Nuclear accumulation of active Smad complexes is crucial for transduction of transforming growth factor β （TGF-β）- superfamily signals from transmembrane receptors into the nucleus. It is now clear that the nucleo...Nuclear accumulation of active Smad complexes is crucial for transduction of transforming growth factor β （TGF-β）- superfamily signals from transmembrane receptors into the nucleus. It is now clear that the nucleocytoplasmic distributions of Smads, in both the absence and the presence of a TGF-β-superfamily signal, are not static, but instead the Smads are continuously shuttling between the nucleus and the cytoplasm in both conditions. This article presents the evidence for continuous nucleocytoplasmic shuttling of Smads. It then reviews different mechanisms that have been proposed to mediate Smad nuclear import and export, and discusses how the Smad steady-state distributions in the absence and the presence of a TGF-β-superfamily signal are established. Finally, the biological relevance of continuous nucleocytoplasmic shuttling for signaling by TGF-β superfamily members is discussed.展开更多
The epidermal growth factor receptor （EGFR） is a member of the ErbB/EGFR family, including EGFR/Herl, ErbB2/Her2, ErbB-3/Her3, and ErbB-4/Her4. EGFR exerts its effects through the receptor tyrosine kinase phosphoryl...The epidermal growth factor receptor （EGFR） is a member of the ErbB/EGFR family, including EGFR/Herl, ErbB2/Her2, ErbB-3/Her3, and ErbB-4/Her4. EGFR exerts its effects through the receptor tyrosine kinase phosphorylation and activation of important downstream signaling pathways in normal and neoplastic cells, mainly the Ras GTPase/MAP kinase （MAPK）, STAT3, and phosphatidylinositide 3 kinase-AKT pathways. EGFR deregulation is common in malignant glioma, especially primary glioblastoma, and exists in three forms： gene overexpression （amplification）, autocrine effects of EGFR activation, and activating receptor mutation （EGFRvlII）. However, some EGFR abnormalities have also been found in low-grade gliomas, including the nuclear localization of EGFR, expression in the microfoci of anaplastic transformation, and association with neovascularization in the mesenchyma of the glioma, which suggests that some unknown EGFR-related mechanisms are possibly responsible for its central role in the initiation and progression of malignant glioma. Uncovering these mechanisms will have potential value in the development of radio- therapy, chemotherapy, and EGFR-targeted therapy for glioma.展开更多
We study the Bc meson rare decay in order to search for the Majorana neutrino signal. It is found that the corresponding decay rate is sensitive to the Majorana neutrino mass and mixing angles. The signal of B~ --~ li...We study the Bc meson rare decay in order to search for the Majorana neutrino signal. It is found that the corresponding decay rate is sensitive to the Majorana neutrino mass and mixing angles. The signal of B~ --~ lil l~ Mm induced by the Majorana neutrino within the mass region mr 〈 mn 〈mB may be observed at LHCb.展开更多
文摘Nuclear accumulation of active Smad complexes is crucial for transduction of transforming growth factor β （TGF-β）- superfamily signals from transmembrane receptors into the nucleus. It is now clear that the nucleocytoplasmic distributions of Smads, in both the absence and the presence of a TGF-β-superfamily signal, are not static, but instead the Smads are continuously shuttling between the nucleus and the cytoplasm in both conditions. This article presents the evidence for continuous nucleocytoplasmic shuttling of Smads. It then reviews different mechanisms that have been proposed to mediate Smad nuclear import and export, and discusses how the Smad steady-state distributions in the absence and the presence of a TGF-β-superfamily signal are established. Finally, the biological relevance of continuous nucleocytoplasmic shuttling for signaling by TGF-β superfamily members is discussed.
文摘The epidermal growth factor receptor （EGFR） is a member of the ErbB/EGFR family, including EGFR/Herl, ErbB2/Her2, ErbB-3/Her3, and ErbB-4/Her4. EGFR exerts its effects through the receptor tyrosine kinase phosphorylation and activation of important downstream signaling pathways in normal and neoplastic cells, mainly the Ras GTPase/MAP kinase （MAPK）, STAT3, and phosphatidylinositide 3 kinase-AKT pathways. EGFR deregulation is common in malignant glioma, especially primary glioblastoma, and exists in three forms： gene overexpression （amplification）, autocrine effects of EGFR activation, and activating receptor mutation （EGFRvlII）. However, some EGFR abnormalities have also been found in low-grade gliomas, including the nuclear localization of EGFR, expression in the microfoci of anaplastic transformation, and association with neovascularization in the mesenchyma of the glioma, which suggests that some unknown EGFR-related mechanisms are possibly responsible for its central role in the initiation and progression of malignant glioma. Uncovering these mechanisms will have potential value in the development of radio- therapy, chemotherapy, and EGFR-targeted therapy for glioma.
基金Supported by the National Science Foundation of China under Grant No.11275114China Postdoctoral Science Foundation under Grant No.2012T50604Natural Science Foundation of Shandong Province under Grant No.ZR2011AQ013
文摘We study the Bc meson rare decay in order to search for the Majorana neutrino signal. It is found that the corresponding decay rate is sensitive to the Majorana neutrino mass and mixing angles. The signal of B~ --~ lil l~ Mm induced by the Majorana neutrino within the mass region mr 〈 mn 〈mB may be observed at LHCb.
