11 research outputs found
Calculation of magnetic anisotropy energy in SmCo5
SmCo5 is an important hard magnetic material, due to its large magnetic
anisotropy energy (MAE). We have studied the magnetic properties of SmCo5 using
density functional theory (DFT) calculations where the Sm f-bands, which are
difficult to include in DFT calculations, have been treated within the LDA+U
formalism. The large MAE comes mostly from the Sm f-shell anisotropy, stemming
from an interplay between the crystal field and the spin-orbit coupling. We
found that both are of similar strengths, unlike some other Sm compounds,
leading to a partial quenching of the orbital moment (f-states cannot be
described as either pure lattice harmonics or pure complex harmonics), an
optimal situation for enhanced MAE. A smaller portion of the MAE can be
associated with the Co-d band anisotropy, related to the peak in the density of
states at the Fermi energy. Our result for the MAE of SmCo5, 21.6 meV/f.u.,
agrees reasonably with the experimental value of 13-16 meV/f.u., and the
calculated magnetic moment (including the orbital component) of 9.4 mu_B agrees
with the experimental value of 8.9 mu_B.Comment: Submitted to Phys. Rev.
Negative regulation of constitutive NF-κB and JNK signaling by PKN1-mediated phosphorylation of TRAF1
Quasiparticle recombination and 2Δ-phonon-trapping in superconducting tunneling junctions
Measurements of effective quasiparticle recombination times and of densities of electronic states at the Fermi level in superconducting Al- and Pb-films
Quasiparticle recombination time in superconducting tin and normal electronic density of states at the fermi surface from tunnel junction experiments
GPCR-CARMA3-NF-kappaB Signaling Axis: A Novel Drug Target for Cancer Therapy
G protein-coupled receptors (GPCRs) play pivotal roles in regulating various cellular functions. It has been well established that GPCR activates NF-κB and aberrant regulation of GPCR-NF-κB signaling axis leads to cancers. However, how GPCRs induce NF-κB activation remains largely elusive. Recently, it has been shown that a novel scaffold protein, CARMA3, is indispensable in GPCR-induced NF-κB activation. In CARMA3-deficient mouse embryonic fibroblast cells, some GPCR ligand-, like lysophosphatidic acid (LPA), induced NF-κB activation is completely abolished. Mechanistically, upon GPCR activation, CARMA3 is linked to the membrane by β-arrestin 2 and phosphorylated by some PKC isoform. Phosphorylation of CARMA3 unfolds its steric structure and recruits its downstream effectors, which in turn activate the IKK complex and NF-κB. Interestingly, GPCR (LPA)-CARMA3-NF-κB signaling axis also exists in ovarian cancer cells, and knockdown of CARMA3 results in attenuation of ovarian cancer migration and invasion, suggesting a novel target for cancer therapy. In this review, we summarize the biology of CARMA3, discuss the GPCR (LPA)-CARMA3-NF-κB signaling axis in ovarian cancer and speculate its potential role in other types of cancers. With a strongly increasing tendency to identify more LPA-like ligands, such as endothelin-1 and angiotensin II, which also activate NF-κB through CARMA3 and contribute to myriad diseases, GPCR- CARMA3-NF-κB signaling axis is emerging as a novel drug target for various types of cancer and other myriad diseases