3,183 research outputs found
Data on the transcriptional regulation of DNA damage induced apoptosis suppressor (DDIAS) by ERK5/MEF2B pathway in lung cancer cells
No full textAbstractThe data included in this article are associated with the article entitled “DNA-damage-induced apoptosis suppressor (DDIAS) is upregulated via ERK5/MEF2B signaling and promotes β-catenin-mediated invasion” (J.Y. Im, S.H. Yoon, B.K. Kim, H.S. Ban, K.J. Won, K.S. Chung, K.E. Jung, M. Won) [1]. Quantitative RT-PCR data revealed that genetic or pharmacological inhibition of extracellular signal-regulated kinase 5 (ERK5) suppresses DDIAS transcription in response to epidermal growth factor (EGF) in Hela cells. p300 did not interact with myocyte enhancer factor 2B (MEF2B), a downstream target of ERK5 and affect transcription of DDIAS. Moreover, DDIAS transcription is activated by ERK5/MEF2B signaling on EGF exposure in the non-small cell lung cancer cells (NSCLC) NCI-H1703 and NCI-H1299. DDIAS knockdown suppresses lung cancer cell invasion by decreasing β-catenin protein level on EGF exposure
Supplemental Material, Revision_final_supple_minor_revision - Single-Factor SOX2 Mediates Direct Neural Reprogramming of Human Mesenchymal Stem Cells via Transfection of <i>In Vitro</i> Transcribed mRNA
No full textSupplemental Material, Revision_final_supple_minor_revision for Single-Factor SOX2 Mediates Direct Neural Reprogramming of Human Mesenchymal Stem Cells via Transfection of In Vitro Transcribed mRNA by Bo-Eun Kim, Soon Won Choi, Ji-Hee Shin, Jae-Jun Kim, Insung Kang, Byung-Chul Lee, Jin Young Lee, Myoung Geun Kook, and Kyung-Sun Kang in Cell Transplantation</p
Chao cai liao yong yu ya bo chang ju jiao: ge xiang yi xing hao sun cai liao yu ti du guang xue na mi bo dao guan
No full textKwok, Hui Kin = 超材料用於亞波長聚焦 : 各向異性耗損材料與梯度光學納米波導管 / 郭栩健.Thesis M.Phil. Chinese University of Hong Kong 2015.Includes bibliographical references (leaves 67-69).Abstracts also in Chinese.Title from PDF title page (viewed on 26, September, 2016).Kwok, Hui Kin = Chao cai liao yong yu ya bo chang ju jiao : ge xiang yi xing hao sun cai liao yu ti du guang xue na mi bo dao guan / Guo Xujian
SPAM1/HYAL5 double deficiency in male mice leads to severe male subfertility caused by a cumulus‐oocyte complex penetration defect
No full textThe glycosylphosphatidylinositol-anchored sperm hyaluronidases (Hyals), sperm adhesion molecule 1 (SPAM1) and HYAL5, have long been believed to assist in sperm penetration through the cumulus-oocyte complex (COC), but their role in mammalian fertilization remains unclear. Previously, we have shown that mouse sperm devoid of either Spam1 or Hyal5 are still capable of penetrating the COC and that the loss of either Spam1 or Hyal5 alone does not cause male infertility in mice. In the present study, we found that Spam1/Hyal5 double knockout (dKO) mice produced significantly fewer offspring compared with wild-type (WT) mice, and this was due to defective COC dispersal. A comparative analysis between WT and Spam1/Hyal5 dKO epididymal sperm revealed that the absence of these 2 sperm Hyals resulted in a marked accumulation of sperm on the outside of the COC. This impaired sperm activity is likely due to the deficiency in the sperm Hyals, even though other somatic Hyals are expressed normally in the dKO mice. The fertilization ability of the Spam1/Hyal5 dKO sperm was restored by adding purified human sperm Hyal to the in vitro fertilization medium. Our results suggest that Hyal deficiency in sperm may be a significant risk factor for male sterility.-Park, S., Kim, Y.-H., Jeong, P.-S., Park, C., Lee, J.-W., Kim, J.-S., Wee, G., Song, B.-S., Park, B.-J., Kim, S.-H., Sim, B.-W., Kim, S.-U., Triggs-Raine, B., Baba, T., Lee, S.-R., Kim, E. SPAM1/HYAL5 double deficiency in male mice leads to severe male subfertility caused by a cumulus-oocyte complex penetration defect.
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Understanding metastatic growth through the traction force of human breast cancer cells
No full textCancer is a hard disease to control because of its ability to spread to different parts of the body. Cancer cells can spread out from a primary tumor to distant organs which gives rise to new cancer cell colonies and more tumors over time. This process is known as metastasis and causes over 90% of human cancer deaths.
Cell traction force (CTF) coordinates many cellular functions such as cell migration. Cell migration plays a critical role in the spread of cancer. Therefore, CTF plays a significant role the the biological process of metastasis.
The goal of this experiment is to simultaneously measure the deformation field around the cells and cellular responses between two different substrate rigidities. Past experiments have been mostly done with different substrate rigidities separately. However, it is more realistic to measure cellular contractility with two different substrate rigidities simultaneously. These conditions better reflect physiological conditions because there are varying rigidities within the human body
Study of interaction between incident silicon and germanium fluxes and SiO2 layer using solid-source molecular beam epitaxy
No full textThe dependence on the substrate temperature and the flux rates of the behavior of impinging elemental Si and Ge fluxes on a SiO2 surface. including SiO2 etching and the deposition of polycrystalline Si and SiGe films, was investigated by using the solid source molecular beam epitaxy (MBE). Flux rates of the source beams and a substrate temperature were in the range of 1 to 5 X 10(13) atoms/cm2s and 710-810-degrees-C, respectively. Under these experimental conditions, the Ge flux was not individually effective to etch the SiO2, but contributed to etching the oxide layer with an accompanying Si flux. The critical flux of Si for SiO2 etching at 740-degrees-C was determined to be about 1 X 10(13) atoms/cm2s.This work was supported by the Ministry of Communications of Kore
A Novel Malate Dehydrogenase 2 Inhibitor Suppresses Hypoxia-Inducible Factor-1 by Regulating Mitochondrial Respiration.
No full textWe previously reported that hypoxia-inducible factor (HIF)-1 inhibitor LW6, an aryloxyacetylamino benzoic acid derivative, inhibits malate dehydrogenase 2 (MDH2) activity during the mitochondrial tricarboxylic acid (TCA) cycle. In this study, we present a novel MDH2 inhibitor compound 7 containing benzohydrazide moiety, which was identified through structure-based virtual screening of chemical library. Similar to LW6, compound 7 inhibited MDH2 activity in a competitive fashion, thereby reducing NADH level. Consequently, compound 7 reduced oxygen consumption and ATP production during the mitochondrial respiration cycle, resulting in increased intracellular oxygen concentration. Therefore, compound 7 suppressed the accumulation of HIF-1α and expression of its target genes, vascular endothelial growth factor (VEGF) and glucose transporter 1 (GLUT1). Moreover, reduction in ATP content activated AMPK, thereby inactivating ACC and mTOR the downstream pathways. As expected, compound 7 exhibited significant growth inhibition of human colorectal cancer HCT116 cells. Compound 7 demonstrated substantial anti-tumor efficacy in an in vivo xenograft assay using HCT116 mouse model. Taken together, a novel MDH2 inhibitor, compound 7, suppressed HIF-1α accumulation via reduction of oxygen consumption and ATP production, integrating metabolism into anti-cancer efficacy in cancer cells
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