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Unknown,Transcriptomics,Genomics,Proteomics

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FSTL1 promotes keratinocyte migration.

ABSTRACT: This study identifies FSTL1 as key component of intiating keratinocyte migration in skin Total RNA from N/TERT-1 keratinocytes transfected with a non-targeting siRNA or Smartpool siRNA against FSTL1 were subjected to microarray analysis

ORGANISM(S): Homo sapiens

SUBMITTER: Prabha Sampath

PROVIDER: E-GEOD-41615 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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'See-saw' expression of microRNA-198 and FSTL1 from a single transcript in wound healing.

Sundaram Gopinath M GM Common John E A JE Gopal Felicia E FE Srikanta Satyanarayana S Lakshman Krishnaswamy K Lunny Declan P DP Lim Thiam C TC Tanavde Vivek V Lane E Birgitte EB Sampath Prabha P

Nature 20130210 7439

Post-transcriptional switches are flexible effectors of dynamic changes in gene expression. Here we report a new post-transcriptional switch that dictates the spatiotemporal and mutually exclusive expression of two alternative gene products from a single transcript. Expression of primate-specific exonic microRNA-198 (miR-198), located in the 3'-untranslated region of follistatin-like 1 (FSTL1) messenger RNA, switches to expression of the linked open reading frame of FSTL1 upon wounding in a huma ...[more]

PMID: 23395958

Similar Datasets

MicroRNA-198 an inhibitor of keratinocyte migration

Project description:This study identifies miR-198 as a potential inhibitor of keratinocyte migration in skin This study identifies genes differentially expressed during the early phases of wound healing using an ex vivo organ culture model of human skin Total RNA from N/TERT-1 keratinocytes transfected with a negative control miRNA or miR-198 were subjected to microarray analysis Skin from elective plastic surgery were subjected to wounding using ex vivo organ culture model. Total RNA from skin biopsies were isolated at 0hr and 24hr post injury and subjected to mircoarray analysis

2013-03-02 | E-GEOD-37967 | biostudies-arrayexpress

Down-regulation of SFRP1 in a mammary epithelial cell line

Project description:Microarray data to accompany Gauger et al. (2009) Cancer Cell International paper A treated X untreated design was used whereby immortalized human mammary epithelial cell lines (TERT cells) were modified to stably express an siRNA that knocked down SFRP1 expression. These "treated" cells were labeled with Cy5 and four replicate harvests were hybridized to Agilent 4by44k whole genome microarrays, along with a Cy3 labeled untreated control. The untreated control consisted of 4 pooled harvests of the parent cell line in normal growth conditions at 60-80% confluence.

2010-05-08 | E-GEOD-15948 | biostudies-arrayexpress

Transcription profiling of mouse skin after acute withdrawal of TERT

Project description:TERT is an essential protein component of telomerase, a ribonuclearprotein complex that protects chromosomal ends. Ectopic expression of TERT in mouse skin activates hair follicle stem cells and induces active growth phase of hair cycles, called anagen. This activity of TERT is independent of its reverse transcriptase function, indicating that this is a non-telomeric function of TERT. We performed time-course microarray analysis using conditional bi-transgenic mice (iK5-TERT) to understand the mechanism of this novel non-telomeric function of TERT. Experiment Overall Design: Hair follicles of iK5-TERT mice at postnatal day 60 is in TERT-induced anagen. To those mice, we injected either PBS, to maintain TERT transgene expression, or doxycycline, to rapidly extinguish transgene expression. We then took time-course dorsal skin biopsies (0,6,12,24 hr) of these mice and analyzed differential gene expressions using Affymetrix Genechips and various bioinformatic tools, including SAM, to discover TERT-regulated genes.

2008-06-17 | E-GEOD-9725 | biostudies-arrayexpress

Genomic copy number profiling of different generations of Atm-/-TERT-ER T-cell lymphomas and associated resistant tumors following telomerase inhibition

Project description:Genomic copy numbers of various generations of Atm-/-TERT-ER mice treated with 4-OHT or vehicle were profiled. Genomic copy numbers of transplanted G3 Atm-/-TERT-ER T-cell lymphomas with telomerase or ALT T-cell lymphomas were developed in various generations of Atm-/-TERT-ER mice with 4-OHT or vehicle treatment. These tumors were profiled with aCGH. G3 Atm-/-TERT-ER tumors were transplanted into SCID mice treated with 4-OHT or vehicle. Cells maintained on vehicle eventually developed ALT-dependent resistance. We used aCGH to profile telomerase+ tumors vs. ALT+ tumors from the same parental lines.

2012-01-17 | E-GEOD-35045 | biostudies-arrayexpress

Global proteome analysis of ATF4 targets during ER stress.

