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MOLECULAR-CELL-D-18-00192: Pole instability drives replication stress, abnormal development and tumorigenesis

NIAID Data Ecosystem2026-03-10 收录

细胞极性研究

肿瘤发生机制

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Unprocessed images for "Pole instability drives replication stress, abnormal development and tumorigenesis" MOLECULAR-CELL-D-18-00192

应用场景：

创建时间：

2018-03-19

肿瘤发生机制

Wnt信号通路调控

Bcl9 and Pygo function within the Wnt enhanceosome to effect β-catenin-dependent transcription. Whether they also mediate β-catenin-dependent neoplasia is unclear. Here we assess their roles in intest

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

肿瘤发生机制

癌基因协同作用

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 K

NIAID Data Ecosystem10

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

肿瘤发生机制

MYC调控机制

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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The FGFR4-G388R Polymorphism Promotes Mitochondrial STAT3 Serine Phosphorylation to Facilitate Pituitary Growth Hormone Cell Tumorigenesis

肿瘤发生机制

FGFR4多态性功能

Pituitary tumors are common intracranial neoplasms, yet few germline abnormalities have been implicated in their pathogenesis. Here we show that a single nucleotide germline polymorphism (SNP) substit

NIAID Data Ecosystem20

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

肿瘤发生机制

Wnt信号通路靶基因

Nearly all colorectal cancers have dysregulated Wnt signalling, predominantly through the mutation of the Apc (Adenomatous Polyposis Coli) gene. Therefore it is of vital importance to elucidate the ke

NIAID Data Ecosystem10

MOLECULAR-CELL-D-18-00192: Pole instability drives replication stress, abnormal development and tumorigenesis

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