1,536 research outputs found
sj-xls-3-ict-10.1177_15347354241233258 – Supplemental material for The Herbal Combination Shu Gan Jie Yu Regulates the SNCG/ER-a/AKT-ERK Pathway in DMBA-Induced Breast Cancer and Breast Cancer Cell Lines Based on RNA-Seq and IPA Analysis
Supplemental material, sj-xls-3-ict-10.1177_15347354241233258 for The Herbal Combination Shu Gan Jie Yu Regulates the SNCG/ER-a/AKT-ERK Pathway in DMBA-Induced Breast Cancer and Breast Cancer Cell Lines Based on RNA-Seq and IPA Analysis by Yi Zhao, Linan Zhao, Tao Wang, Zhenghao Liu, Suyuan Tang, Hongxia Huang, Li Wu and Youzhi Sun in Integrative Cancer Therapies</p
sj-docx-1-ict-10.1177_15347354241233258 – Supplemental material for The Herbal Combination Shu Gan Jie Yu Regulates the SNCG/ER-a/AKT-ERK Pathway in DMBA-Induced Breast Cancer and Breast Cancer Cell Lines Based on RNA-Seq and IPA Analysis
Supplemental material, sj-docx-1-ict-10.1177_15347354241233258 for The Herbal Combination Shu Gan Jie Yu Regulates the SNCG/ER-a/AKT-ERK Pathway in DMBA-Induced Breast Cancer and Breast Cancer Cell Lines Based on RNA-Seq and IPA Analysis by Yi Zhao, Linan Zhao, Tao Wang, Zhenghao Liu, Suyuan Tang, Hongxia Huang, Li Wu and Youzhi Sun in Integrative Cancer Therapies</p
sj-docx-2-ict-10.1177_15347354241233258 – Supplemental material for The Herbal Combination Shu Gan Jie Yu Regulates the SNCG/ER-a/AKT-ERK Pathway in DMBA-Induced Breast Cancer and Breast Cancer Cell Lines Based on RNA-Seq and IPA Analysis
Supplemental material, sj-docx-2-ict-10.1177_15347354241233258 for The Herbal Combination Shu Gan Jie Yu Regulates the SNCG/ER-a/AKT-ERK Pathway in DMBA-Induced Breast Cancer and Breast Cancer Cell Lines Based on RNA-Seq and IPA Analysis by Yi Zhao, Linan Zhao, Tao Wang, Zhenghao Liu, Suyuan Tang, Hongxia Huang, Li Wu and Youzhi Sun in Integrative Cancer Therapies</p
sj-pdf-1-jva-10.1177_11297298221115003 – Supplemental material for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis
Supplemental material, sj-pdf-1-jva-10.1177_11297298221115003 for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis by Yunfeng Li, Zhenwei Shi, Yunyun Zhao, Zhengli Tan, Hongxia Guo and Zhaoxuan Lu in The Journal of Vascular Access</p
sj-pdf-2-jva-10.1177_11297298221115003 – Supplemental material for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis
Supplemental material, sj-pdf-2-jva-10.1177_11297298221115003 for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis by Yunfeng Li, Zhenwei Shi, Yunyun Zhao, Zhengli Tan, Hongxia Guo and Zhaoxuan Lu in The Journal of Vascular Access</p
sj-pdf-3-jva-10.1177_11297298221115003 – Supplemental material for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis
Supplemental material, sj-pdf-3-jva-10.1177_11297298221115003 for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis by Yunfeng Li, Zhenwei Shi, Yunyun Zhao, Zhengli Tan, Hongxia Guo and Zhaoxuan Lu in The Journal of Vascular Access</p
A resilient formin-derived cortical actin meshwork in the rear drives actomyosin-based motility in 2D confinement
Cell migration is driven by the establishment of disparity between the cortical properties of the softer front and the more rigid rear allowing front extension and actomyosin-based rear contraction. However, how the cortical actin meshwork in the rear is generated remains elusive. Here we identify the mDia1-like formin A (ForA) from Dictyostelium discoideum that generates a subset of filaments as the basis of a resilient cortical actin sheath in the rear. Mechanical resistance of this actin compartment is accomplished by actin crosslinkers and IQGAP-related proteins, and is mandatory to withstand the increased contractile forces in response to mechanical stress by impeding unproductive blebbing in the rear, allowing efficient cell migration in two-dimensional-confined environments. Consistently, ForA supresses the formation of lateral protrusions, rapidly relocalizes to new prospective ends in repolarizing cells and is required for cortical integrity. Finally, we show that ForA utilizes the phosphoinositide gradients in polarized cells for subcellular targeting
