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YTHDF2-KIF26B-Wnt signaling forms a positive-feedback regulatory loop to maintain ISC stemness

ABSTRACT: YTHDF2-KIF26B-Wnt signaling forms a positive-feedback regulatory loop to maintain ISC stemness

PROVIDER: PRJNA1227416 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32463875_1.fastq.gz	Fastqsanger.gz
	SRR32463875_2.fastq.gz	Fastqsanger.gz
	SRR32463876_1.fastq.gz	Fastqsanger.gz
	SRR32463876_2.fastq.gz	Fastqsanger.gz
	SRR32463877_1.fastq.gz	Fastqsanger.gz

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YTHDF2-KIF26B-Wnt signaling forms a positive-feedback regulatory loop to maintain ISC stemness

Project description:m6A modification plays a regulatory role in the stemness of small intestinal epithelial stem cells (ISCs), which is crucial for the renewal of intestinal epithelium and the maintenance of homeostasis. Although existing research has demonstrated that METTL3, as an m6A ‘writer’, is a crucial protein in the regulation of the stemness of ISCs, the mechanism by which the function of downstream ‘reader’ proteins is regulated has not been fully elucidated. In this study, we found that the knockout of Ythdf2 could significantly down-regulate the expression of the stemness marker gene Lgr5, suggesting that this ‘reader’ protein plays an important role in the regulation of the stemness of ISCs. Upon exploring the specific downstream mechanisms, we discovered that YTHDF2 promoted the Wnt signaling pathway by regulating the expression of KIF26B. This helps maintain the expression of Lgr5 in stem cells, thus preserving the stemness of these cells. Meanwhile, the expression of YTHDF2 itself is also regulated by the Wnt signaling pathway. Overall, YTHDF2 forms a positive-feedback regulatory loop centered around the Wnt signaling pathway. This loop ensures that ISCs remain in a stem-cell state, enabling the intestinal epithelium to function stably and properly.

2025-05-12 | GSE290302 | GEO

Microarray profiling of YTHDF2 deficient mouse oocytes

Project description:To study the role of the protein YTHDF2 during female gametogenesis, its gene was conditionally deleted in oocytes. Total RNA samples from YTHDF2 deficient GV and MII oocytes (and control oocytes) were subjected to array profiling.

2018-02-12 | E-MTAB-5576 | biostudies-arrayexpress

Microarray analysis of YTHDF2-deficient leukemic stem cells

Project description:YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To study the role of YTHDF2 in leukemia, total RNA from Ythdf2CKO (n=4) and Ythdf2CTL (n=4) leukemic stem cells were used for Affymetrix global gene expression analysis.

2019-04-05 | E-MTAB-7782 | biostudies-arrayexpress

O-GlcNAcylation of YTHDF2 antagonizes ERK-dependent phosphorylation and inhibits lung carcinoma

Project description:The intracellular O-linked N-acetylglucosamine (O-GlcNAc) glycosylation mediates many signal transduction events and regulates tumorigenesis. Previously the RNA N6-methyladenosine (m6A) reader, YTH (YT521-B homology) domain 2 (YTHDF2), has been shown to be O-GlcNAcylated on Ser-263 during Hepatitis B virus (HBV) infection and promote HBV-related hepatocellular carcinoma. Herein we mapped YTHDF2 O-GlcNAcylation at Thr-49 via electron-transfer dissociation mass spectrometry under unperturbed conditions. We show that YTHDF2 Thr-49 O-GlcNAcylation antagonizes Extracellular-signal regulated kinase (ERK)-dependent phosphorylation at Ser-39 and promotes YTHDF2 degradation. The downstream signaling pathway of YTHDF2 in lung carcinoma are thus upregulated, which leads to the downregulation of c-Myc. We further used mouse xenograft models to show that YTHDF2-T49A mutants increased lung cancer mass and size. Our work reveals a key role of YTHDF2 O-GlcNAcylation in tumorigenesis and suggests that O-GlcNAcylation exerts distinct functions under different biological stress.

2026-02-09 | PXD045137 | Pride

YTHDF2 regulates self non-coding RNA metabolism to control TLR3 activation in Inflammation

Project description:To elucidate the roles of YTHDF2 in the UV response in Human Keratinocyte (HaCaT) cells, the YTHDF2 interactome was analyzed through immunoprecipitation using a YTHDF2-specific antibody. Control IgG served as a negative control in this study. The cells were treated with UVB at 20 mJ/cm², and one hour post-treatment, alterations in the binding partners interacting with YTHDF2, along with their post-translational modifications, were analyzed using proteomics.

2025-09-10 | PXD059422 | Pride

CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (YTHDF2-RIPseq)

Project description:CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (YTHDF2-RIPseq)

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MOF forms a positive feedback regulation with ERα to suppress endometrial cancer progression

Project description:MOF forms a positive feedback regulation with ERα to suppress endometrial cancer progression

| PRJNA445964 | ENA

YTHDF2-m6A-NF-kB axis controls anti-tumor immunity through regulating intratumoral Treg survival and function

Project description:N6-methyladenosine (m6A) in messenger RNA (mRNA) regulates immune cells in homeostasis and in response to infection and inflammation. The function of YTHDF2 in the tumor microenvironment (TME) in these contexts has not been explored. We discovered that loss of Ythdf2 in regulatory T (Treg) cells can reduce tumor growth in mice while maintaining peripheral homeostasis. In the tumor microenvironment, Ythdf2-deficient Treg cells have impaired function and poor survival. The elevated tumor necrosis factor (TNF) signaling in the TME grants the location-specific function of YTHDF2, which participates in the feedback regulation of NF-kB signaling by accelerating the degradation of m6A-modified, NF-kB negative regulators, Nlrc3, Nfkbie, and Traf3. TME-specific regulation of Treg by YTHDF2 points to YTHDF2 as a target for anti-cancer immunotherapy, where intratumoral Treg cells can be targeted to enhance antitumor immune response, while avoiding Treg cells in the periphery to minimize undesired inflammations.

2023-06-07 | GSE230418 | GEO

The RNA m6A reader YTHDF2 controls NK cell anti-tumor and anti-viral immunity

Project description:N6-methyladenosine (m6A) is the most prevalent post-transcriptional modification on RNA. NK cells are the predominant innate lymphoid cells that mediate anti-viral and anti-tumor immunity. However, whether and how m6A modifications affect NK cell immunity remains unknown. Here, we discover that YTHDF2, a well-known m6A reader, is upregulated in NK cells upon activation by cytokines, tumors, and cytomegalovirus infection. Ythdf2 deficiency in NK cells impairs NK cell anti-tumor and anti-viral activity in vivo. YTHDF2 maintains NK cell homeostasis and terminal maturation, correlating with modulating NK cell trafficking and regulating Eomes, respectively. YTHDF2 promotes NK cell effector function and is required for IL-15-mediated NK cell survival and proliferation by forming a STAT5-YTHDF2 positive feedback loop. Transcriptome-wide screening identifies Tardbp to be involved in cell proliferation or survival as a YTHDF2-binding target in NK cells. Collectively, we elucidate the biological roles of m6A modifications in NK cells and highlight a new direction to harness NK cell anti-tumor immunity.

2021-05-08 | GSE174027 | GEO

YTHDF2-m6A-NF-kB axis controls anti-tumor immunity through regulating intratumoral Treg survival and function [RIP-seq]

2023-06-07 | GSE216958 | GEO