Transcriptome profiling of RNA from specific Hnrnpa2b1 overexpression in iWAT
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE176376 | GEO | 2026/04/03
REPOSITORIES: GEO
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Project description:Transcriptome profiling of RNA from specific Hnrnpa2b1 overexpression in iWAT
| PRJNA736041 | ENA
Project description:To identify HNRNPA2B1 binding sites on endogenous nuclear RNAs, we performed HITS-CLIP for endogenous HNRNPA2B1 and RNA-seq to analyze the nuclear RNA under either METTL3 or HNRNPA2B1 depletion. Wild type MDA-MB-231 cells were subjected to the HITS-CLIP procedure on immunoprecipitated HNRNPA2B1 associated RNA obtained from the nuclear fraction (Licatalosi D, et al. 2008, Nature 456:464-U22). For RNA-seq, nuclear RNA was extracted from MDA-MB-231 or Hela cells knocked down for METTL3 or HNRNPA2B1.
2015-06-20 | E-GEOD-70061 | biostudies-arrayexpress
Project description:To investigate the role of hnRNPA2B1 in the progression of hepatocellular carcinogenesis, we established a Huh7 cell line in which the hnRNPA2B1 gene was knocked out by crisper/cas9.
2023-09-01 | GSE226544 | GEO
Project description:To identify HNRNPA2B1 binding sites on endogenous nuclear RNAs, we performed HITS-CLIP for endogenous HNRNPA2B1 and RNA-seq to analyze the nuclear RNA under either METTL3 or HNRNPA2B1 depletion.
2015-06-20 | GSE70061 | GEO
Project description:HNRNPA2B1, an RNA-binding protein, plays a key role in primary microRNA processing, alternative splicing, mRNA metabolism and transport. Interestingly, hnRNPA2B1 also works as an N6-methyladenosine(m6A) reader and is critical during tumorigenesis of various tissue types. However, its role in colon cancer is still unclear. In this study, we aimed to elucidate the biological functions of hnRNPA2B1 and to explore its underlying mechanisms in colon cancer. Methods We examined the expression of hnRNPA2B1 in Oncomine and TCGA databases. Then verified the findings in colon cancer cells and clinical samples with western blotting and immunohistochemistry (IHC). We used CRISPR/Cas9 directed gene editing to knockout hnRNPA2B1 expression in human colon cancer cell line SW480 and carried out both in vivo and in vitro experiments. The results were further confirmed by RNA-seq analysis. We found that hnRNPA2B1 significantly promoted colon cancer cell proliferation both in vitro and in vivo, while knockout of hnRNPA2B1 induced apoptosis and cell cycle arrest in SW480. RNA-seq analysis revealed that the ERK/MAPK pathway was activated by hnRNPA2B1 upregulation. In addition, both hnRNPA2B1 and MAPK pathway were activated in clinical colon cancer specimens and positively correlated. Mechanistically, hnRNPA2B1 appeared to be an upstream regulator of the ERK/MAPK pathway and inhibition of MAPK signaling blocked the effects of hnRNPA2B1. Taken together, our data demonstrated that the RNA-binding protein hnRNPA2B1 promotes cell proliferation and regulates cell cycle and apoptosis of human colon cancer by activating the ERK/MAPK signaling, which may provide a new insight into the development of hnRNPA2B1 as a potential therapeutic target for treatment of colon cancer.
2021-06-09 | GSE169211 | GEO
Project description:m6A modification is prevalent on messenger RNA and plays a crucial role in various eukaryotic biological processes, including growth, development, disease, and aging. hnRNPA2B1, a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family, has been identified as an m6A reader. In this study, hnRNPA2B1 was shown to promote osteogenesis differentiation of human adipose-derived stem cells (hASCs) in vitro. Furthermore, the overexpression of hnRNPA2B1 facilitated bone defect healing in in vivo models of bone defects. hnRNPA2B1 RIP-seq, mRNA-seq, and MERIP-seq were used to identify PHC2 as the target gene of hnRNPA2B1. hnRNPA2B1 enhances the stability of PHC2 mRNA through m6A regulation. PHC2 binds to the promoter region of GATA6 and represses GATA6 expression by increasing H3K27me3 levels. GATA6, in turn, inhibits BMP signaling pathways and the osteogenesis differentiation of hASCs. hnRNPA2B1-PHC2-GATA6-BMP axis offers a promising perspective for the development of stem cell based bone tissue engineering.
