29 research outputs found
Fractal Reconnection in Solar and Stellar Environments
Recent space based observations of the Sun revealed that magnetic
reconnection is ubiquitous in the solar atmosphere, ranging from small scale
reconnection (observed as nanoflares) to large scale one (observed as long
duration flares or giant arcades). Often the magnetic reconnection events are
associated with mass ejections or jets, which seem to be closely related to
multiple plasmoid ejections from fractal current sheet. The bursty radio and
hard X-ray emissions from flares also suggest the fractal reconnection and
associated particle acceleration. We shall discuss recent observations and
theories related to the plasmoid-induced-reconnection and the fractal
reconnection in solar flares, and their implication to reconnection physics and
particle acceleration. Recent findings of many superflares on solar type stars
that has extended the applicability of the fractal reconnection model of solar
flares to much a wider parameter space suitable for stellar flares are also
discussed.Comment: Invited chapter to appear in "Magnetic Reconnection: Concepts and
Applications", Springer-Verlag, W. D. Gonzalez and E. N. Parker, eds. (2016),
33 pages, 18 figure
Gefitinib Induces Epidermal Growth Factor Receptor Dimers Which Alters the Interaction Characteristics with 125I-EGF
The tyrosine kinase inhibitor gefitinib inhibits growth in some tumor types by targeting the epidermal growth factor receptor (EGFR). Previous studies show that the affinity of the EGF-EGFR interaction varies between hosting cell line, and that gefitinib increases the affinity for some cell lines. In this paper, we investigate possible mechanisms behind these observations. Real-time interaction analysis in LigandTracer® Grey revealed that the HER2 dimerization preventing antibody pertuzumab clearly modified the binding of 125I-EGF to EGFR on HER2 overexpressing SKOV3 cells in the presence of gefitinib. Pertuzumab did not affect the binding on A431 cells, which express low levels of HER2. Cross-linking measurements showed that gefitinib increased the amount of EGFR dimers 3.0–3.8 times in A431 cells in the absence of EGF. In EGF stimulated SKOV3 cells the amount of EGFR dimers increased 1.8–2.2 times by gefitinib, but this effect was cancelled by pertuzumab. Gefitinib treatment did not alter the number of EGFR or HER2 expressed in tumor cell lines A431, U343, SKOV3 and SKBR3. Real-time binding traces were further analyzed in a novel tool, Interaction Map, which deciphered the different components of the measured interaction and supports EGF binding to multiple binding sites. EGFR and HER2 expression affect the levels of EGFR monomers, homodimers and heterodimers and EGF binds to the various monomeric/dimeric forms of EGFR with unique binding properties. Taken together, we conclude that dimerization explains the varying affinity of EGF – EGFR in different cells, and we propose that gefitinib induces EGFR dimmers, which alters the interaction characteristics with 125I-EGF