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| Autism literature | Calcineurin literature |
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| Fatemi [28] reported a reduction of Bcl-2 (a regulatory protein for control of programmed brain cell death) levels in the cerebellum of patients with autism. |
Erin et al. [30] observed that calcineurin occurred as a complex with Bcl-2 in various regions of rat and mouse brains. |
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Roesler et al. [47] reported on a translocation in the GRPR gene, the mammalian bombesin-like gastrin-releasing peptide, being associated with autism. |
Corral et al. [48] showed that bombesin promotes the activation of the nuclear factor of activated T cells (NFAT) through a Ca(2+)/calcineurin-linked pathway. |
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Huber et al. [14] showed evidence of an important functional role of fragile X protein, an identified cause of autism, in regulating activity-dependent synaptic plasticity in the brain. | Winder and Sweatt [49] described the critical role of protein phosphatase 1, protein phosphatase 2A, and calcineurin in the activity-dependent alterations of synaptic plasticity. |
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Belmonte et al. [45] reviewed neuropathological studies of the cerebral cortex in autism indicating abnormal synaptic and columnar structure and neuronal migration defects. |
Chen et al. [50] reported about the decrease in protein ubiquitination in synaptosomes and in nonneuronal cells that may play a role in the regulation of synaptic function by a calcineurin antagonist FK506. |
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Vorstman et al. [51] stated that autism spectrum disorders and subthreshold autistic symptoms are common in children with 22q11.2 deletion syndrome. |
Sivagnanasundaram et al. [52] examined the differential expression of gene mapping to human chromosome 22q11.2 in 22q11.2 deletion syndrome and found the decreased expression of calmodulin 1 encoding a calcium-dependent protein involved in the calmodulin-calcineurin regulated pathway, which is implicated in learning and memory. |
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| Mouridsen et al. [53] observed two autoimmune conditions associated with infantile autism: ulcerative colitis in mothers and type 1 diabetes in fathers. | Winter and Schatz [54] listed immunosuppression by calcineurin inhibitors as one of the promising strategies for intervention in autoimmune type 1 diabetes mellitus. |
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| Román [55] proposed that morphological brain changes in autism may be produced by maternal hypothyroxinemia resulting in low triiodothyronine in the foetal brain during pregnancy. |
Sinha et al. [56] found that calcineurin was compromised in young progeny when they investigated the maternal hypothyroxinemia effect during pregnancy on the brains of young progeny. |
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| Omura [57] published the results of measurements of asbestos accumulation where relatively high levels of asbestos were found in autism. |
Li et al. [58] investigated the role of reactive oxygen species, by asbestos, in activation of nuclear factor of activated T cells (NFAT). They found that pretreatment of cells with cyclosporin A, a pharmacological inhibitor of calcineurin, blocked asbestos-induced NFAT activation. |
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| Thornton [59] argued that artificially generated electromagnetic radiation may play an important role in the mirror neuron dysfunction associated with autism. |
Manikonda et al. [60] indicated that exposure to extremely low-frequency electromagnetic fields caused increased activity of calcineurin in the hippocampal region of rats. |
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Barnard et al. [61] revealed that adults with autism showed impaired performance on the tests of working memory. |
Runyan et al. [62] illustrated how the inhibition of calcium activated phosphatase calcineurin causes impaired working memory. |
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