Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast

ABSTRACT: Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast

PROVIDER: PRJNA1128162 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29554516_1.fastq.gz	Fastqsanger.gz
	SRR29554516_2.fastq.gz	Fastqsanger.gz
	SRR29554517_1.fastq.gz	Fastqsanger.gz
	SRR29554517_2.fastq.gz	Fastqsanger.gz
	SRR29554518_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast

Project description:All cells must detect, interpret and adapt to multiple and concurrent stimuli. While signaling pathways are highly specialized, different pathways often share components or have components with overlapping functions. In the yeast Saccharomyces cerevisiae, the high osmolarity glycerol (HOG) pathway has two seemingly redundant branches, mediated by Sln1 and Sho1. Both branches are activated by osmotic pressure, leading to phosphorylation of the MAPKs Hog1 and Kss1. The mating pathway is activated by pheromone, leading to phosphorylation of the MAPKs Fus3 and Kss1. Given that Kss1 is shared by the two pathways, we investigated its role in signal coordination. We activated both pathways with a combination of salt and pheromone, in cells lacking the shared MAPK and in cells lacking either of the redundant branches of the HOG pathway. By systematically evaluating MAPK activation, translocation, and transcription programs, we determined that Sho1 mediates cross talk between the HOG and mating pathways and does so through Kss1. Further, we show that Kss1 initiates a transcriptional program that is distinct from that induced by Hog1 and Fus3. Our findings reveal how redundant and shared components coordinate concurrent signals and thereby adapt to sudden environmental changes.

2024-06-29 | GSE270781 | GEO

MAPK

Project description:MAPK

| PRJNA1054526 | ENA

Expression profiling of MAPK inhibition in WM266-4 BRAF V600D mutant melanoma cell line

Project description:Extracellular signal regulated kinases, ERK1 and ERK2 are often considered as redundant due to their high homology, large number of overlapping substrates, and ability to substitute for each other in genetically engineered mouse models. We have investigated the individual contribution of ERK1 and ERK2 to the survival of human melanoma cell lines driven by oncogenic BRAF. ERK2, but not ERK1 activity, was crucial to drive survival and maintain transcriptional output of the MAPK pathway. Furthermore, we found that ERK2 DEF-domain interactions were crucial for transcriptional regulation and survival in some cells, but not in others, whereas ERK2-substrate interactions at the D-docking motif were largely dispensable. We used microarrays to examine the global impact of gene expression by imhibiting different nodes of MAPK pathway.

2018-12-31 | GSE57721 | GEO

c-Fos mediates cell proliferation, invasion and drug-resistance of lung adenocarcinoma through MAPK signal pathway

Project description:Lung cancer is the main cause of cancer-related death in men and women all over the world. Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer, with the overall 5-year survival rate is less than 20% . We found the mRNA expression of c-Fos in LUAD clinical samples was decreased significantly compared to adjacent normal control. Overexpression of c-Fos inhibited LUAD cell proliferation, colony formation, and induced cell apoptosis while c-Fos knockdown promoted cell proliferation, colony formation, and suppressed cell apoptosis. Cell cycle showed little difference after c-Fos knockdown but overexpression of c-Fos increased the distribution of G1 phase when decreased G2 phase cells. Knockdown of c-Fos reduced the sensitivity of LUAD cells to cisplatin but overexpression of c-Fos increased the efficacy of cisplatin both in vitro and in vivo. MAPK signaling pathway was enriched after c-Fos was overexpressed in LUAD cells. The expression of c-Jun, c-Myc and DUSP1 was greatly inhibited after c-Fos overexpression but incresed after c-Fos knockdown, which suggests c-Fos regulated MAPK signaling pathway in LUAD. Furthermore, c-Fos was shown to interact with c-Jun and overexpression of c-Jun partially recovered the expression of c-Jun, c-Myc and DUSP1 caused by c-Fos overexpression. Cell proliferation was also rescued when apoptosis was decreased followed by c-Jun overexpression. In contrast, knockdown of c-Jun inhibited cell proliferation and promoted cell apoptosis in LUAD cells when reduced the level of c-Jun, c-Myc and DUSP1. In summary, c-Fos inhibits cell proliferation, promotes apoptosis and increses cisplatin-sensitivity of lung adenocarcinoma cells via regulating MAPK signaling by interacting with c-Jun in certain LUADs.

2023-09-20 | GSE213590 | GEO

Cross-talk between enhancers, structural elements and activating transcription factors maintains the 3D architecture and expression of the CFTR gene.

Project description:Here we examine the mechanisms by which multiple cis-regulatory elements (CREs) at the CFTR locus coordinate its expression in intestinal epithelial cells. Using CRISPR/Cas9 to remove CREs, individually and in tandem, followed by assays of gene expression and higher-order chromatin structure (4C-seq), we reveal the cross-talk and dependency of two cell-specific intronic enhancers. The results also suggest an internal monitoring mechanism at the locus whereby alternative enhancers may be recruited when the normal sites are lost. Of note, activating transcription factors such as FOXA2 may contribute to this mechanism. Also, by deleting the 5' topologically-associating domain (TAD) boundary, we illustrate its relative contribution to normal mechanisms of CFTR gene expression and 3D gene architecture.

2024-10-17 | GSE186272 | GEO

Dong M. oryzae MAPK pathway mutants

Project description:Gene expression profiling in MAPK-related mutants of Magnaporthe oryzae

2012-06-19 | E-MEXP-3658 | biostudies-arrayexpress

Metabolism-dependent secondary effect of anti-MAPK cancer therapy on DNA repair [MAPK inhibitors]

Project description:Metabolism-dependent secondary effect of anti-MAPK cancer therapy on DNA repair [MAPK inhibitors]

| PRJNA973618 | ENA

Shared periodic performer movements coordinate interactions in duo improvisations.

Project description:Human interaction involves the exchange of temporally coordinated, multimodal cues. Our work focused on interaction in the visual domain, using music performance as a case for analysis due to its temporally diverse and hierarchical structures. We made use of two improvising duo datasets-(i) performances of a jazz standard with a regular pulse and (ii) non-pulsed, free improvizations-to investigate whether human judgements of moments of interaction between co-performers are influenced by body movement coordination at multiple timescales. Bouts of interaction in the performances were manually annotated by experts and the performers' movements were quantified using computer vision techniques. The annotated interaction bouts were then predicted using several quantitative movement and audio features. Over 80% of the interaction bouts were successfully predicted by a broadband measure of the energy of the cross-wavelet transform of the co-performers' movements in non-pulsed duos. A more complex model, with multiple predictors that captured more specific, interacting features of the movements, was needed to explain a significant amount of variance in the pulsed duos. The methods developed here have key implications for future work on measuring visual coordination in musical ensemble performances, and can be easily adapted to other musical contexts, ensemble types and traditions.

| S-EPMC5830756 | biostudies-literature

ID1 and CEBPA coordinate epidermal progenitor cell

Project description:ID1 and CEBPA coordinate epidermal progenitor cell

| PRJNA888130 | ENA

Enteric glial hub cells coordinate intestinal motility

Project description:Enteric glial hub cells coordinate intestinal motility

| PRJNA973609 | ENA