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Biopreservation and Biobanking (1)
The Journal of Experimental Medicine (1)
Asadullah, Khusru (1)
Di Cristofano, Antonio (1)
Döcke, Wolf-Dietrich (1)
Gross, Durdana (1)
Igney, Frederik H. (1)
Pandolfi, Pier Paolo (1)
Qin, Yi (1)
Schmitz, Arndt A. (1)
Schmitz, Arndt A.P. (1)
Schoepe, Stefanie (1)
Sterry, Wolfram (1)
Van Aelst, Linda (1)
Vonk, Richardus (1)
Zhao, Mingming (1)
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Willingness to Donate Human Samples for Establishing a Dermatology Research Biobank: Results of a Survey
Igney, Frederik H.
Biopreservation and Biobanking
There is a rising need for biomaterial in dermatological research with regard to both quality and quantity. Research biobanks as organized collections of biological material with associated personal and clinical data are of increasing importance. Besides technological/methodological and legal aspects, the willingness to donate samples by patients and healthy volunteers is a key success factor. To analyze the theoretical willingness to donate blood and skin samples, we developed and distributed a questionnaire. Six hundred nineteen questionnaires were returned and analyzed. The willingness to donate samples of blood (82.5%) and skin (58.7%) is high among the population analyzed and seems to be largely independent of any expense allowance. People working in the healthcare system, dermatological patients, and higher qualified individuals seem to be in particular willing to donate material. An adequate patient insurance as well as an extensive education about risks and benefits is requested. In summary, there is a high willingness to donate biological samples for dermatological research. This theoretical awareness fits well with our own experiences in establishing such a biobank.
Phosphoinositide 3-Kinase–Dependent Membrane Recruitment of P62dok Is Essential for Its Negative Effect on Mitogen-Activated Protein (Map) Kinase Activation
Di Cristofano, Antonio
Pandolfi, Pier Paolo
Van Aelst, Linda
The Journal of Experimental Medicine
A major pathway by which growth factors, such as platelet-derived growth factor (PDGF), regulate cell proliferation is via the receptor tyrosine kinase/Ras/mitogen-activated protein kinase (MAPK) signaling cascade. The output of this pathway is subjected to tight regulation of both positive and negative regulators. One such regulator is p62dok, the prototype of a newly identified family of adaptor proteins. We recently provided evidence, through the use of p62dok-deficient cells, that p62dok acts as a negative regulator of growth factor–induced cell proliferation and the Ras/MAPK pathway. We show here that reintroduction of p62dok into p62dok−/− cells can suppress the increased cell proliferation and prolonged MAPK activity seen in these cells, and that plasma membrane recruitment of p62dok is essential for its function. We also show that the PDGF-triggered plasma membrane translocation of p62dok requires activation of phosphoinositide 3-kinase (PI3-kinase) and binding of its pleckstrin homology (PH) domain to 3′-phosphorylated phosphoinositides. Furthermore, we demonstrate that p62dok can exert its negative effect on the PDGFR/MAPK pathway independently of its ability to associate with RasGAP and Nck. We conclude that p62dok functions as a negative regulator of the PDGFR/Ras/MAPK signaling pathway through a mechanism involving PI3-kinase–dependent recruitment of p62dok to the plasma membrane.
growth factors; cell proliferation; membrane lipids; signal transduction; protein-serine-threonine kinase
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