Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mycoplasma gallisepticum WhiA knockdown and overexpression

ABSTRACT: Proteomes of Mycoplasma gallisepticum strains with overexpression and knockdown of WhiA transcription factor. The overexpression was introduced on a transposon vector carrying M. gallisepticum whiA gene with strong constitutive promoter and strong SD sequence. The knockdown was made by CRISPRi. dCas9 protein and sgRNA against whiA gene were introduced on a transposon vector.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Mycoplasma Gallisepticum S6

SUBMITTER: Aleksandr Zubov

LAB HEAD: Gleb Fisunov

PROVIDER: PXD026928 | Pride | 2021-06-25

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Similar Datasets

Data on nucleoid-associated proteins isolated from Mycoplasma gallisepticum after intracellular infection

Project description:Mycoplasma gallisepticum belongs to the class Mollicutes. It causes chronic respiratory disease in avian species. M. gallisepticum is characterized by lack of cell wall; reduced genome size and the volume of its nucleoid is comparable to the size of the whole cell. As a result of genome reduction, M. gallisepticum has a limited variety of DNA-binding proteins (DBP) and transcription factors. It was shown, however, that mycoplasmas demonstrate a wide range of differential expression in response to various stress factors, which promotes effective adaptation to unfavorable conditions. We assume that in the case of mycoplasmas, which are characterized by a combination of the reduction of known gene expression regulation systems and a high adaptive potential, the coordination of gene expression can be provided due to local changes in the structure and spatial organization of the chromosome. The study of the dynamic changes of the proteomic profile of M. gallisepticum nucleoid may assist in revealing its mechanisms of functioning, regulation of chromosome organization and stress adaptation including its changes upon invasion of the host cells.

2021-03-31 | PXD025107 | Pride

Overexpression of miR-9 and miR-9* in 32D cells

Project description:Overexpression of miR-9 and miR-9* in 32D cells, cells grown under IL-3 conditions and miR-9 and miR-9* were introduced with retroviral vectors containing about ~150 bp up and downstream of mmu-mir-9-2. Expression was determined to find out the effect of miR-9/9*overexpression on the transcriptome level compared to introduction of empty vector control.

2012-11-01 | GSE41942 | GEO

Overexpression of miR-9 and miR-9* in 32D cells

2012-11-01 | E-GEOD-41942 | biostudies-arrayexpress

RNA-seq of HNSCC cell lines with over-expression and knockdown of MMP10

Project description:To investigate MMP10 downstream targets involved in the regulation of tongue cancer metastasis, transcriptome sequencing of MMP10 overexpression (AW13516) and knockdown clones (AW8507 and CAL27) was performed. 1) For stable overexpression of MMP10 in AW13516 cell line, pBABEpuro-MMP10 construct was used. pBABE-puro empty vector was used as control for overexpression. Transfection was carried out using lipofectamine kit (Cat No. L3000015, Invitrogen) in 293FT cells and virus was collected after 48 hours. AW13516 cells were infected with viral particles to generate stable MMP10-overexpression or vector control clones. Stable MMP10-overexpression clones generated and used for RNA-seq are: a) AW13516-vector control; b) AW13516-MMP10 overexpression clones. 2) For shRNA mediated stable knockdown of MMP10 in CAL27 and AW8507 cell lines, 3 lentiviral shRNA constructs targeting MMP10 were used. A short hairpin non-targeting (sh-NT) construct was used as vector control. Transfection and infection with viral particles was performed as described in the overexpression study. Stable MMP10-knockdown clones generated and used for RNA-seq are: a) AW8507 shRNA-NT vector control, b) AW8507 MMP10 shRNA-1, c) AW8507 MMP10 shRNA-2, d) AW8507 MMP10 shRNA-3, e) CAL27 shRNA-NT vector control, f) CAL27 MMP10 shRNA-1, g) CAL27 MMP10 shRNA-2, h) CAL27 MMP10 shRNA-3. To identify the differentially expressed genes, cuffdiff and NOISeq tools were used, and overlapping significantly differentially expressed genes (-1.5<log2FC>1.5; p-value<0.05 or prob>0.95) were identified for further characterization.

2023-01-04 | E-MTAB-11185 | biostudies-arrayexpress

The mechanism of elevated S100A6 (Calcyclin) Enhances Tumorigenesis in clear cell renal cell carcinoma

Project description:Among all types of urological cancers, the clear cell renal cell carcinoma is the second leading cause of death in adults. This is mainly due to lack of promising prognosis or predictors, and effective target therapy. S100A6 (calcyclin), a member of S100 family of proteins, is reported to be elevated in many types of cancers. In the present study, we analyzed the expression of S100A6 in mRNA, in proteins and tissues. The mechanism of enhancing tumorigenesis was studied to understand the role of S100A6 in clear cell renal cell carcinoma tumorigenesis. Microarray and bioinformatic analyses were performed in the stable transfection of overexpression and knockdown of S100A6, comparing with each empty vector control in order to find the different expression genes and explore the mechanism. The microarray analysis of clear cell renal cell carcinoma 786-O cell line treated with overexpression and knockdown S100A6. Four samples: overexpression S100A6 sample and vector control sample, knockdown S100A6 and vector control sample, each sample had three replicates.

