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GEF-H1 mediated gene expression changes in BMDCs in response to microtubule destabilization

ABSTRACT: GEF-H1 mediated gene expression changes in BMDCs in response to microtubule destabilization

PROVIDER: PRJNA558066 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9884650_1.fastq.gz	Fastqsanger.gz
	SRR9884650_2.fastq.gz	Fastqsanger.gz
	SRR9884651_1.fastq.gz	Fastqsanger.gz
	SRR9884651_2.fastq.gz	Fastqsanger.gz
	SRR9884652_1.fastq.gz	Fastqsanger.gz

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GEF-H1 mediated gene expression changes in BMDCs in response to microtubule destabilization

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GEF-H1-IRF5 mediated gene expression changes in BMDM by MDP recognition

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Hypoxia inhibits HUNK-mediated phosphorylation of GEF-H1 for epithelial-to-mesenchymal transition

Project description:Hypoxia regulates epithelial to mesenchymal transition (EMT) of cancer cells. However, the mechanism underlying hypoxia-mediated EMT remains largely unknow. Here, utilizing colorectal cell carcinoma (CRC) as a model, we find that HUNK inhibits EMT and suppresses metastasis of CRC cells via its substrate GEF-H1 in a kinase-dependent manner. Mechanistically, HUNK directly phosphorylates GEF-H1 at ser645 site, which activates RhoA and consequently leads to a cascade of phosphorylation of LIMK1/CFL-1, thereby stabilizing F-actin and inhibiting EMT. Moreover, hypoxia suppresses HUNK activity and dephosphorylates GEF-H1 to promote EMT. Clinically, the expression levels of both HUNK and phosphorylation of GEH-H1 ser645 are not only downregulated in CRC tissues with metastasis compared to that without metastasis, but also positively correlated among these tissues. Our findings highlight the importance of hypoxia-regulated HUNK kinase activity and phosphorylation of GEF-H1 in regulation of EMT and metastasis of CRC.

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Measuring the effect of ROCK inhibition on microtubule destabilization response

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Measuring the effect of pan-Rho inhibition on microtubule destabilization response

Project description:In this study, we sought to measure what changes cells experienced upon microtubule destabilization after inhibiting Rho GTPases. We used human pulmonary microvascular endothelial cells (HPMECs) as a model to measure cell response to microtubule depolymerization in a sensitive cell type.

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Measuring the effect of ROCK inhibition on microtubule destabilization response

Project description:Measuring the effect of ROCK inhibition on microtubule destabilization response

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GEF-H1 Signaling upon Microtubule Destabilization Is Required for Dendritic Cell Activation and Specific Anti-tumor Responses.

Project description:Dendritic cell (DC) activation is a critical step for anti-tumor T cell responses. Certain chemotherapeutics can influence DC function. Here we demonstrate that chemotherapy capable of microtubule destabilization has direct effects on DC function; namely, it induces potent DC maturation and elicits anti-tumor immunity. Guanine nucleotide exchange factor-H1 (GEF-H1) is specifically released upon microtubule destabilization and is required for DC activation. In response to chemotherapy, GEF-H1 drives a distinct cell signaling program in DCs dominated by the c-Jun N-terminal kinase (JNK) pathway and AP-1/ATF transcriptional response for control of innate and adaptive immune responses. Microtubule destabilization, and subsequent GEF-H1 signaling, enhances cross-presentation of tumor antigens to CD8 T cells. In absence of GEF-H1, anti-tumor immunity is hampered. In cancer patients, high expression of the GEF-H1 immune gene signature is associated with prolonged survival. Our study identifies an alternate intracellular axis in DCs induced upon microtubule destabilization in which GEF-H1 promotes protective anti-tumor immunity.

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Project description:GEF-H1-IRF5 mediated gene expression changes in BMDM by MDP recognition

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Hypoxia inhibits HUNK-mediated phosphorylation of GEF-H1 for epithelial-to-mesenchymal transition

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