23 research outputs found

    A dynamic mode of mitotic bookmarking by transcription factors.

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    During mitosis, transcription is shut off, chromatin condenses, and most transcription factors (TFs) are reported to be excluded from chromosomes. How do daughter cells re-establish the original transcription program? Recent discoveries that a select set of TFs remain bound on mitotic chromosomes suggest a potential mechanism for maintaining transcriptional programs through the cell cycle termed mitotic bookmarking. Here we report instead that many TFs remain associated with chromosomes in mouse embryonic stem cells, and that the exclusion previously described is largely a fixation artifact. In particular, most TFs we tested are significantly enriched on mitotic chromosomes. Studies with Sox2 reveal that this mitotic interaction is more dynamic than in interphase and is facilitated by both DNA binding and nuclear import. Furthermore, this dynamic mode results from lack of transcriptional activation rather than decreased accessibility of underlying DNA sequences in mitosis. The nature of the cross-linking artifact prompts careful re-examination of the role of TFs in mitotic bookmarking

    Preparation and Characterization of Cu2ZnSnS4 Thin Films and Solar Cells Fabricated from Quaternary Cu-Zn-Sn-S Target

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    CZTS thin films were fabricated through sputtering from a quaternary Cu-Zn-Sn-S target, followed by a sulfurization process. CZTS thin-film solar cells were also fabricated and a highest efficiency of 4.04% was achieved. It has been found that obvious Zn loss occurs during the sputtering and poorly crystallized CZTS are formed in the sputtered films. The Zn loss leads to the appearance of SnS. A sulfurization process can obviously improve the crystallinity of CZTS and films with grain size of several hundred nanometers can be obtained after sulfurization. The optical band gap of the films is estimated to be 1.57 eV. The electrical properties of the 4.04% efficient solar cell were investigated and it has been found that cell has obvious deficiency in minority carrier lifetime. This deficiency should be responsible for the low Jsc and low Voc of our cell

    Resetting Human Naïve Pluripotency

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    The rodent naive pluripotent state is believed to represent the preimplantation inner cell mass state of the developing blastocyst and can derive self-renewing pluripotent embryonic stem cells (ESCs) in vitro. Nevertheless, human ESCs exhibit epigenetic, metabolic, and transcriptomic characteristics more akin to primed pluripotent stem cells (PSCs) derived from the postimplantation epiblast. Understanding the genetic and epigenetic mechanisms that constrain human ESCs in the primed state is crucial for the human naive pluripotent state resetting and numerous applications in regenerative medicine. In this review, we begin by defining the naive and primed states in the murine model and compare the epigenetic characteristics of those states to the human PSCs. We also examine the various reprogramming schemes to derive the human naive pluripotent state. Finally, we discuss future perspectives of studying and deriving the human naive PSCs in the context of cellular engineering and regenerative medicine

    Thermocapillary Flow in an Annular Two-Layer Liquid System

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     By means of a hybrid lattice Boltzmann method, thermocapillary flow, driven by the surface tension owing to a horizontal temperature gradient along the interface in immiscible two-layer liquid system, is simulated numerically. The dynamic behavior of the interface is captured by using phase-field theory. The dependence of flow and interface deformation on the density ratio, Capillary number and aspect ratio, is investigated

    MiR-324-5p Suppresses Hepatocellular Carcinoma Cell Invasion by Counteracting ECM Degradation through Post-Transcriptionally Downregulating ETS1 and SP1.

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    Hepatocellular carcinoma (HCC) is one of the common malignancies, which is highly metastatic and the third common cause of cancer deaths in the world. The invasion and metastasis of cancer cells is a multistep and complex process which is mainly initiated by extracellular matrix (ECM) degradation. Aberrant expression of microRNA has been investigated in HCC and shown to play essential roles during HCC progression. In the present study, we found that microRNA-324-5p (miR-324-5p) was downregulated in both HCC cell lines and tissues. Ectopic miR-324-5p led to the reduction of HCC cells invasive and metastatic capacity, whereas inhibition of miR-324-5p promoted the invasion of HCC cells. Matrix metalloproteinase 2 (MMP2) and MMP9, the major regulators of ECM degradation, were found to be downregulated by ectopic miR-324-5p, while upregulated by miR-324-5p inhibitor. E26 transformation-specific 1 (ETS1) and Specificity protein 1 (SP1), both of which could modulate MMP2 and MMP9 expression and activity, were presented as the direct targets of and downregulated by miR-324-5p. Downregulation of ETS1 and SP1 mediated the inhibitory function of miR-324-5p on HCC migration and invasion. Our study demonstrates that miR-324-5p suppresses hepatocellular carcinoma cell invasion and might provide new clues to invasive HCC therapy
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