Project description:Cancer cells exploit many of the cellular adaptive responses to support their survival needs. One such critical pathway in eukaryotic cells is the unfolded protein response (UPR) that is important in normal physiology as well as disease states, including cancer. Since UPR can serve as a lever between survival and death, regulated control of its activity is critical for tumor formation and growth although the underlying mechanisms are poorly understood. Here we show that one of the main transcriptional effectors of UPR, activating transcription factor 4 (ATF4), is essential for prostate cancer (PCa) growth and survival. To identify ATF4 target genes that mediate the ISR outcome and to get insight into its mechanism of action in PCa, we performed global proteomic expression profiling in parallel with transcriptomic expression profiling. These data show that ATF4 regulates important metabolic pathways in PCa cells.

2019-07-22 | PXD012858 | Pride

Anti-telomerase therapy provokes ALT and mitochondrial adaptive mechanisms

Project description:This SuperSeries is composed of the following subset Series: GSE35044: Expression profiles of Telomerase+ vs. ALT+ G3 Atm-/-TERT-ER T-cell lymphomas GSE35045: Genomic copy number profiling of different generations of Atm-/-TERT-ER T-cell lymphomas and associated resistant tumors following telomerase inhibition Refer to individual Series

2012-01-17 | E-GEOD-35046 | biostudies-arrayexpress

Transcription profiling of human cells transfected with a miR-34a LNA inhibitor to investigate its role in oncogene-induced senescence

Project description:To understand the role of miR-34a in oncogene-induced senescence, we tested global mRNA expression using microarrays of TIG3 TERT/ deltaB-RAF:ER cells transfected with a miR-34a LNA inhibitor or a scrambled control LNA in the presence or absence of deltaB-RAF activation.<br>TIG3 TERT/ deltaB-RAF:ER cells are primary human diploid fibroblasts immortalized by hTERT. deltaB-RAF is constitutively active due to truncation of the regulatory N-terminal domain and fused to the hormone-binding domain of the oestrogen receptor, which was modified to respond to 4-hydroxytamoxifen (4-OHT) but not beta-estradiol.<br>TIG3 TERT/ deltaB-RAF:ER cells were treated with 500nM 4-OHT or equal amounts of ethanol the day after seeding at 1E6 per 10cm plate, in three biological replicates. After 2 days of 4-OHT treatment, cells were transfected with LNA-miR-34a or a control LNA-scramble using Lipofectamine 2000 (Invitrogen). Total RNA was harvested 24 h post-transfection (3 days of 4-OHT treatment in total) using TRIzol reagent. Affymetrix microarray analysis (HG-U133 Plus 2.0 human) was performed.

2009-08-01 | E-MEXP-2241 | biostudies-arrayexpress

The lncRNA TAZ-AS202 promotes lung cancer progression through stabilization of the E2F1 transcription factor and activation of Ephrin signaling

Project description:Silencing of TAZ (WWTR1) and lncRNA TAZ-AS202 (WWTR1-AS1-202) by siRNA transfection on A549 cell line of lung cancer

2023-12-07 | E-MTAB-12507 | biostudies-arrayexpress

Molecular characterization of immortalization of human MSCs by a combination of p53 knockdown and TERT overexpression

Project description:Gene expression profile of p53 knockdown MSCs or p53 knockdown+TERT MSCs was compared with that of control MSCs. Our data show p53 knockdown prolongs the lifespan of MSCs, and a combination of p53 knockdown and TERT overexpression is sufficient to immortalize MSCs. The results provide important information about the molecular basis underlying p53 knockdown in MSCs and immortalization-related genes of MSCs. Total RNA obtained from p53 knockdown MSCs or p53 knockdown+TERT MSCs from three patients were compared with control MSCs.

2011-04-13 | E-GEOD-28546 | biostudies-arrayexpress

Expression profiles of immortal lung fibroblasts

Project description:Activation of telomerase often endows cancer cells, but rarely normal somatic cells, with immortality. Especially, fetal lung fibroblasts are known to be hardly immortalized by TERT overexpression. We here established an immortal non-transformed lung fibroblast cell line only by TERT transfection, as well as an immortal transformed cell line by transfection of TERT and SV40 early antigens. Comparing the expression profiles of these cell lines with those of mortal cell strains with elongated lifespan after TERT transfection, 51 genes, including 19 upregulated and 32 downregulated, were explored to be the candidates responsible for regulation of cellular proliferation of lung fibroblasts. These included the genes previously reported to be involved in cellular proliferation, transformation, or self-renewal capacity, and those highly expressed in lung tissues obtained from patients with idiopathic pulmonary fibrosis or hypersensitivity pneumonitis. This set of lung fibrobrast cell lines/strains of identical genetic background with different proliferative capacity, mortal and immortal non-transformed fibroblasts may become useful model cells for research on lung fibroblast growth regulation and the candidate genes explored in this study may provide promising biomarkers or molecular targets of pulmonary fibrosis. Keywords: Cell type comparison We analyzed 6 arrays with Affymetrix, 4 arrays with Agilent, and 7 arrays with CodeLink oligonucleotide microarrays for lung fibroblasts with various lifespan with or without transfection of TERT and/or SV40 early antigens.

2010-05-22 | E-GEOD-9077 | biostudies-arrayexpress

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