List of Publications
There are numbers of autism related research can be found in Malaysia that generally focus on the ASD, learning disorder, communication aids, therapy and many more. The list of publications is provided below:
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2017 |
Hakim, N H A; Majlis, B Y; Suzuki, H; Tsukahara, T Neuron-specific splicing Journal Article BioScience Trends, 11 (1), pp. 16-22, 2017, ISSN: 18817815, (cited By 0). Abstract | Links | BibTeX | Tags: Alternative RNA Splicing, Alternative Splicing, Animals, Antibody Specificity, Biological, Biological Model, Diseases, Genetics, Human, Metabolism, Models, Nerve Cell, Neurons, Organ Specificity, RNA Splicing @article{Hakim201716, title = {Neuron-specific splicing}, author = {N H A Hakim and B Y Majlis and H Suzuki and T Tsukahara}, url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85014435502&doi=10.5582%2fbst.2016.01169&partnerID=40&md5=8a5044dbf3b905fc2553520a048bcd59}, doi = {10.5582/bst.2016.01169}, issn = {18817815}, year = {2017}, date = {2017-01-01}, journal = {BioScience Trends}, volume = {11}, number = {1}, pages = {16-22}, publisher = {International Advancement Center for Medicine and Health Research Co., Ltd.}, abstract = {During pre-mRNA splicing events, introns are removed from the pre-mRNA, and the remaining exons are connected together to form a single continuous molecule. Alternative splicing is a common mechanism for the regulation of gene expression in eukaryotes. More than 90% of human genes are known to undergo alternative splicing. The most common type of alternative splicing is exon skipping, which is also known as cassette exon. Other known alternative splicing events include alternative 5' splice sites, alternative 3' splice sites, intron retention, and mutually exclusive exons. Alternative splicing events are controlled by regulatory proteins responsible for both positive and negative regulation. In this review, we focus on neuronal splicing regulators and discuss several notable regulators in depth. In addition, we have also included an example of splicing regulation mediated by the RBFox protein family. Lastly, as previous studies have shown that a number of splicing factors are associated with neuronal diseases such as Alzheime's disease (AD) and Autism spectrum disorder (ASD), here we consider their importance in neuronal diseases wherein the underlying mechanisms have yet to be elucidated.}, note = {cited By 0}, keywords = {Alternative RNA Splicing, Alternative Splicing, Animals, Antibody Specificity, Biological, Biological Model, Diseases, Genetics, Human, Metabolism, Models, Nerve Cell, Neurons, Organ Specificity, RNA Splicing}, pubstate = {published}, tppubtype = {article} } During pre-mRNA splicing events, introns are removed from the pre-mRNA, and the remaining exons are connected together to form a single continuous molecule. Alternative splicing is a common mechanism for the regulation of gene expression in eukaryotes. More than 90% of human genes are known to undergo alternative splicing. The most common type of alternative splicing is exon skipping, which is also known as cassette exon. Other known alternative splicing events include alternative 5' splice sites, alternative 3' splice sites, intron retention, and mutually exclusive exons. Alternative splicing events are controlled by regulatory proteins responsible for both positive and negative regulation. In this review, we focus on neuronal splicing regulators and discuss several notable regulators in depth. In addition, we have also included an example of splicing regulation mediated by the RBFox protein family. Lastly, as previous studies have shown that a number of splicing factors are associated with neuronal diseases such as Alzheime's disease (AD) and Autism spectrum disorder (ASD), here we consider their importance in neuronal diseases wherein the underlying mechanisms have yet to be elucidated. |
2012 |
