Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CASPARIAN STRIP INTEGRITY FACTOR 2 (CIF2) peptide induces SCHENGEN3 (SGN3) receptor-kinase dependent transcriptional changes

ABSTRACT: CASPARIAN STRIP INTEGRITY FACTOR 2 (CIF2) peptide induces SCHENGEN3 (SGN3) receptor-kinase dependent transcriptional changes

PROVIDER: PRJNA602947 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10959623.fastq.gz	Fastqsanger.gz
	SRR10959624.fastq.gz	Fastqsanger.gz
	SRR10959625.fastq.gz	Fastqsanger.gz
	SRR10959626.fastq.gz	Fastqsanger.gz
	SRR10959627.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 54

Similar Datasets

CASPARIAN STRIP INTEGRITY FACTOR 2 (CIF2) peptide induces SCHENGEN3 (SGN3) receptor-kinase dependent transcriptional changes

Project description:Here we show that the CASPARIAN STRIP INTEGRITY FACTOR 2 peptide induces SCHENGEN3 (SGN3) receptor-kinase dependent transcriptional changes both in short-term (30 min) and long-term (480 min) transcriptional changes in roots of Arabidopsis thaliana. We deposit RNA-seq data of wildtype, sgn3, and cif1,2 with or without the CIF2 peptide treatment. Wildtype and cif1,2 presented large transcriptional changes, while the sgn3 receptor mutant showed almost no difference after the treatment.

2020-04-22 | GSE144182 | GEO

Stimulation with M.tb peptide pool induces multiple signaling pathways involved in providing protection during M.tb infection

Project description:M.tb Peptide pool induces an intricate network of signaling pathways in DCs and T cells which leads to enhanced cytokine production and T cell activation.

2021-01-06 | GSE164258 | GEO

Endodermis-specific Receptor-like Kinase (ERK1) is required for the deposition of lignin in the Casparian strip in the root

Project description:The Casparian strip constitutes a physical diffusion barrier formed by the polar deposition of lignin in the root endodermis. The polar deposition of lignin is thought to be mediated by the scaffolding activity of membrane bound Casparian Strip domain proteins (CASPs) and the dirigent domain-containing protein Enhanced Suberin1 (ESB1). Here, we show that the endodermis-specific receptor-like kinase (ERK1), is part of this machinery, playing an essential role in the localization of CASP proteins and in the deposition of lignin, which ultimately are required for the formation of afunctional Casparian strip. ERK1 is localized to the cytoplasm and nucleus of the endodermis, and is part of a signalling pathway that implicates the circadian clock regulator Time for Coffee (TIC). In addition, we found that loss of ERK1 and TIC disrupts the Casparian strip organisation and alters composition of the root microbiome.

2021-09-08 | PXD013861 | Pride

Identification of a DAMP receptor and its cognate peptide ligand in sweet potato (Ipomoea batatas)

Project description:We identified a leucine-rich repeat receptor kinase (IbLRR-RK1) that is induced upon wounding and herbivory, and related to peptide-elicitor receptors (PEPRs) from tomato and Arabidopsis. We also identified a gene encoding a precursor protein comprising a peptide ligand (IbPep1) for IbLRR-RK1. RNAseq of I. batatas reveals differentially expressed genes (DEGs) upon IbPep1 and IbHypSysIV treatment

2023-04-01 | GSE227409 | GEO

Escalating-dose peptide immunotherapy induces progressive immunoregulatory changes in self-reactive T cells

