N6-methyladenosine RNA methylome analyses in cyclophosphamide-treated neonatal rat cardiac myocytes.
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE184294 | GEO | 2021/09/23
REPOSITORIES: GEO
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Project description:N6-methyladenosine RNA methylome analyses in cyclophosphamide-treated neonatal rat cardiac myocytes.
| PRJNA763909 | ENA
Project description:To analyze the gene expression of non-bacterial bladdder inflammation, mouse cyclophosphamide(CYP)-induced model of cystitis was adapted. Forty-eight hour after CYP or vehicle treatment, total RNA was extracted from CYP-treated group (CYP150) and control group (CYP0). We used microarrays to detail the gene expression underlying bladder inflammation.
2014-03-18 | GSE55986 | GEO
Project description:To analyze the gene expression of non-bacterial bladdder inflammation, mouse cyclophosphamide(CYP)-induced model of cystitis was adapted. Forty-eight hour after CYP or vehicle treatment, total RNA was extracted from CYP-treated group (CYP150) and control group (CYP0). We used microarrays to detail the gene expression underlying bladder inflammation. Five-week-old female Balbc/A mice were injected intraperitoneally with 150mg/kg body weight of CYP diluted in 15ml/kg body weight of saline. Mice injected with saline alone served as controls. Treated mice were killed 48 hours after administaration and the whole bladders harvested. Total RNA was extracted and microarray analysis was performed.
2014-03-18 | E-GEOD-55986 | biostudies-arrayexpress
Project description:During cyclophosphamide (CYP) induced ctstitis progression differential expression of microRNAs (miRs) play a role in urinary bladder inflammation and detrusor function. We identified eight UBs miRs that are known to be involved in various other bladder pathologies which exhibited altered expression in CYP mice and e predicted to have a role in inflammation and smooth muscle function (miR-34c-5p, -34b-3p, -212-3p, -449a-5p, -21a-3p, -376b-3p, -376b-5p and -409-5p).
2023-09-18 | GSE243239 | GEO
Project description:Although internal PolyA RNA modification N6-methyladenosine (m6A) plays essential roles in diverse biological processes, technology to detect precise m6A sites at transcriptome-wide scale is lacking. Here, we discovered that m6A interferes A (Adenine) – U (Uracil) or A-T (Thymidine) pairing. Based on differential hybridization between methylated vs. unmethylated RNAs to a DNA probe, we developed tiling microarray to pinpoint m6A sites in mouse transcriptome. We validated some of the identified sites and provided evidence to suggest that one functional mechanism of m6A is to block small RNA targeting to methylated mRNA. We designed a custom tiling array with to examine the precise location of m6A within meRIP-seq peaks from mouse embryonic stem cells determined in our previous publication (Wang et al., 2014). Each custom two-channel Agilent tiling array harbors 947,952 probes. Each probe is 25 nucleotides (nt), and any two adjacent probes in the genomic coordinate overlap each other by 19 nt. The Cy5 or red channel corresponds to Mettl14 knockout (M14) or DZA mutant mESC cell line, and Cy3 or green channel is associated with wild type cell line treated with scramble hairpin (SCR). Thus, in principle a higher Cy5/Cy3 signal for each probe reflects an increased hybridization to the oligonucleotide due to de-methylation of a particular RNA molecule in M14 or DZA condition relative to the SCR control. Moreover, we employed additional arrays with both channels dedicated for M14 as an external control for technical difference between the Cy5 and Cy3 dye (details below). For each comparison, we have three biological replicates, and therefore there are 9 tiling arrays in total (i.e., 3 arrays for M14 vs SCR, 3 arrays for DZA vs SCR, and 3 arrays for M14 vs M14).
