Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigating the role of YAP and FOS in driving OnF reporgramming during tumor intiation

ABSTRACT: To investigate the role of YAP and FOS in early OnF reporgramming, we knocked down either gene during tumor intiation induced by APC depletion.

ORGANISM(S): Mus musculus

PROVIDER: GSE263047 | GEO | 2024/10/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Investigating the role of FOS/AP-1 in OnF reprogramming during tumor intiation

Project description:To investigate the role of FOS/AP-1 in early OnF reprogramming, we blocked its activity during tumor intiation by overexpressing a dominant negative form of FOS.

2024-10-17 | GSE263056 | GEO

Transcriptional profiling of AKSP tumoroids following knockdown of either YAP or FOS.

Project description:To elucidate the role of YAP and FOS in sustaining the OnF state in davnaced CRC, we knocked down either gene in AKSP tumoroids.

2024-10-17 | GSE263055 | GEO

Elucidating the role of RXR in driving the OnF porgram along the CRC malignancy contiuum.

Project description:To investigate the role of RXR during eraly OnF reporgramming, we perturbed the APC/RXR regulatory axis during tumor intiation. To investigate the role of RXR in sustaining the OnF state in advanced CRC, we perturbed its expression in AKSP tumoroids.

2024-10-17 | GSE263045 | GEO

Transcriptional profiling of intestinal organoids following ectopic expression of YAP (S6) +/- FOS.

Project description:To elucidate the roles of YAP and FOS/AP-1 in driving OnF reporgramming, we tested the effects of their ecotpic expression in healthy intestinal organoids. The sequential overperession recapitulates the chornnology of deregulation of both axes during CRC evolution.

2024-10-17 | GSE263050 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [JUN_WT_M14_in_JUN_KO]

Project description:The transcriptional coactivators YAP/TAZ are the critical downstream regulators of the Hippo pathway that regulate gene expression in response to changes in pathway activity, mainly by binding to TEAD transcription factors. Uncontrolled transcriptional output of YAP/TAZ can lead to rapid induction of aggressive tumor growth. AP-1 is a dimeric basic leucine zipper (bZIP) transcription factor complex with JUN and FOS proteins being the most abundant members of this family. Unlike FOS, JUN can also form homodimers, but in the cell, JUN presumably preferentially forms heterodimers with members of the FOS family, which act as potent transcriptional activators. Previous studies identified substantial co-occupancy of YAP/TAZ and AP-1 at genomic sites, and they demonstrated that JUN/FOS heterodimers cooperate with the YAP/TAZ and TEAD transcription factors to drive YAP/TAZ target gene expression. Here, we now elucidate a negative feedback mechanism in which high YAP activity is restrained by the recruitment of homodimeric JUN::JUN/NCOR1 repressor complexes and show that this noncanonical JUN function is part of a tumor suppressor mechanism in the liver.

2024-06-30 | GSE235967 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [CutRun_in_constitutive_5SA_MCF10A]

2024-06-30 | GSE235963 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [SLAM_Seq]

2024-06-30 | GSE235616 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [TruSeq]

2024-06-30 | GSE235615 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [3primeSeq_siY]

2024-06-30 | GSE235614 | GEO

A non-canonical repressor function of JUN restrains YAP activity and suppresses YAP-dependent liver cancer growth [3prime_Seq_JUNoe]

2024-06-30 | GSE235613 | GEO