Homo sapiens Transcriptome or Gene expression. Homo sapiens
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This study was designed to explore the molecular mechanism of bladder cancer through an RNA-seq
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2019-03-04
相关数据集
denovo_DESeq.zip
The differentially abundant genes in each pairwise comparison of treatments
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Osteomodulin and proline/arginine-rich end leucine rich repeat protein contribute to bladder cancer initiation and progression by controling transition between epithelial and mesenchymal cells through regulation of TGF-b and EGF pathways. Osteomodulin and proline/arginine-rich end leucine rich repeat protein contribute to bladder cancer initiation and progression by controling transition between epithelial and mesenchymal cells through regulation of TGF-b and EGF pathways
Two secreted proteins, osteomodulin (OMD) and proline/arginine-rich end leucine repeat protein (PRELP), are specifically expressed in bladder epithelial umbrella cells. At the initiation of human blad
NIAID Data Ecosystem00
RNA sequencing of human and mouse cells with either endogenous or exogenous overexpression of APOBEC2 cytidine deaminase-like protein
To identify transcriptome-wide effects of the APOBEC2 cytidine deaminase-like protein, human HEK-293T and mouse C2C12 cells were transiently transfected with either an empty-vector control construct o
NIAID Data Ecosystem00
Therapeutic targeting of CD146/MCAM highlights its supportive function in prostate cancer bone metastasis
To identify the putative mechanisms of action of MCAM, we performed RNA-sequencing to define the transcriptional changes induced by MCAM knockdown. A biological triplicate for MCAM knockdown cells and
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A novel tsRNA, m7G-3' tiRNA LysTTT, promotes bladder cancer malignancy via regulating ANXA2 phosphorylation. A novel tsRNA, m7G-3' tiRNA LysTTT, promotes bladder cancer malignancy via regulating ANXA2 phosphorylation
Emerging evidence indicates that tRNA-derived small RNAs (tsRNAs) with the most abundant RNA modifications play an important role in many complex physiological and pathological processes. However, the
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