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Neil Smyth

Researcher at University of Southampton

Publications -  83
Citations -  5973

Neil Smyth is an academic researcher from University of Southampton. The author has contributed to research in topics: Laminin & Basement membrane. The author has an hindex of 44, co-authored 81 publications receiving 5492 citations. Previous affiliations of Neil Smyth include Southampton General Hospital & Max Planck Society.

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Epidermal transglutaminase (TGase 3) is the autoantigen of dermatitis herpetiformis.

TL;DR: It is demonstrated that epidermal transglutaminase, rather than tissue transglutanase, is the dominant autoantigen in dermatitis herpetiformis and explain why skin symptoms appear in a proportion of patients having gluten sensitive disease.
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Matrix assembly, regulation, and survival functions of laminin and its receptors in embryonic stem cell differentiation

TL;DR: This study used differentiating embryoid bodies derived from mouse embryonic stem cells null for γ1-laminin, β1-integrin and α/β-dystroglycan to dissect the contributions of laminin domains and interacting receptors to this process.
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Integrin α2-Deficient Mice Develop Normally, Are Fertile, but Display Partially Defective Platelet Interaction with Collagen

TL;DR: It is demonstrated that integrin α2β1 significantly contributes to platelet adhesion to (fibrillar) collagen, which is confirmed by the abolished adhesion of α2-deficient platelets to soluble collagen, indicating that α2 β1 plays a supportive rather than an essential role in platelet-collagen interactions.
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Compound genetic ablation of nidogen 1 and 2 causes basement membrane defects and perinatal lethality in mice.

TL;DR: Nidogen 1 and 2 do not appear to be crucial in establishing tissue architecture during organ development; instead, they are essential for late stages of lung development and for maintenance and/or integrity of cardiac tissue, which are not compatible with postnatal survival.
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Preemptive ramipril therapy delays renal failure and reduces renal fibrosis in COL4A3-knockout mice with Alport syndrome.

TL;DR: The data in COL4A3 -/- mice as an animal-model for Alport syndrome suggest that ramipril might as well delay renal failure in humans with AS, and an antiproteinuric and antifibrotic nephroprotective effect in mice is mediated by down-regulation of TGF-beta1.