Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning

ABSTRACT: AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning

PROVIDER: PRJNA428246 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6492321.fastq.gz	Fastqsanger.gz
	SRR6492322.fastq.gz	Fastqsanger.gz
	SRR6492323.fastq.gz	Fastqsanger.gz
	SRR6492324.fastq.gz	Fastqsanger.gz
	SRR6492325.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning

Project description:RNA-seq of RNA isolated from E10.5 mandibular prominence of 3 control and 3 Tfap2a;Tfap2b;Wnt1CRE mutant mouse embryos.

2018-01-03 | GSE108678 | GEO

Transcription profiling following expression of the transcription factor Hoxa2 in first branchial arch cells

Project description:Branchial arches are transient tissue bands in the head region of all vertebrate embryos. Although initially formed from similar components, each arch will give rise to different head and neck structures.<br><br>To understand the molecular control of inter-branchial arch identity, we forced expression of the transcription factor Hoxa2 (the main determinant of second branchial arch fate) in first branchial arch mice cells, and analyzed changes in global expression.<br><br>

2013-12-13 | E-MEXP-3837 | biostudies-arrayexpress

ChIP-seq for histone H3K27Ac on mouse first branchial arch at E11.5

Project description:H3K27Ac ChIP-seq on mouse first branchial arch (BA1) at embryonic day (E) 11.5.

2020-01-06 | E-MTAB-7966 | biostudies-arrayexpress

ChIP-Seq of mouse second branchial arch cells with antibody against Hoxa2

Project description:Chromatin immunoprecipitation of Hoxa2 in second branchial arch cells from E11.5 mouse embryos detected by SOLiD sequencing

2012-01-17 | E-MTAB-711 | biostudies-arrayexpress

AP-2? and AP-2? cooperatively orchestrate homeobox gene expression during branchial arch patterning.

Project description:The evolution of a hinged moveable jaw with variable morphology is considered a major factor behind the successful expansion of the vertebrates. DLX homeobox transcription factors are crucial for establishing the positional code that patterns the mandible, maxilla and intervening hinge domain, but how the genes encoding these proteins are regulated remains unclear. Herein, we demonstrate that the concerted action of the AP-2? and AP-2? transcription factors within the mouse neural crest is essential for jaw patterning. In the absence of these two proteins, the hinge domain is lost and there are alterations in the size and patterning of the jaws correlating with dysregulation of homeobox gene expression, with reduced levels of Emx, Msx and Dlx paralogs accompanied by an expansion of Six1 expression. Moreover, detailed analysis of morphological features and gene expression changes indicate significant overlap with various compound Dlx gene mutants. Together, these findings reveal that the AP-2 genes have a major function in mammalian neural crest development, influencing patterning of the craniofacial skeleton via the DLX code, an effect that has implications for vertebrate facial evolution, as well as for human craniofacial disorders.

| S-EPMC5825845 | biostudies-literature

Genome-wide identification of AP-2α targets in bladder cells by RNA-seq (Control vs AP-2α KD)

Project description:TFAP2A (AP-2α) is a member of the transcription factor AP-2 family, functions as a tumor suppressor by regulating the expression of various cancer-related genes; its expression is positively correlated with chemosensitivity and survival of cancer patients.

2020-12-08 | GSE128714 | GEO

Genome-wide identification of AP-2α targets in bladder cells by RNA-seq (Control vs AP-2α OE)

2020-12-08 | GSE128715 | GEO

AP-2α pull down from E12.5 cortex

Project description:Identificatin of interaction partners of AP-2α via pull down from the cortex of E12.5 mice followed by quantitative mass spectrometry.

2023-12-11 | PXD047202 | Pride

Genome-wide identification of AP-2α by ChIP-chip in breast cancer cell line MCF7

Project description:The AP-2 family of transcription factors is involved in the regulation of embryonic development, cell proliferation and tumorigenesis. To date, five members of the AP-2 family have been identified: AP-2α, AP-2β, AP-2γ, AP-2δ and AP-2ε. All AP-2 proteins bind as homo- or heterodimers to the consensus sequence of 5'- GCCNNNGGC-3' and directly regulate transcription of their target genes. Among these, AP-2α is the best-characterized gene.

2020-12-08 | GSE128589 | GEO

AP-2α Regulates S-phase and is a Marker for Sensitivity to PI3K-inhibitor Buparlisib in Colon Cancer [ChIP-seq]

Project description:Abstract:AP-2α (encoded by TFAP2A) functions as a tumor suppressor and influences response to therapy in several cancer types. We aimed to characterize regulation of the transcriptome by AP-2α in colon cancer. Results: Knockout of TFAP2A induced significant alterations in the transcriptome including repression of TGM2, identified as a primary gene target of AP-2α. Loss of AP-2α delayed progression through S-phase into G2/M and decreased phosphorylation of AKT, effects that were mediated through regulation of TGM2. Buparlisib (BKM120) repressed in vitro invasiveness of HCT116 and LS-180; however, loss of AP-2α induced resistance to Buparlisib. Similarly, Buparlisib repressed PHH3 and growth of tumor xenografts and increased overall survival of tumor-bearing mice, whereas, loss of AP-2α induced resistance to the effect of PI3K inhibition. Conclusion: Loss of AP-2α in colon cancer leads to prolonged S-phase through altered activation of AKT leading to resistance to the PI3K inhibitor, Buparlisib. The findings demonstrate an important role for AP-2α in regulating progression through the cell cycle and indicates that AP-2α is a marker for response to PI3K inhibitors.

2021-06-01 | GSE155165 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data