Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells

ABSTRACT: Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells

PROVIDER: PRJNA688896 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13337075.fastq.gz	Fastqsanger.gz
	SRR13444945_1.fastq.gz	Fastqsanger.gz
	SRR13444945_2.fastq.gz	Fastqsanger.gz
	SRR13444946_1.fastq.gz	Fastqsanger.gz
	SRR13444946_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells

Project description:Up-regulation of the neuropeptide NTS in a subgroup of lung cancers has been linked to poor prognosis. However, the regulatory pathway centered on NTS in lung cancer remains unclear. Here we identified the NTS specific enhancer in lung adenocarcinoma cells. The AF4/FMR2 (AFF) family protein AFF1 occupies the NTS enhancer and inhibits NTS transcription. Clustering analysis of lung adenocarcinoma gene expression data demonstrated that NTS is highly positively correlated with the expression of the oncogenic factor CPS1. Detailed analyses demonstrated that NTS antagonizes the IL6 pathway in regulating CPS1. Thus, our analyses revealed a novel NTS centered regulatory axis, consisting of AFF1 as a master transcription suppressor and IL6 as an antagonist in lung adenocarcinoma cells.

2021-03-23 | GSE164098 | GEO

Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells.

Project description:Upregulation of the neuropeptide neurotensin (NTS) in a subgroup of lung cancers has been linked to poor prognosis. However, the regulatory pathway centered on NTS in lung cancer remains unclear. Here we identified the NTS-specific enhancer in lung adenocarcinoma cells. The AF4/FMR2 (AFF) family protein AFF1 occupies the NTS enhancer and inhibits NTS transcription. Clustering analysis of lung adenocarcinoma gene expression data demonstrated that NTS expression is highly positively correlated with the expression of the oncogenic factor CPS1. Detailed analyses demonstrated that the IL6 pathway antagonizes NTS in regulating CPS1. Thus, our analyses revealed a novel NTS-centered regulatory axis, consisting of AFF1 as a master transcription suppressor and IL6 as an antagonist in lung adenocarcinoma cells.

| S-EPMC7949158 | biostudies-literature

The E3 Ubiquitin Ligase AFF1 targets ARF19 to the proteasome

Project description:Auxin critically regulates nearly every aspect of plant growth and development. Auxin-driven transcriptional responses are mediated through the AUXIN RESPONSE FACTOR (ARF) family of transcription factors. Although ARF protein stability is regulated via the 26S proteasome, molecular mechanisms underlying ARF stability and turnover are unknown. Here, we report the identification and functional characterization of an F-Box E3 ubiquitin ligase, which we have named AUXIN RESPONSE FACTOR F-BOX1 (AFF1). AFF1 directly interacts with ARF19 and regulates its accumulation. Mutants defective in AFF1 display ARF19 protein hyperaccumulation, mild auxin resistance, and developmental defects. Together, our data suggest a new mechanism, namely control of ARF protein stability, in regulating auxin responsiveness.

2022-06-09 | GSE172353 | GEO

Distinct roles of the two SEC scaffold proteins, AFF1 and AFF4, in regulating RNA Pol II transcription elongation [RNA-seq]

Project description:The P-TEFb-containing super elongation complex (SEC) plays the essential role in transcriptional elongation control. The AF4/FMR2 family members AFF1 and AFF4 are the central scaffold proteins of SEC, associated with different human diseases. However, their specific roles in transcriptional control remain unclear. Here, we report that AFF1 and AFF4 show distinct genomic distribution patterns around TSS. AFF1 binds upstream of TSS, while AFF4 is enriched downstream of TSS. Pol II occupancies are reduced genome-widely after depletion of AFF1, but not AFF4. Interestingly, in a subset of active genes with broad AFF4 binding signature, AFF4 disruption causes slow elongation and early termination, while AFF1 deletion mirrors the transcriptional defects observed in the fast Pol II mutant. Furthermore, AFF4 knockdown leads to increased AFF1 levels at chromatin, and vice versa. In summary, our data demonstrate that AFF1 and AFF4 function, to some extent, antagonistically to ensure proper Pol II transcription.

2023-07-02 | GSE207812 | GEO

Distinct roles of the two SEC scaffold proteins, AFF1 and AFF4, in regulating RNA Pol II transcription elongation [ChiP-seq 3]

2023-07-02 | GSE224753 | GEO

Distinct roles of the two SEC scaffold proteins, AFF1 and AFF4, in regulating RNA Pol II transcription elongation [ChIP-seq 2]

2023-07-02 | GSE207810 | GEO

Distinct roles of the two SEC scaffold proteins, AFF1 and AFF4, in regulating RNA Pol II transcription elongation [ChIP-seq 1]

2023-07-02 | GSE207320 | GEO

Distinct roles of the two SEC scaffold proteins, AFF1 and AFF4, in regulating RNA Pol II transcription elongation [RNA-seq 2]

2023-07-02 | GSE224754 | GEO

Effects of VNS on the NTS

Project description:Effects of VNS on the NTS

| PRJNA783894 | ENA