Role of MiR-155 Signal Pathway in Regulating Podocyte Injury Induced by TGF-β1 by Xu Lin, Xintng Zhen, Haiting Huang, Haohao Wu, Yanwu You, Pengwei Guo, Xiangjun Gu, Fafen Yang

“…Moreover, the number of apoptotic podocytes was increased after exposure to TGF-β1 and this was alleviated after miR-155 knockdown. Knocking down miR-155 also decreased an apoptosis rate of TGF-β1-treated podocytes. …”
Get full text

CX3CL1/CX3CR1 signal mediates M1-type microglia and accelerates high-altitude-induced forgetting by Xueting Wang, Yuqi Xie, Yun Niu, Baolan Wan, Yapeng Lu, Qianqian Luo, Li Zhu

“…M1-type polarized microglia are suspected to be responsible for CNS injury under hypoxic conditions, but the exact molecular mechanism is still unelucidated.MethodsCX3CR1 knock out and wide type mice were exposed to a simulated plateau at 7000 m for 48 h to construct the model of hypobaric hypoxia-induced memory impairment. …”
Get full text

Nebivolol Desensitizes Myofilaments of a Hypertrophic Cardiomyopathy Mouse Model by Sabrina Stücker, Sabrina Stücker, Nico Kresin, Nico Kresin, Lucie Carrier, Lucie Carrier, Felix W. Friedrich, Felix W. Friedrich

“…Furthermore, we investigated actions of nebivolol and epigallocatechin-gallate, which has been shown to desensitize myofilaments for Ca2+ in mouse and human HCM models, in cardiac strips of HCM patients with a mutation in the most frequently mutated HCM gene MYBPC3.Methods and Results: Nebivolol effects were tested on contractile parameters and force-Ca2+ relationship of skinned ventricular muscle strips isolated from Mybpc3-targeted knock-in (KI), wild-type (WT) mice and cardiac strips of three HCM patients with MYBPC3 mutations. …”
Get full text

Consolidated bioprocessing of lignocellulose for production of glucaric acid by an artificial microbial consortium by Chaofeng Li, Xiaofeng Lin, Xing Ling, Shuo Li, Hao Fang

“…Results The opi1 gene was knocked out because of its negative regulation on myo-inositol synthesis, which is the limiting step of d-glucaric acid production by S. cerevisiae. …”
Get full text

Discoidin domain receptor 1(DDR1) promote intestinal barrier disruption in Ulcerative Colitis through tight junction proteins degradation and epithelium apoptosis by Xiaoli Li, Qianqian Li, Bin Xiong, Huiling Chen, Xiaochun Wang, Dekui Zhang

“…Methods: The DDR1 expression level in non-inflamed and inflamed colon samples from IBD patients were assessed. DDR1 knock-out (DDR1-/-) and wild-type (WT) mice were administered dextran sulfate sodium (DSS) to induce colitis and assessed based on colitis symptoms. …”
Get full text

PDK1- and PDK2-mediated metabolic reprogramming contributes to the TGFβ1-promoted stem-like properties in head and neck cancer by Wan-Hsuan Sun, Yun-Hsuan Chen, Hou-Hsuan Lee, Yu-Wen Tang, Kuang-Hui Sun

“…Methods Levels of PDK1 and PDK2 were evaluated in HNC tissue microarrays by immunohistochemistry to explore potential clinical relevance. PDK1 and PDK2 were knocked down by the lentivirus shRNA system to investigate their role in TGFβ1-promoted tumor progression in vitro. …”
Get full text

Intracellular and extracellular promoters of metastasis to different organs by Hebert, Jess Dale.

Get full text

A CRISPR Interference System for Efficient and Rapid Gene Knockdown in Caulobacter crescentus by Guzzo, Mathilde, Castro, Lennice K., Reisch, Christopher R., Guo, Monica S., Laub, Michael T.

“…CRISPR interference (CRISPRi) is a powerful new tool used in different organisms that provides a fast, specific, and reliable way to knock down gene expression. Caulobacter crescentus is a well-studied model bacterium, and although a variety of genetic tools have been developed, it currently takes several weeks to delete or deplete individual genes, which significantly limits genetic studies. …”
Get full text

Microglia and Myelin: Improved Tools and Molecular Interactions by Kaiser, Tobias

“…Harnessing the microglia-specific Tmem119 locus and CRISPR/Cas, I engineered knock-in mice expressing EGFP or CreERT2 and show that these lines are highly specific in discerning microglia from other closely related myeloid cells. …”
Get full text

Antigen-specific memory T cell distribution in non-lymphoid tissue by Olurinde, Mobolaji O