One-laser interferometric broadband coherent anti-Stokes Raman scattering
We introduce an interferometric technique for eliminating the non-resonant background of broadband coherent anti-Stokes Raman scattering (CARS) microscopy. CARS microscopy has been used for imaging a number of biological samples and processes, but the studies are mostly limited to detecting lipids in biological systems by probing the C-H stretch. Non-resonant background and incoherent noise sources can easily overwhelm less intense signals from other molecular vibrations. In this study, we demonstrate a one-laser broadband interferometric technique that separates the spontaneous Raman scattering-related component of the CARS signal from the non-resonant background using liquid benzonitrile as a model system.Tak W. Kee, Hongxia Zhao, and Marcus T. Ciceron
Mechanistic principles underlying regulation of the actin cytoskeleton by phosphoinositides
The actin cytoskeleton powers membrane deformation during many cellular processes, such as migration, morphogenesis, and endocytosis. Membrane phosphoinositides, especially phosphatidylinositol 4,5-bisphosphate [PI(4,5)P-2], regulate the activities of many actinbinding proteins (ABPs), including profilin, cofilin, Dia2, N-WASP, ezrin, and moesin, but the underlying molecular mechanisms have remained elusive. Moreover, because of a lack of available methodology, the dynamics of membrane interactions have not been experimentally determined for any ABP. Here, we applied a combination of biochemical assays, photobleaching/activation approaches, and atomistic molecular dynamics simulations to uncover the molecular principles by which ABPs interact with phosphoinositide-rich membranes. We show that, despite using different domains for lipid binding, these proteins associate with membranes through similar multivalent electrostatic interactions, without specific binding pockets or penetration into the lipid bilayer. Strikingly, our experiments reveal that these proteins display enormous differences in the dynamics of membrane interactions and in the ranges of phosphoinositide densities that they sense. Profilin and cofilin display transient, low-affinity interactions with phosphoinositide-rich membranes, whereas F-actin assembly factors Dia2 and N-WASP reside on phosphoinositide-richmembranes for longer periods to performtheir functions. Ezrin and moesin, which link the actin cytoskeleton to the plasma membrane, bindmembranes with very high affinity and slow dissociation dynamics. Unlike profilin, cofilin, Dia2, and N-WASP, they do not require high "stimulus-responsive" phosphoinositide density for membrane binding. Moreover, ezrin can limit the lateral diffusion of PI(4,5)P-2 along the lipid bilayer. Together, these findings demonstrate that membrane-interaction mechanisms of ABPs evolved to precisely fulfill their specific functions in cytoskeletal dynamics.Peer reviewe
?-Catenin/TCF pathway upregulates STAT3 expression in human esophageal squamous cell carcinoma
Precise roles of ?-catenin/TCF pathway involved in esophageal tumorigenesis remain elusive. Here we found STAT3 overexpression in esophageal cancer cells and tissues, and its overexpression in esophageal squamous cell carcinoma (ESCC) tissues correlated with ?-catenin cytoplasmic/nuclear accumulation. A functional TCF binding element was detected in STAT3 promoter which specifically bound to TCF4. Transfected ?-catenin induced STAT3 transcriptional activity dose-dependently, and also enhanced STAT3 mRNA and protein levels. These inductions were specifically abolished by dominant-negative TCF4. These results suggest that STAT3 is a target of ?-catenin/TCF pathway and might participate in esophageal tumorigenesis
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