2013-11-25 | E-GEOD-52708 | biostudies-arrayexpress

Expression analysis in mouse jejunum enteroids following over-expression of the zinc finger transcription factor PLAGL2

Project description:We examined mRNA level changes in two mouse enteroids clones expressing different levels of PLAGL2 from a constitutive Piggybac transposon vector.

2018-07-01 | GSE115532 | GEO

Gene expression profiles induced by knockdown and overexpression of p63 variants in MCF-10A mammary epithelial cell line

Project description:p63 is critical for epithelial development yet little is known about the transcriptional programmes it regulates. The p63 transactivating (TA) isoforms contain an amino-terminal exon that encodes a p53-like transactivation domain, whereas ÎN-isoforms lack this domain but contain the common DNA binding domain (DBD), suggesting that TAp63 and ÎNp63 isoforms may have opposing functions. By characterising transcriptional changes and cellular effects following modulation of p63 expression, we have defined a vital role for p63 in cellular adhesion. Knockdown of p63 expression caused downregulation of cell adhesion-associated genes, cell detachment and anoikis in mammary epithelial cells and keratinocytes. Conversely, overexpression of the TAp63Î³ or ÎNp63Î± isoforms of p63 upregulated cell adhesion molecules, increased cellular adhesion and conferred resistance to anoikis. Total RNA was isolated 48 h after retroviral or adenoviral infection and was subjected to reverse transcription, labelling and hybridization. The knockdown samples were performed in duplicate with shRNA vector control, shRNA targetting all isoforms of p63 (shDBD) and shRNA targetting p63 isoforms containing the transactivating (TA) domains. The overexpression samples were performed in triplicate with vector control, overexpression of the ÎNp63Î± isoform, and overexpression of the TAp63Î³ isoforms.

2010-03-23 | E-GEOD-20286 | biostudies-arrayexpress

RNA-seq of H9 hESC line carrying shRB expression cassette, and H9 hESC line carrying shRB expression cassette in addition to CRISPR/Cas9-mediated nonsense mutations on RBL1 and RBL2

Project description:In order to investigate the roles of retinoblastoma family genes during early human development, mutant H9 human embryonic stem cells were generated. Frameshift mutations were introduced in RBL1 and RBL2 genes using the CRISPR/Cas9 technology, and then the shRNA-expression cassette to knockdown RB upon tetracycline treatment was integrated. These cells were cultured in definitive endoderm differentiation conditions for 3 or 6 days with/without tetracycline.

2022-06-20 | E-MTAB-11109 | biostudies-arrayexpress

MAGE-A1 Promotes Proliferation, Migration and Invasion of Human Melanoma Cells through RNA-SEQ Analysis via Affecting C-JUN-IL8-ARHGAP29 Network

Project description:To define the role of MAGE-A1 in melanoma growth and metastasis, we performed RNA-seq analysis on MAGE-A1 overexpression (OE) and knockdown (KD) models in A375 human melanoma cell line. Our results revealed that overexpression of MAGE-A1 dramatically promoted proliferation, migration, and invasion of human melanoma cells in vitro and down-regulated of MAGE-A1 inhibited tumor cell proliferation and invasion. Furthermore, MAGE-A1 exerts its tumor promoting activity via activating including ERK-MAPK signaling pathway by RNA-seq analysis. mRNA profiles of MAGE-A1 over expression (OE), knockdown (KD), pcDNA-vector control, and pRNAT-scramble control in A375 cell line were generated using Ion torrent

2016-01-04 | E-GEOD-66859 | biostudies-arrayexpress

mRNA expression data from adenoma, gene modified, and colorectal cancer organoid.

Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids. To assess the expression profiling of genome-engineered organoids, we prepared total-RNA from cultured adenoma, carcinoma and genome-engineered organoids. We produced two types of genome-engineered organoids using the CRISPR/Cas9 or lentivirus vector system. Each engineered gene and engineered methods are described as a single alphabet and method name, respectively, in the sample characteristics field. The abbreviations for the engineered genes are as follows. 1) Genome-engineered organoids with CRISPR/Cas9 A = APC deletion; K = KRAS G12V knock in; S = Smad4 deletion; T = TP53 deletion; P = PIK3CA E545K knock in. 2) Genome-engineered organoids with Lent virus vector B = CTNNB1 S33Y overexpression; K = KRAS G12V overexpression; S = Smad4 shRNA overexpression; T = TP53 shRNA overexpression; P = PIK3CA E545K overexpression.

2015-01-18 | E-GEOD-57965 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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