首页/数据集/Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression

Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression

ChEBI2013-05-11 更新2026-07-21 收录

肿瘤发生机制

基因功能调控

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-46821 数据链接链接失效反馈

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资源简介：

Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression

应用场景：

创建时间：

2013-05-11

肿瘤发生机制

细胞衰老调控

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p53 amyloid formation induced cellular transformation and tumor formation in xenograft model

p53

肿瘤发生机制

p53 mutation and its subsequent loss of function along with gain of oncogenic functions is associated with cancer. However, the exact mechanism of how altered p53 acts as an oncogene is not clear yet.

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YAP1 and PRDM14 converge to regulate cell survival and tumorigenesis

肿瘤发生机制

疾病靶点发现

The transcriptional co-activator YAP1 oncogene is the downstream effector of the Hippo pathway, which regulates tissue homeostasis, organ size, regeneration and tumorigenesis. Multiple cancers are dep

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NGS-mRNA in lung tissues in RAG1-/- and in RAG1-/- Sgo1-/+ mice

基因表达分析

肿瘤发生机制

We compared lung mRNA expression profiles between RAG1-/- control and RAG1-/- Sgo1-/+ chromosome instability model mice. RAG1-/-Sgo1-/+ mice developed significantly more spontaneous lung tumors. Char

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Homo sapiens Transcriptome or Gene expression. Homo sapiens

转录组测序

基因功能调控

The IBTK gene encodes the major protein isoform IBtkα, that was recently characterized as substrate receptor of Cul3-dependent E3 ligase, regulating ubiquitination coupled to proteasomal degradation o

NIAID Data Ecosystem50

Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression

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