scholarly journals Expression and subcellular localization of HSPC117 in min pig tissues and the PK15 cell line

2019 ◽  
Vol 27 ◽  
pp. 301-306
Author(s):  
Hong Ma ◽  
Bo Fu ◽  
Xu Zhang ◽  
Liang Wang ◽  
Zhongqiu Li ◽  
...  
Author(s):  
Yang Lin ◽  
Xiaoyong Pan ◽  
Hong-Bin Shen

Abstract Motivation Long non-coding RNAs (lncRNAs) are generally expressed in a tissue-specific way, and subcellular localizations of lncRNAs depend on the tissues or cell lines that they are expressed. Previous computational methods for predicting subcellular localizations of lncRNAs do not take this characteristic into account, they train a unified machine learning model for pooled lncRNAs from all available cell lines. It is of importance to develop a cell-line-specific computational method to predict lncRNA locations in different cell lines. Results In this study, we present an updated cell-line-specific predictor lncLocator 2.0, which trains an end-to-end deep model per cell line, for predicting lncRNA subcellular localization from sequences.We first construct benchmark datasets of lncRNA subcellular localizations for 15 cell lines. Then we learn word embeddings using natural language models, and these learned embeddings are fed into convolutional neural network, long short-term memory and multilayer perceptron to classify subcellular localizations. lncLocator 2.0 achieves varying effectiveness for different cell lines and demonstrates the necessity of training cell-line-specific models. Furthermore, we adopt Integrated Gradients to explain the proposed model in lncLocator 2.0, and find some potential patterns that determine the subcellular localizations of lncRNAs, suggesting that the subcellular localization of lncRNAs is linked to some specific nucleotides. Availability The lncLocator 2.0 is available at www.csbio.sjtu.edu.cn/bioinf/lncLocator2 and the source code can be found at https://github.com/Yang-J-LIN/lncLocator2. Supplementary information Supplementary data are available at Bioinformatics online.


Blood ◽  
2006 ◽  
Vol 107 (3) ◽  
pp. 1133-1140 ◽  
Author(s):  
Christian Kardinal ◽  
Marc Dangers ◽  
Angelika Kardinal ◽  
Alexandra Koch ◽  
Dominique Tobias Brandt ◽  
...  

AbstractWe have investigated the role of tyrosine phosphorylation of the cyclin-dependent kinase (cdk) inhibitor p27Kip1 using the acute promyelocytic leukemia cell line NB4 together with granulocyte colony-stimulating factor (G-CSF). Short-term G-CSF stimulation resulted in a rapid tyrosine dephosphorylation of p27Kip1 accompanied by a change in its binding preferences to cdks. On G-CSF stimulation, p27Kip1 dissociated from cdk4 and associated with cdk2. Binding assays with recombinant p27Kip1 confirmed that tyrosine-phosphorylated p27Kip1 preferentially bound to cdk4, whereas unphosphorylated protein preferentially associated with cdk2. In addition, studies with p27Kip1 point mutations revealed a decisive role of Tyr88 and Tyr89 in binding to cdk4. Furthermore, phosphorylation of Tyr88 and Tyr89 was accompanied by strong nuclear translocation of p27Kip1. Taken together, this report provides the first evidence that tyrosine phosphorylation of p27Kip1 plays a crucial role in binding to cdks and its subcellular localization. Moreover, both effects are mediated by application of G-CSF.


2012 ◽  
Vol 61 (3) ◽  
pp. 211-215 ◽  
Author(s):  
MAGDALENA KIMSA ◽  
BARBARA STRZALKA-MROZIK ◽  
MALGORZATA KIMSA ◽  
JOLANTA ADAMSKA ◽  
JOANNA GOLA ◽  
...  

The present study focuses on the assessment of porcine endogenous retrovirus (PERV) release from PK15 cells in a time dependent manner. The highest amount of PERV A RNA was detected in PK15 cells after 16 hours of culture. The highest amount of PERV B RNA was detected in PK15 cells after 20 hours. The highest amount of both subtypes RNAs was detected in culture medium after 32 hours of culture. The peaks of PERV reverse transcriptase (RT) activity were detected after 28 h of culture in PK15 cells and after 32 hours in the culture medium. The monitoring of PERV release from PK15 cell line may be useful for the evaluation of PERV replication.


2014 ◽  
Vol 39 (4) ◽  
pp. 404-408
Author(s):  
Wei LUO ◽  
Dun ZHAO ◽  
Da-liang JIANG ◽  
Xing-long YU

2016 ◽  
Vol 36 (6) ◽  
Author(s):  
Chaohui Dai ◽  
Li Sun ◽  
Lihuai Yu ◽  
Guoqiang Zhu ◽  
Shenglong Wu ◽  
...  

As a critical adapter protein in Toll-like receptor (TLR)/Interleukin (IL)-1R signalling pathway, myeloid differentiation protein 88 (MyD88) plays an important role in immune responses and host defence against pathogens. The present study was designed to provide a foundation and an important reagent for the mechanistic study of MyD88 and its role TLR/IL-1R signalling pathways in porcine immunity. Lentivirus-mediated RNAi was used to generate a porcine PK15 cell line with a silenced MyD88 gene and quantitative real-time PCR (qPCR) and Western blotting were used to detect changes in the expression of critical genes in the Toll-like receptor 4 (TLR4) signalling pathway. ELISA was used to measure the levels of seven proinflammatory cytokines–interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α), IL-6, IL-8, IL-12, macrophage inflammatory protein (MIP)-1α and MIP-1β–in cell culture supernatants after MyD88 silencing. We successfully obtained a PK15 cell line with 61% MyD88 mRNA transcript down-regulated. In PK15 cells with MyD88 silencing, the transcript levels of TLR4 and IL-1β were significantly reduced, whereas there were no significant changes in the expression levels of cluster of differentiation antigen 14 (CD14), interferon-α (IFN-α) or TNF-α. The ELISA results showed that the levels of most cytokines were not significantly changed apart from IL-8 without stimulation, which was significantly up-regulated. When cells were induced by lipopolysaccharide (LPS) (0.1 μg/ml) for 6 h, the global level of seven proinflammatory cytokines up-regulated and the level of IL-1β, TNF-α, IL-6, IL-8 and IL-12 of Blank and negative control (NC) group up-regulated more significantly than RNAi group (P<0.05), which revealed that the MyD88 silencing could reduce the TLR4 signal transduction which inhibited the release of proinflammatory cytokines and finally leaded to immunosuppression.


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