Cheah, P -S; Ramshaw, H S; Thomas, P Q; Toyo-Oka, K; Xu, X; Martin, S; Coyle, P; Guthridge, M A; Stomski, F; Buuse, Van Den M; Wynshaw-Boris, A; Lopez, A F; Schwarz, Q P Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency Journal Article Molecular Psychiatry, 17 (4), pp. 451-466, 2012, ISSN: 13594184, (cited By 58). Abstract | Links | BibTeX | Tags: 14-3-3 Proteins, Animal Experiment, Animal Model, Animal Tissue, Animals, Article, Autism, Behaviour Disorder, Bipolar Disorder, Brain, Cell Movement, Cells, Cognitive Defect, Controlled Study, Cultured, Disease Models, Disrupted in Schizophrenia 1 Protein, Embryo, Female, Gene, Gene Deletion, Genetic Predisposition to Disease, Glutamic Acid, Hippocampal Mossy Fiber, Hippocampus, Human, Hyperactivity, Inbred C57BL, Isoprotein, Knockout, Learning, Male, Maze Learning, Memory, Mice, Motor Activity, Mouse, Neurogenesis, Neuronal Migration Disorder, Neurons, Neuropsychiatry, Nonhuman, Priority Journal, Protein 14-3-3, Protein 14-3-3 Zeta, Protein Deficiency, Protein Interaction, Recognition, Risk Factor, Schizophrenia, Sensory Gating, Synapse, Unclassified Drug @article{Cheah2012451, title = {Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency}, author = {P -S Cheah and H S Ramshaw and P Q Thomas and K Toyo-Oka and X Xu and S Martin and P Coyle and M A Guthridge and F Stomski and M Van Den Buuse and A Wynshaw-Boris and A F Lopez and Q P Schwarz}, url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84859007028&doi=10.1038%2fmp.2011.158&partnerID=40&md5=7f507fef31a192a10b3cde7bf69b5442}, doi = {10.1038/mp.2011.158}, issn = {13594184}, year = {2012}, date = {2012-01-01}, journal = {Molecular Psychiatry}, volume = {17}, number = {4}, pages = {451-466}, abstract = {Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Here, we show that deletion of 14-3-3ζ causes neurodevelopmental anomalies similar to those seen in neuropsychiatric disorders such as schizophrenia, autism spectrum disorder and bipolar disorder. 14-3-3ζ-Deficient mice displayed striking behavioural and cognitive deficiencies including a reduced capacity to learn and remember, hyperactivity and disrupted sensorimotor gating. These deficits are accompanied by subtle developmental abnormalities of the hippocampus that are underpinned by aberrant neuronal migration. Significantly, 14-3-3ζ- deficient mice exhibited abnormal mossy fibre navigation and glutamatergic synapse formation. The molecular basis of these defects involves the schizophrenia risk factor, DISC1, which interacts isoform specifically with 14-3-3ζ. Our data provide the first evidence of a direct role for 14-3-3ζ deficiency in the aetiology of neurodevelopmental disorders and identifies 14-3-3ζ as a central risk factor in the schizophrenia protein interaction network. © 2012 Macmillan Publishers Limited All rights reserved.}, note = {cited By 58}, keywords = {14-3-3 Proteins, Animal Experiment, Animal Model, Animal Tissue, Animals, Article, Autism, Behaviour Disorder, Bipolar Disorder, Brain, Cell Movement, Cells, Cognitive Defect, Controlled Study, Cultured, Disease Models, Disrupted in Schizophrenia 1 Protein, Embryo, Female, Gene, Gene Deletion, Genetic Predisposition to Disease, Glutamic Acid, Hippocampal Mossy Fiber, Hippocampus, Human, Hyperactivity, Inbred C57BL, Isoprotein, Knockout, Learning, Male, Maze Learning, Memory, Mice, Motor Activity, Mouse, Neurogenesis, Neuronal Migration Disorder, Neurons, Neuropsychiatry, Nonhuman, Priority Journal, Protein 14-3-3, Protein 14-3-3 Zeta, Protein Deficiency, Protein Interaction, Recognition, Risk Factor, Schizophrenia, Sensory Gating, Synapse, Unclassified Drug}, pubstate = {published}, tppubtype = {article} } Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Here, we show that deletion of 14-3-3ζ causes neurodevelopmental anomalies similar to those seen in neuropsychiatric disorders such as schizophrenia, autism spectrum disorder and bipolar disorder. 14-3-3ζ-Deficient mice displayed striking behavioural and cognitive deficiencies including a reduced capacity to learn and remember, hyperactivity and disrupted sensorimotor gating. These deficits are accompanied by subtle developmental abnormalities of the hippocampus that are underpinned by aberrant neuronal migration. Significantly, 14-3-3ζ- deficient mice exhibited abnormal mossy fibre navigation and glutamatergic synapse formation. The molecular basis of these defects involves the schizophrenia risk factor, DISC1, which interacts isoform specifically with 14-3-3ζ. Our data provide the first evidence of a direct role for 14-3-3ζ deficiency in the aetiology of neurodevelopmental disorders and identifies 14-3-3ζ as a central risk factor in the schizophrenia protein interaction network. © 2012 Macmillan Publishers Limited All rights reserved. |