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Transcriptional profiling of intestinal changes following KRasG12D mutation in an APC deficient mutation

NIAID Data Ecosystem2026-04-30 收录

肿瘤发生机制

癌基因协同作用

数据链接：

https://www.ncbi.nlm.nih.gov/sra/SRP175263 数据链接链接失效反馈

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资源简介：

Activation of KRas in the intestinal epithelium alongside APC loss under the control of VilCreER Overall design: Expression data from whole intestine comparing VilCreER APCfl/fl to VilCreER APCfl/fl KRasG12D

应用场景：

创建时间：

2022-11-23

肿瘤发生机制

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Transcriptome changes following loss of Apc in the intestine. Mus musculus

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OncoSig: a new algorithm for the accurate and systematic de novo prediction of Oncoprotein-centric Signaling networks. OncoSig: a new algorithm for the accurate and systematic de novo prediction of Oncoprotein-centric Signaling networks

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We introduce a new algorithm, OncoSig, to address the deficiencies of canonical pathways through the accurate, context-specific prediction of proteins representing both known and novel functional memb

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Aneuploidy, oncogene amplification, and epithelial to mesenchymal transition define spontaneous transformation of murine epithelial cells [CGH]

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Human epithelial cancers are defined by a recurrent distribution of specific chromosomal aneuploidies. In our model system, mouse bladder and kidney epithelial cells spontaneously immortalize, transf

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MYC binding to the E-box in the 5-UTR of Nle1 predisposes mice to intestinal tumors

肿瘤发生机制

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Nle1 encodes a WD40 repeats-containing protein highly conserved in eukaryotes and involved in Notch signaling pathway. Previous studies have shown that inhibition/loss-of-function of NLE1 alleviates d

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Transcriptional profiling of intestinal changes following KRasG12D mutation in an APC deficient mutation

资源简介：

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