Evolution of Anemone AR NOAA 10798 and the Related Geo-Effective Flares and CMEs

We present a detailed examination of the features of the Active Region (AR) NOAA 10798. This AR generated coronal mass ejections (CMEs) that caused a large geomagnetic storm on 24 August 2005 with the minimum Dst index of -216 nT. We examined the evolution of the AR and the features on/near the solar surface and in the interplanetary space. The AR emerged in the middle of a small coronal hole, and formed a {\it sea anemone} like configuration. H$\alpha$ filaments were formed in the AR, which have southward axial field. Three M-class flares were generated, and the first two that occurred on 22 August 2005 were followed by Halo-type CMEs. The speeds of the CMEs were fast, and recorded about 1200 and 2400 km s$^{-1}$, respectively. The second CME was especially fast, and caught up and interacted with the first (slower) CME during their travelings toward Earth. These acted synergically to generate an interplanetary disturbance with strong southward magnetic field of about -50 nT, which was followed by the large geomagnetic storm.Comment: 32 pages, 9 figures, JGR accepte

VEGF-A/NRP1 stimulates GIPC1 and Syx complex formation to promote RhoA activation and proliferation in skin cancer cells

Neuropilin-1 (NRP1) has been identified as a VEGF-A receptor. DJM-1, a human skin cancer cell line, expresses endogenous VEGF-A and NRP1. In the present study, the RNA interference of VEGF-A or NRP1 suppressed DJM-1 cell proliferation. Furthermore, the overexpression of the NRP1 wild type restored shNRP1-treated DJM-1 cell proliferation, whereas NRP1 cytoplasmic deletion mutants did not. A co-immunoprecipitation analysis revealed that VEGF-A induced interactions between NRP1 and GIPC1, a scaffold protein, and complex formation between GIPC1 and Syx, a RhoGEF. The knockdown of GIPC1 or Syx reduced active RhoA and DJM-1 cell proliferation without affecting the MAPK or Akt pathway. C3 exoenzyme or Y27632 inhibited the VEGF-A-induced proliferation of DJM-1 cells. Conversely, the overexpression of the constitutively active form of RhoA restored the proliferation of siVEGF-A-treated DJM-1 cells. Furthermore, the inhibition of VEGF-A/NRP1 signaling upregulated p27, a CDK inhibitor. A cell-penetrating oligopeptide that targeted GIPC1/Syx complex formation inhibited the VEGF-A-induced activation of RhoA and suppressed DJM-1 cell proliferation. In conclusion, this new signaling pathway of VEGF-A/NRP1 induced cancer cell proliferation by forming a GIPC1/Syx complex that activated RhoA to degrade the p27 protein