation and Catalysis of TPPI, the Enzyme Deficient in Classic Late-Infantile Neuronal Ceroid Lipofuscinosis

Proteomic approach for the elucidation of biological defects in autism : Current investigations in autism brain tissue research

Receptor Interactions of [beta]-N-Oxalyl-L-[alpha],[beta]-Diaminopropionic Acid, the Lathyrus sativus Putative Excitotoxin, with Synaptic Membranes

Receptor interactions of β-N-oxalyl-L-α, β-diaminopropionic acid, the Lathyrus sativus putative excitotoxin, with synaptic membranes

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