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YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [MeDIP-Seq]

ABSTRACT: YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [MeDIP-Seq]

PROVIDER: PRJNA860811 | ENA |

REPOSITORIES: ENA

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Similar Datasets

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis

Project description:YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis

| PRJNA860801 | ENA

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [ChIP-Seq]

Project description:YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [ChIP-Seq]

| PRJNA860812 | ENA

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [RNA-Seq]

Project description:YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [RNA-Seq]

| PRJNA860810 | ENA

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [MeDIP-Seq]

Project description:We use m6A-seq to report the most comprehensive survey to date of mRNA in spermatogonial stem cells (SSCs) and neural stem cell-like cells (iNSCs)

2025-07-21 | GSE208724 | GEO

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-07-21 | GSE208726 | GEO

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [RNA-Seq]

Project description:The expression profile data was obtained by RNA-Seq data.

2025-07-21 | GSE208725 | GEO

YTHDF1 phase separation triggers the fate transsition of spermatogonial stem cells by activating IκB-NFκB-CCND1 axis [ChIP-Seq]

Project description:We use ChIP-seq to report the most comprehensive survey to date of chromatin organization in spermatogonial stem cells (SSCs) and neural stem cell-like cells (iNSCs)

2025-07-21 | GSE208723 | GEO

YTHDF1-N6-methyladenosine-ARHGEF2 axis promoted colorectal tumorigenesis and metastasis

Project description:N6-methyladenosine (m6A) governs the fate of RNAs through m6A readers. Colorectal cancer (CRC) exhibits aberrant m6A modifications and expression of m6A regulators. However, little is known about how m6A readers interpret oncogenic m6A methylome for malignant transformation. m6A reader YTHDF1 was overexpressed by copy number gain/amplification in majority of CRCs. YTHDF1 high expression and CNVs predict increased risk of CRC relapse. Transcriptome profiles of YTHDF1-high tumors exhibit highly metastatic features. YTHDF1 promoted CRC tumor cell and organoid proliferation and enhanced metastasis. Ythdf1 knockout dampened tumor growth in carcinogen-induced CRC model. Through multiomic integration, RhoA activator ARHGEF2 was characterized as the key functional YTHDF1 target based on its m6A and YTHDF1-binding signal, translation efficiency changes, protein correlations with YTHDF1 in clinical samples, and disrupted RhoA features by YTHDF1 knockdown. Moreover, YTHDF1-ARHGEF2 co-regulation was observed in YTHDF1-overexpressing metastatic sites and carcinogen-induced Ythdf1-null CRC tumors. ARHGEF2 overexpression significantly rescued RhoA signaling, tumor cell survival and invasiveness impaired by YTHDF1 knockdown both in vitro and in vivo, further confirming the essential function of ARHGEF2.

2022-01-18 | GSE159425 | GEO

YTHDF1 links hypoxia adaptation and non-small cell lung cancer progression

Project description:10plex TMT labelling quantification expriments were performed to access the knockdown effect of YTHDF1 in cells.3 shGFPs control samples, 3 YTHDF1 shRNA-2 knockdown samples , 3 YTHDF1 shRNA-3 knockdown samples and 1 mixture sample were labelled by TMT 10-plex reagents.

2019-09-27 | PXD015182 | Pride

Role of disorder in IκB-NFκB interaction.

Project description:The paradigmatic transcription factors of the NFκB family provide an increasingly complex view of the mechanism of signal-mediated transcriptional activation. Although the primary event, phosphorylation and subsequent ubiquitin-dependent degradation of IκBα, the inhibitor of the canonical NFκB (p50/p65), is reasonably well understood, the means whereby the activation is turned off by postinduction repression are less well understood. Recent work highlighted in this review suggests that the inhibitor IκBα participates in the "stripping" of NFκB from the DNA, and that this process relies heavily on the disordered and weakly ordered segments of IκBα. Kinetic and equilibrium measurements in vitro as well as genetic screens in vivo convincingly demonstrate not only that IκBα greatly increases the dissociation rate of NFκB from DNA but also that further control of the process is mediated by the extremely short half-life of free IκBα, doubtless a result of the overall weakly folded nature of the free protein. These studies illustrate the versatility of protein systems that use not only well-structured proteins and protein complexes but also the full range of available weakly structured and disordered states to maximize functional efficiency and metabolic control.

| S-EPMC3575514 | biostudies-literature

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