Get full text

Non-viral drug delivery systems for immune modulation by Fuller, Jason E., Ph. D. Massachusetts Institute of Technology

Get full text

High-throughput sequencing of RNA 5'- and 3'-termini yields insights into viral and vertebrate gene expression by Koppstein, David N. P. (David Neal Pira)

Get full text

Severe acute respiratory syndrome coronavirus envelope protein ion channel activity promotes virus fitness and pathogenesis by Verdiá-Báguena, Carmina, Castaño-Rodriguez, Carlos, Alcaraz, Antonio, Torres, Jaume, Enjuanes, Luis, Fernandez-Delgado, Raul, Nieto-Torres, Jose L., DeDiego, Marta L., Jimenez-Guardeño, Jose M., Regla-Nava, Jose A., Aguilella, Vicente M.

“…In contrast, mice infected with mutants lacking IC activity, which did not incorporate mutations within E gene during the experiment, recovered from disease and most survived. Knocking down E protein IC activity did not significantly affect virus growth in infected mice but decreased edema accumulation, the major determinant of acute respiratory distress syndrome (ARDS) leading to death. …”
Get full text
Get full text

Calcium-dependent and synapsin-dependent pathways for the presynaptic actions of BDNF by Cheng, Qing, Song, Sang-Ho, Augustine, George James

“…In contrast, the sustained component was unaffected in these conditions but was eliminated by U0126, an inhibitor of the MAP kinase (MAPK) pathway, as well as by genetic deletion of synapsins in neurons from a synapsin triple knock-out (TKO) mouse. Thus, two pathways mediate the ability of BDNF to enhance spontaneous glutamate release: the transient component arises from calcium influx through TRPC3 channels, while the sustained component is mediated by MAPK phosphorylation of synapsins. …”
Get full text
Get full text

PERILAKU SAMBUNGAN KOMPOSIT KAYU-BETON DENGAN ALAT SAMBUNG SEKRUP KUNCI TERHADAP BEBAN LATERAL by , EFA SURIANI, , Ali Awaludin, ST., M.Eng., Ph.D

“…In its development, the wooden house can be made in the form of assembled or knocked down. So, what if the connection should be investigated with beams foundation is connected with using a lag-screw and foundation pedestals replaced with concrete foundations without reinforcement. …”

Targeting the SREBP-1/Hsa-Mir-497/SCAP/FASN Oncometabolic Axis Inhibits the Cancer Stem-Like and Chemoresistant Phenotype of Non-Small Cell Lung Carcinoma Cells by Tiong, Tung-Yu, Weng, Pei-Wei, Wang, Chun-Hua, Setiawan, Syahru Agung, Yadav, Vijesh Kumar, Pikatan, Narpati Wesa, Fong, Iat-Hang, Yeh, Chi-Tai, Hsu, Chia-Hung, Kuo, Kuang-Tai

“…Methods: We analyzed SREBP-1 levels and biological functions in clinical samples and the human NSCLC cell lines H441 and A549 through shRNA-based knock down of SREBP function, cisplatin-resistant clone generation, immunohistochemical staining of clinical samples, and cell viability, sphere-formation, Western blot, and quantitative PCR assays. …”
Get full text

Elucidating the molecular mechanism of TET2 function in hematopoiesis by Huang, W

“…I constructed the Tet2-knock-out (KO) HPC-7 cell and characterized the cell differentiation phenotype caused by Tet2 depletion. …”

Regulation of RNA polymerase II transcription by Spt4 in Saccharomyces cerevisiae by Uzun, Ü

“…With the same technique, the position of Spt5 on RNAPII was investigated in wild type (WT) and spt4 knock-out (spt4∆) cells. RNAPII dynamics were examined using NET-seq in spt4∆ cells or cells in which Spt4 has been anchored away to the cytoplasm (Spt4 AA). …”

Investigating the effect of H3K4 and H3K79 methylation on gene expression noise in Saccharomyces cerevisiae by Khushaim, W

“…The increase in noise that was observed on the loss of H3K4me3 was reduced to the wild-type level in the double knock-out of DOT1 and SPP1. In conclusion, this study provides evidence that gene expression noise may be regulated by histone methylation, particularly H3K4 and H3K79, and that Dot1 (H3K79me3) could redundantly function with Spp1 (H3K4me3).…”

Investigating the systemic pathological mechanisms of FUS and TDP-43 by Ali, Z

“…This project investigated the systemic pathological mechanisms of FUS and TDP-43 using physiological knock-in mouse models carrying disease-relevant mutations. …”