Project description:Peptide immunotherapy aims to specifically restore tolerance to the administered self-antigen and prevent autoimmunity without the perturbation of normal immune function. We have developed a dose escalation protocol for subcutaneous delivery of the MHC II-restricted myelin basic protein peptide analogue Ac1-9[4Y] to T cell receptor transgenic (Tg4) mice. Dose escalation allows safe administration of high doses of peptide, which effectively induces antigen-specific tolerance and suppresses the development of experimental autoimmune encephalomyelitis, a model for the human condition multiple sclerosis. CD4+ T cells isolated from treated mice are anergic and suppressive in vitro and respond to stimulation by secretion of the immunoregulatory cytokine IL-10. To understand the molecular changes occurring throughout the course of dose-escalation immunotherapy, we undertook microarray analysis of CD4+ T cells at different the stages of treatment, using Tg4 Rag-1 deficient mice, which lack naturally occurring regulatory T cells and have a monoclonal CD4+ T cell population

2014-07-14 | GSE46036 | GEO

A Staphylococcus pro-apoptotic peptide induces acute exacerbation of pulmonary fibrosis

Project description:A Staphylococcus pro-apoptotic peptide induces acute exacerbation of pulmonary fibrosis

2020-04-22 | PXD017818 | Pride

the peptide PDTLN1 induces the expression of a set of genes in P19 cells

Project description:the peptide PDTLN1 induces the expression of a set of genes in P19 cells

| PRJNA752880 | ENA

Peptide-mediated inhibition of the transcriptional regulator Elongin BC induces apoptosis in cancer cells

Project description:Peptide-mediated inhibition of the transcriptional regulator Elongin BC induces apoptosis in cancer cells

| PRJNA882408 | ENA

Cardiac specific deletion of natriuretic peptide receptor A induces different myocardial expression of circular RNA and mRNA involved with metabolism in mice

Project description:Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are not only important biological markers, but also regulators of cardiac functions. The natriuretic peptide A receptor (NPRA), also called NPR1 or guanylyl cyclase A (GC-A), binds with ANP or BNP ligand and fulfils transmembrane signalling transduction by elevating the intracellular levels of cGMP. However, the comprehensive effects and mechanisms downstream to NPRA are still largely to be elucidated. Here, the cardiac expressing profiles of mRNA in the mice with myocardium-specific deletion of NPRA were analyzed. It was found that differently expressed mRNAs were detected and proved by Gene Ontology (GO) and pathway analysis to be mainly related to the metabolic process. Moreover, circular RNAs (circRNAs) were scrutinized, and subsequently a possible regulatory network consisting of circRNAs- MicroRNAs (miRNAs) -mRNAs was predicted and constructed by ceRNA (competing endogenous RNA) analysis. In conclusion, NPRA plays possible roles in cardiac metabolism, which might be mediated by circRNAs via endogenous competition mechanisms.

2020-12-08 | GSE140678 | GEO

An estrogen receptor α-derived peptide improves glucose homeostasis during obesity

Project description:Estrogen improves insulin sensitivity and increases energy expenditure, contributing to sexual dimorphism regarding type 2 diabetes mellitus (T2DM) susceptibility. Estrogen receptor α (ERα) plays a crucial role in mediating estrogen action on glucose and energy homeostasis. However, the underlying mechanisms remain incompletely understood. Here, we found a ligand-independent effect of ERα on the regulation of glucose homeostasis and identified an ERα-derived peptide as a potential insulin sensitizer. Deficiency of ERα but not ERβ in the liver impaired glucose homeostasis in male, female, and ovariectomized (OVX) female mice. Mechanistic studies revealed that ERα promoted hepatic insulin sensitivity by suppressing ubiquitination-induced IRS1 degradation. The ERα 1-280 domain mediated the ligand-independent effect of ERα on insulin sensitivity. Furthermore, we designed a peptide based on ERα 1-280 domain and found that ERα-derived peptide interacted with IRS1, increased IRS1 stability through suppressing its ubiquitination, and enhanced insulin sensitivity. Importantly, administration of ERα-derived peptide into obese mice significantly increased insulin sensitivity, attenuated glucose intolerance, and improved serum lipid profiles. These findings pave the way for the therapeutic intervention of T2DM by targeting the ligand-independent effect of ERα and indicate that ERα-derived peptide is a potential insulin sensitizer for the treatment of T2DM.

2024-04-05 | GSE262841 | 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