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John K. Heath

Researcher at University of Birmingham

Publications -  167
Citations -  17235

John K. Heath is an academic researcher from University of Birmingham. The author has contributed to research in topics: Leukemia inhibitory factor & Receptor. The author has an hindex of 57, co-authored 161 publications receiving 16652 citations. Previous affiliations of John K. Heath include Jewish General Hospital & Thermo Fisher Scientific.

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Inhibition of pluripotential embryonic stem cell differentiation by purified polypeptides

TL;DR: DIA and human interleukin DA/leukaemia inhibitory factor have been identified as related multifunctional regulatory factors with distinct biological activities in both early embryonic and haemopoetic stem cell systems.
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Transforming growth factor beta modulates the expression of collagenase and metalloproteinase inhibitor.

TL;DR: The observations suggest that TGF‐beta exerts a selective effect on extracellular matrix deposition by modulating the action of other growth factors on metalloproteinase and TIMP expression.
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Aggressiveness, hypoalgesia and high blood pressure in mice lacking the adenosine A2a receptor.

TL;DR: It was found that A2aR-knockout mice were viable and bred normally, and male mice were much more aggressive towards intruders, whereas caffeine, which normally stimulates exploratory behaviour, became a depressant of exploratory activity.
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Mesoderm induction in early Xenopus embryos by heparin-binding growth factors.

TL;DR: It is reported that pure basic fibroblast growth factor (bFGF), at very low concentrations and with high specificity, closely mimics the effect of the ventrovegetal (W) signal and that the transmission of the natural VV signal can be blocked by heparin, suggesting that it may be aHeparin-binding factor such as bFGF.
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PDGF-A signaling is a critical event in lung alveolar myofibroblast development and alveogenesis

TL;DR: The two PDGF null phenotypes reveal analogous morphogenetic functions for myofibroblast-type cells in lung and kidney organogenesis, and show that PDGF-B is required in the ontogeny of kidney mesangial cells.