2025-03-10 | GSE291171 | GEO
Project description:m6A modification is prevalent on messenger RNA and plays a crucial role in various eukaryotic biological processes, including growth, development, disease, and aging. hnRNPA2B1, a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family, has been identified as an m6A reader. In this study, hnRNPA2B1 was shown to promote osteogenesis differentiation of human adipose-derived stem cells (hASCs) in vitro. Furthermore, the overexpression of hnRNPA2B1 facilitated bone defect healing in in vivo models of bone defects. hnRNPA2B1 RIP-seq, mRNA-seq, and MERIP-seq were used to identify PHC2 as the target gene of hnRNPA2B1. hnRNPA2B1 enhances the stability of PHC2 mRNA through m6A regulation. PHC2 binds to the promoter region of GATA6 and represses GATA6 expression by increasing H3K27me3 levels. GATA6, in turn, inhibits BMP signaling pathways and the osteogenesis differentiation of hASCs. hnRNPA2B1-PHC2-GATA6-BMP axis offers a promising perspective for the development of stem cell based bone tissue engineering.
2025-03-10 | GSE291175 | GEO
Project description:Exosomes are released by most cells to the extracellular environment, and are involved in cell-to-cell-communication. Exosomes contain specific repertoires of mRNAs, miRNAs and other non-coding RNAs that can be functionally transferred to recipient cells. However, the mechanisms that control the specific loading of RNA species into exosomes remain unknown. Here we describe short sequence motifs present in miRNAs that control their localization into exosomes. The protein hnRNPA2B1 specifically binds exosomal miRNAs through the recognition of these motifs and controls their loading into exosomes. Moreover, hnRNPA2B1 in exosomes is sumoylated, and sumoylation controls the binding of hnRNPA2B1 to miRNAs. The loading of miRNAs into exosomes can be modulated by mutagenesis of the identified motifs or changes in hnRNPA2B1 expression levels. These findings identify hnRNPA2B1 as a key player in miRNA sorting into exosomes and provide potential tools for the packaging of selected regulatory RNAs into exosomes and their use in biomedical applications.
2014-04-16 | PXD000350 | Pride
Project description:Deciphering the rapid expression and the underlying mechanisms of antibacterial effectors is critical to host defense against bacterial infection. Bacterial infection can reprogram cellular metabolism, however, the immunometabolism and its cross-talk with epigenetics in the regulation of antibacterial innate immunity remain to be fully understood. Here we report that nuclear hnRNPA2B1 is required to antibacterial innate response by promoting Il1b transcription. Myeloid-specific Hnrnpa2b1-deficient mice are susceptible to bacterial infection, resulting from IL-1β production insufficiency. The screenings identify the metabolite adenine in the nucleus to be able to bind and activate hnRNPA2B1. Adenine directly recruits hnRNPA2B1 to Il1b enhancers for increasing chromatin accessibility to promote Il1b transcription through NCL and FTO-mediated DNA 6mA demethylation of Il1b gene enhancers. Furthermore, bacterial infection elevates nuclear adenine levels, and in vivo administration of adenine protects mice from bacterial infection through hnRNPA2B1-IL1 circuit. Our findings provide an undiscovered paradigm of cross-regulation between epigenetic and metabolic pathways in antibacterial innate immunity, adding insight and proposing new approach to the treatment of bacterial infections.
2025-04-28 | GSE263373 | GEO
Project description:Deciphering the rapid expression and the underlying mechanisms of antibacterial effectors is critical to host defense against bacterial infection. Bacterial infection can reprogram cellular metabolism, however, the immunometabolism and its cross-talk with epigenetics in the regulation of antibacterial innate immunity remain to be fully understood. Here we report that nuclear hnRNPA2B1 is required to antibacterial innate response by promoting Il1b transcription. Myeloid-specific Hnrnpa2b1-deficient mice are susceptible to bacterial infection, resulting from IL-1β production insufficiency. The screenings identify the metabolite adenine in the nucleus to be able to bind and activate hnRNPA2B1. Adenine directly recruits hnRNPA2B1 to Il1b enhancers for increasing chromatin accessibility to promote Il1b transcription through NCL and FTO-mediated DNA 6mA demethylation of Il1b gene enhancers. Furthermore, bacterial infection elevates nuclear adenine levels, and in vivo administration of adenine protects mice from bacterial infection through hnRNPA2B1-IL1 circuit. Our findings provide an undiscovered paradigm of cross-regulation between epigenetic and metabolic pathways in antibacterial innate immunity, adding insight and proposing new approach to the treatment of bacterial infections.
2025-04-28 | GSE263374 | GEO