More From John Neville

CCNB1, CCNB2, CCNA1, CCNA2, SYT1, SYT2, CKS2, CKS1B, CCNB3, SKP1, CDK1, RPS23, RPS27A, ZFAND4, RPS27, RPS27l, BUB1, BUB1B could play significant roles in the aetiology of schizophrenia by acting as points of contact between ALDH18A1 and SEC23IP (COP2). By John Neville
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Fourteen genes and their paralogues (CCNB1, CCNB2, CCNA1, CCNA2, SYT1, SYT2, CKS2, CKS1b, CCNB3, RPS23, RPS27A, ZFAND4, RPS27, RPS27l, BUB1, BUB1B, SKP1, CDK1), which putatively act as points of... More > contact between ALDH18A1 and COP2 associated genes, particularly SEC23IP and CSNK1D, are identified which could play significant roles in the aetiology of schizophrenia. Many of these genes are found at the same genetic locations as deletion/duplication disorders and/or CNVs that have been reported on as being associated with schizophrenia.< Less
A hypothesis that proposes that in ALDH18A1 spastic paraplegia, the failure to produce specific proline residues required for the binding of SEC23IP as part of the COP2 transport process could be causative of symptoms and may be a viable treatment target By John Neville
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It is hypothesized that a failure or partial failure of ALDH18A1/PYCR1 to produce specific proline residues could be causative of symptoms in ALDH18A1 spastic paraplegia and also of symptoms in... More > ALDH18A1/PYCR1 cutis laxa. If so, any such missing proline residues may be viable treatment targets. In the case of ALDH18A1 spastic paraplegia, these proline residues would be required for the binding of SEC23IP/PI3P, whilst in the case of ALDH18A1/PYCR1 cutis laxa, the proline residues would be required for the formation of elastin. Contains approximately forty blank pages.< 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
Purpose-driven Rapid Evolutionary Selection. By John Neville
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A hypothesis is proposed in which the over-function of a pathway that results from an immune response reaction or simply the overuse of an organ or body part in turn results in rapid mutational... More > changes that support this over-function. In other words, rapid purpose-driven selection. The hotspot conversion paradox is also discussed.< Less