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DYRK1A Inhibition via Harmine

ABSTRACT: DYRK1A Inhibition via Harmine

PROVIDER: PRJNA1130459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29665264_1.fastq.gz	Fastqsanger.gz
	SRR29665264_2.fastq.gz	Fastqsanger.gz
	SRR29665265_1.fastq.gz	Fastqsanger.gz
	SRR29665265_2.fastq.gz	Fastqsanger.gz
	SRR29665266_1.fastq.gz	Fastqsanger.gz

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DYRK1A Inhibition via Harmine

Project description:Chemical inhibition of DYRK1A (e.g. using harmine) inhibits Th17 and promotes Treg differentiation. To better understand the mechanisms by which DYRK1A regulates Th17 differentiation, we are comparing expression profiles of naïve CD4+ T cells during the course of Th17 differentiation in the presence or absence of harmine.

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DYRK1A Inhibition via Harmine or via Conditional Knockout

Project description:DYRK1A Inhibition via Harmine or via Conditional Knockout

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DYRK1A Inhibition via Conditional Knockout

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DYRK1A Inhibition via Conditional Knockout

Project description:DYRK1A Inhibition via Conditional Knockout

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DYRK1A Inhibition via Harmine or via Conditional Knockout

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

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DYRK1A, a potential therapeutic target for head and neck squamous cell carcinoma

Project description:To identify the activated tyrosine kinase signaling pathways in HNSCC, we carried out phosphotyrosine profiling using a panel of HNSCC cell lines compared to a normal oral keratinocyte. A total of 61 unique phosphosites were identified across these cell lines. Dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A (DYRK1A) was one of the kinases hyperphosphorylated at Y321 in all the HNSCC cell lines compared to the normal oral cell line OKF6/TERT1. Inhibition of DYRK1A using its specific siRNA and inhibitor resulted in a decrease in the invasion and colony formation ability of the HNSCC cell lines. Further, the treatment of mice bearing HNSCC xenograft tumors with DYRK1A inhibitor (harmine) showed regression of tumor growth. Our results demonstrate that DYRK1A could be a novel therapeutic target in HNSCC.

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RNA-sequencing of DYRK1A-deficient (CKO) pre-B and pre-T cells

Project description:Pre-B and pre-T lymphocytes must orchestrate a transition from a highly proliferative state to a quiescent one during development. Cyclin D3 is essential for these cells’ proliferation, but little is known about its post-translational regulation at this stage. Here, we show that the dual specificity tyrosine-regulated kinase 1A (DYRK1A) restrains Cyclin D3 protein levels by phosphorylating T283 to induce its degradation. Loss of DYRK1A activity, via genetic inactivation or pharmacologic inhibition, caused accumulation of Cyclin D3 protein, incomplete repression of E2F-mediated gene transcription, and failure to properly couple cell cycle exit with differentiation. Expression of a non-phosphorylatable Cyclin D3 T283A mutant recapitulated these defects, while inhibition of Cyclin D:CDK4/6 mitigated the effects of DYRK1A inhibition. These data uncover a previously unknown role for DYRK1A in lymphopoiesis, and demonstrate how Cyclin D3 protein stability is negatively regulated during exit from the proliferative phases of B and T cell development. 5 cell populations were analyzed (small pre-B cells, large pre-B cells, quiescent CD4+CD8+ thymocytes, cycling CD4+CD+ thymocytes, and mature granulocytes) from 2 Control mice (pooled) and 2 DYRK1A-deficient mice (pooled) for a total of 10 samples.

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Project description:Intervening in mitochondrial oxidative phosphorylation (OXPHOS) has emerged as a potential therapeutic strategy for certain types of cancers. However, the exploration of targeting OXPHOS for the treatment of liver cancer is still limited, and the regulatory network involved in OXPHOS inhibition remains largely unexplored. Here, employing kinome-based CRISPR screening, we find that OXPHOS inhibitor IACS-010759 exhibits limited effect in liver cancer cells due to the function of dual specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A). Genetic inactivation or pharmacological inhibition of DYRK1A combined with OXPHOS inhibitors activates transforming growth factor β (TGFβ) signalling, which is crucial for OXPHOS inhibition-triggered cell death in liver cancer cells. Mechanistically, DYRK1A directly phosphorylates SMAD3 at Thr132, thereby suppressing the negative impact of TGFβ signalling on the transcription of the glutamine transporter solute carrier family 1 member 5 (SLC1A5). This mechanism compensates for the increased glutamine requirement (?) upon OXPHOS inhibition, leading to the resistance of liver cancer cells to OXPHOS inhibition. Finally, we validated the therapeutic efficacy of targeting OXPHOS in combination with DYRK1A inhibition in multiple liver cancer models in vivo. Our study identifies DYRK1A as a novel regulator of TGF β signalling and elucidates the regulatory mechanisms governing the response to OXPHOS inhibition in tumour cells, providing novel insights into targeting OXPHOS for liver cancer therapy.

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