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Transcriptomic analysis of the knockdown effects of LRRC41 and DDX5

ABSTRACT: Transcriptomic analysis of the knockdown effects of LRRC41 and DDX5

PROVIDER: PRJEB91122 | ENA |

REPOSITORIES: ENA

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Analysis of gene expression changes in RN2 acute myeloid leukemia (AML) cells at 24hrs and 48hrs after Ddx5 knockdown.

2013-12-26 | GSE53599 | GEO

Analysis of gene expression changes in RN2 acute myeloid leukemia (AML) cells at 24hrs and 48hrs after Ddx5 knockdown.

Project description:Ddx5 inhibition in RN2 cells slows cell proliferation and induces apoptosis within 48-72hrs. The aim of this analysis was to gain insight into how Ddx5 inhibition causes this outcome by analyzing gene expression changes in RN2 cells that occur at early timepoints after Ddx5 inhibition that precedes the timepoint when RN2 proliferation/cell death becomes evident in tissue culture (72hrs after inhibition). Derivatives of RN2 AML cells were prepared that encode doxycycline-inducible expression of either of two different shRNAs targeting Ddx5 (shDdx5.1322 and shDdx5.2086) or a negative control shRNA that targets Renilla Luciferase (shRen.713). Six independent cultures of each derivative RN2 cell line (shDdx5.1322, shDdx5.2086, or shRen.713) were treated with doxycycline at timepoint 0 days to induce expression of the indicated shRNA in the RN2 cells. Each shRNA is co-expressed with dsRed in a doxycycline-induced manner and flow cytometry analysis indicated that doxycycline induced expression of dsRed and the shRNA in 70-to-80% of the cells in each culture. RNA was isolated from three independent cultures of each derivative RN2 cell line at either 24hrs and 48hrs after dpxycycline treatment. Therefore this study consists of 18 samples, sequencing results from biological triplicate samples of RN2-shDdx5.1322, RN2-shDdx5.2086, and RN2-shRen.713 at 24hrs post-doxycycline and sequencing results from biological triplicate samples of RN2-shDdx5.1322, RN2-shDdx5.2086, and shRen.713 at 48hrs post-doxycycline.

2013-12-26 | E-GEOD-53599 | biostudies-arrayexpress

Transcriptomic analysis of senescent cells upon PTBP1 knockdown and EXOC7 knockdown

Project description:Transcriptomic analysis of senescent cells upon PTBP1 knockdown and EXOC7 knockdown

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Next-Generation Sequencing Facilitates Quantitative Analysis of Wild Type and DDX5 knockdown of GC Transcriptomes

Project description:Next-Generation Sequencing Facilitates Quantitative Analysis of Wild Type and DDX5 knockdown of GC Transcriptomes

| PRJNA610573 | ENA

Transcriptomic analysis of RNases knockdown in A549 cells.

Project description:Transcriptomic analysis of RNases knockdown in A549 cells.

| PRJNA871880 | ENA

Next-Generation Sequencing Facilitates Quantitative Analysis of Wild Type and DDX5 knockdown of GC Transcriptomes

Project description:We aimed to detect the mRNA expression levels in HGC-27 cells after transduction with lentivirus harboring DDX5 shRNA or non-targeting shRNA.

2021-11-10 | GSE146429 | GEO

Keratinocyte DDX5 in response to IL-36γ

Project description:To compare how WT and DDX5-/- keratinocyte in response toIL-36γ, we performed gene expression profiling analysis using data obtained from RNA-seq of WT and DDX5-/- keratinocyte stimulated by IL-36γ

2022-10-24 | GSE208666 | GEO

DDX5 in colonic tumors

Project description:The Asp-Glu-Ala-Asp (DEAD)-box RNA binding protein, DDX5, is ubiquitously expressed in many cell types, yet its role in RNA metabolism and its downstream function in vivo has not been fully elucidated. In the intestine, DDX5 is highly expressed in the intestinal epithelial cell (IECs) and contributes to tumorigenesis. Here, we used a conditional mouse lines where DDX5 is knocked out in IECs upon Tamoxifen administration to uncover mechanisms underlying DDX5 functions in colon tumors.

2021-12-03 | GSE146014 | GEO

Transcriptomic analysis of primary mouse adipocytes after Rbm43 knockdown

Project description:Transcriptomic analysis of primary mouse adipocytes after Rbm43 knockdown

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DDX5 alleviates osteoarthritic temporomandibular joint by maintaining homeostasis of cartilage metabolism

Project description:Temporomandibular joint osteoarthritis (TMJOA) is a prevalent musculoskeletal disease without effective therapeutic measure. DDX5 regulated the progression of cancer，immune disease, as well as skin inflammation by activating a series of signal transduction pathways. However, the role of DDX5 in TMJOA has not been reported yet. The distribution of DDX5 in human cartilage was performed by HE, Safranin O and Masson staining. Moreover, the expression of DDX5 was unveiled by immunofluorescent analyses. The role of DDX5 in TMJOA was verified by UAC-induced TMJOA mice and Aggrecan-CreERT; DDX5flox/flox mice. The downstream protein expression profile of DDX5 were examined by RNA-Seq analysis. The DDX5 expression remarkably decreased in the condylar cartilage of patients with TMJOA. DDX5 decreased with cartilage degradation in UAC-Induced TMJOA mice. Cartilage specific DDX5 knockout induced cartilage degeneration. Mechanistically, the inhibition expression of DDX5 accelerates cartilage degeneration by activating NF-κB Signaling. Additionally, DDX5 overexpression alleviated the progression of TMJOA under excessive mechanical stress.

2025-10-24 | GSE246357 | GEO

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