Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting METTL3 protein by PROTAC: A Novel Therapeutic Approach for Acute Myeloid Leukemia

ABSTRACT: Targeting METTL3 protein by PROTAC: A Novel Therapeutic Approach for Acute Myeloid Leukemia

PROVIDER: PRJNA1141488 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR30027206_1.fastq.gz	Fastqsanger.gz
	SRR30027206_2.fastq.gz	Fastqsanger.gz
	SRR30027208_1.fastq.gz	Fastqsanger.gz
	SRR30027208_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 5

Similar Datasets

Targeting METTL3 protein by PROTAC: A Novel Therapeutic Approach for Acute Myeloid Leukemia

Project description:Despite numerous studies suggesting that RNA m6A transferase core complex including METTL3 and METTL14 play essential roles in both the initiation and maintenance of Acute myeloid leukemia (AML), effective pharmacological targeting of these two proteins remains elusive. Here, we report the development and evaluation of a novel METTL3 degrader, ZW27941, designed to induce METTL3 degradation via the VHL-mediated proteasomal degradation pathway. ZW27941 exhibited potent and selective degradation of METTL3 and its binding partner METTL14, leading to significant anti-leukemic activity in AML cell lines. Furthermore, ZW27941 demonstrated synergistic or additive effects when combined with standard AML therapeutics, such as Cytarabine and Venetoclax. Our findings suggest that selective METTL3 degraders, exemplified by ZW27941, hold promise as a novel therapeutic approach for AML, particularly when used in combination with existing treatments to enhance efficacy and overcome resistance mechanisms.

2025-06-04 | GSE273361 | GEO

Gene expression in Mon-Mac-6 cells treated with METTL3 PROTAC, WD6305

Project description:We developed a new METTL3 PROTAC, WD6305, which, unlike inhibitors, can reduce the expression of METTL3 protein. Here, we tested the gene expression after dosing by RNA-seq.

2023-11-29 | GSE234985 | GEO

Gene expression in Mon-Mac-6 cells treated with METTL3 PROTAC, WD6305

Project description:Gene expression in Mon-Mac-6 cells treated with METTL3 PROTAC, WD6305

| PRJNA983837 | ENA

Promoter-bound METTL3 maintains myeloid leukemia by m6A-dependent regulation of protein translation

Project description:N6-methyladenosine (m6A) is an abundant internal RNA modification, in both coding and non-coding RNAs, catalyzed by the METTL3/METTL14 methyltransferase complex. We identified METTL3 as an essential gene for acute myeloid leukemia (AML) cell growth in two distinct genetic screens. Down-regulation of METTL3 results in cell cycle arrest, differentiation of leukemic cells and failure to establish leukemia in immunodeficient mice. We show that METTL3, independently of METTL14, associates with chromatin and localizes to the transcriptional start site (TSS) of 83 active genes. The vast majority of these genes have a CAATT-box motif at their TSS, are occupied by a specific set of transcription factors including NFY, WDR5, KLF9 and they harbor specific histone modifications (e.g. H3R2me2s). Promoter bound METTL3 induces m6A modification within the coding region of the associated mRNA transcript and it enhances translation due to relief of ribosome stalling. We show that genes regulated by METTL3 in this way are necessary for AML-leukemia. Together, these data define a new mechanism of gene regulation by METTL3 and identify this enzyme as a novel therapeutic target for AML.

2017-11-28 | GSE94613 | GEO

Effect of PROTAC-mediated BRD4 degradation in acute myeloid leukemia

Project description:Effect of PROTAC-mediated BRD4 degradation in acute myeloid leukemia

| PRJNA382703 | ENA

RNA-seq of the human acute myeloid leukemia cell line MOLM-13 treated with the METTL3 inhibitor UZH2 for 16 h compared to untreated controls

Project description:The METTL3 methyltransferase is responsible for the deposition of N6-methyladenosine (m6A) modifications in RNA and has been identified as essential for survival and proliferation of acute myeloid leukemia (AML) cells in a genome-wide CRISPR screen. In our experiments involving a small-molecule METTL3 inhibitor (UZH2) in the AML cell line MOLM-13, we observed suppression of cell proliferation, induction of apoptosis and differentiation. The aim of RNA-seq experiment was to characterize the transcriptomic changes occurring in MOLM-13 cell line after treatment UZH2. Cell were treated with 10 µM of UZH2 for 16 h and compered to untreated controls (5 % DMSO).

2022-10-01 | E-MTAB-11952 | biostudies-arrayexpress

A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies.

Project description:A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies.

| PRJNA1094882 | ENA

A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies

Project description:A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies

| PRJNA1160801 | ENA

A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies

Project description:A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies

| PRJNA1162874 | ENA

METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data