Search Results: '5q31.1'

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3 results for "5q31.1"
A hypothesis that proposes that many SNPs that are markers of schizophrenia are required for immune response and that these SNPs may be rapidly accumulated as part of one or more immune response reactions. Check preview function for full copy. By John Neville
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It is hypothesized that many SNPs that are markers of schizophrenia could support the over and/or under-expression of pathways required for immune response, for example pathways leading to polyamines... More > and nitric oxide, and that these SNPs may be rapidly acquired by the schizophrenic patient or may have been rapidly acquired by one or more of their ancestors as part of one or more immune response reactions. The over-expression of a gene resulting from an immune response reaction may result in new SNP being acquired at that location. This mutation in turn may result in the over-expression of genes controlling enzymes on the same pathway. Where there is over-expression of further genes then further SNPs may be acquired as a result at the location of these over-expressed genes. In effect a cascade reaction results.< Less
Analysing and attempting to connect the genetic and metabolic derangements underpinning a disorder which is linked to schizophrenia in Irish high density schizophrenia families (see preview to check for availability of free access). By John Neville
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A familial disorder that causes psychosis is described. Associated with the disorder are distinct patterns of physical symptoms and conditions that may be used to assist diagnosis. The proband... More > carries genetic markers that link the disorder to schizophrenia in Irish high density schizophrenia families. The genetic and metabolic derangements underpinning the disorder are analysed and potentially linked. Evidence is considered which supports a working hypothesis in which haplotype SNPs located at IL3 and/or ACSL6 at 5q31.1 result in or from the failure or partial failure of one or more ERE to activate a pathway leading from P5CS to proline.< Less
Describing for the first time a COP2 transport defect that causes psychosis - go to preview function for free access. By John Neville
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In a familial disorder that can cause psychosis that is comorbid with physical symptoms of various metabolic disorders, evidence is presented which indicates that the metabolic derangement in the... More > disorder likely centers on the hypofunction of SAR1B mediated COP2 transport, and the consequential hyperfunction of SAR1B/COP2 autophagy. This metabolic derangement has significant links to five genetic locations, three of which were previously reported on in the disorder – 5q31.1, 17p11.2 and 17p13.1. It is noted that a complete or partial failure of the PI3K product PI3P, or of PI4KA dependent PI4P, to bind with SEC23IP, as part of the COP2 transport process, would be almost entirely consistent with and provide a complete explanation for the presentation of this familial disorder.< Less

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Birth Log Book Birth Log Book By Emily Rumsey
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