2015-09-08 | E-GEOD-62530 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE27421: Mouse bone marrow cyclophosphamide treated vs untreated GSE27422: Mouse peripheral blood leukocytes cyclophosphamide treated vs untreated GSE27423: Mouse spleen cyclophosphamide treated vs untreated Refer to individual Series
2011-04-27 | E-GEOD-27440 | biostudies-arrayexpress
Project description:Purpose:Detect transcriptome-wide mapping of m6A modifications by MeRIP-seq between Rhein and DMSO treated 3T3-L1 differentiation adipocytes at the preadipocytes, MCE stage and differentiation stage. Methods:Total RNA was extracted using TRIzol Reagent followed by chemical fragmentation. The fragmented RNA was incubated with anti-m6A antibody. The desired m6A-enriched RNA eluate was used to construct cDNA library in parallel with input control. Conclusion: Our study revealed the difference of m6A-methylated RNA between DMSO and Rhein treated cells by RNA-seq and MeRIP-seq technologies.
2021-06-01 | GSE173702 | GEO
Project description:We performed a genome-wide analysis of m6A mRNA methylation in SUN-treated human pluripotent stem cells induced myocardial cells (hiPSC-CMs) by methylated RNA immunoprecipitation sequencing (MeRIP-seq).
2022-03-21 | GSE192913 | GEO
Project description:We show that N6-methyladenosine (m6A), the most abundant internal modification in mRNA/lncRNA with still poorly characterized function, alters RNA structure to facilitate the access of RBM for heterogeneous nuclear ribonucleoprotein C (hnRNP C). We term this mechanism m6A-switch. Through combining PAR-CLIP with Me-RIP, we identify 39,060 m6A-switches among hnRNP C binding sites transcriptome-wide. We show that m6A-methyltransferases METTL3 or METTL14 knockdown decreases hnRNP C binding at 16,582 m6A-switches. Taken together, 2,798 m6A-switches of high confidence are identified to mediate RNA-hnRNP C interactions and affect diverse biological processes including cell cycle regulation. These findings reveal the biological importance of m6A and provide insights into the sophisticated regulation of RNA-RBP interactions through m6A-induced RNA structural remodeling. Measure the m6A methylated hnRNP C binding sites transcriptome-wide by PARCLIP-MeRIP; measure the differential hnRNP C occupancies upon METTL3/METTL14 knockdown by PAR-CLIP; measure RNA abundance and splicing level changes upon HNRNPC, METTL3 and METTL14 knockdown
2015-02-27 | E-GEOD-56010 | biostudies-arrayexpress
Project description:Analysis the effect of cyclophosphamide on splenocytes gene expression. Certain chemotherapeutic drugs such as cyclophosphamide can enhance the antitumor efficacy of immunotherapy because of their capacity to modulate innate and adaptive immunity. Indeed, it has been argued that this capacity may be more significant to chemotherapeutic efficacy in general than is presently appreciated. To gain insights into the core mechanisms of chemoimmunotherapy, we methodically profiled the effects of cyclophosphamide on gene expression in bone marrow, spleen and peripheral blood, and on cytokine expression in plasma and bone marrow of tumor-bearing mice. Gene and protein expression were modulated early and transiently by cyclophosphamide, leading to upregulation of a variety of immunomodulatory factors, including danger signals, pattern recognition receptors, inflammatory mediators, growth factors, cytokines, chemokines and chemokine receptors. These factors are involved in sensing cyclophosphamide myelotoxicity and activating repair mechanisms, which, in turn, stimulate immunoactivation events that promote efficacy. In particular, cyclophosphamide induced a T helper 17 (Th17)-related gene signature associated with an increase in Th17, Th1 and activated CD25+CD4+Foxp3- T lymphocytes and a slight recovery of regulatory T-cells. By analyzing gene and protein expression kinetics and their relationship to the antitumor efficacy of different therapeutic schedules of combination, we determined that optimal timing for performing adoptive immunotherapy is approximately 1 day after cyclophosphamide treatment. Together, our findings highlight factors that may propel the efficacy of chemoimmunotherapy, offering a mechanistic glimpse of the important immune modulatory effects of cyclophosphamide Four-condition experiment, Untreated mice - Cyclophosphamide-treated mice 1 day - Cyclophosphamide-treated mice 2 days - Cyclophosphamide-treated mice 5 days. Biological replicates: 5, controls: 5, independently harvested. Two replicates per array.
2011-04-27 | E-GEOD-27423 | biostudies-arrayexpress