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The kinase GSK-3 alters the repertoire of RNA binding proteins present on lipid metabolism transcripts leading to altered expression in the C. elegans nervous system

ABSTRACT: The kinase GSK-3 alters the repertoire of RNA binding proteins present on lipid metabolism transcripts leading to altered expression in the C. elegans nervous system

PROVIDER: PRJNA1208473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31943890.fastq.gz	Fastqsanger.gz
	SRR31943891.fastq.gz	Fastqsanger.gz
	SRR31943892.fastq.gz	Fastqsanger.gz
	SRR31943893.fastq.gz	Fastqsanger.gz
	SRR31943894.fastq.gz	Fastqsanger.gz

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The kinase GSK-3 alters the repertoire of RNA binding proteins present on lipid metabolism transcripts leading to altered expression in the C. elegans nervous system

Project description:The kinase GSK-3 alters the repertoire of RNA binding proteins present on lipid metabolism transcripts leading to altered expression in the C. elegans nervous system

| PRJNA1208484 | ENA

The kinase GSK-3 alters the repertoire of RNA binding proteins present on lipid metabolism transcripts leading to altered expression in the C. elegans nervous system

Project description:Tissue-specific regulation of gene expression is essential for multicellular organisms, and RNA binding proteins play central roles in these molecular processes. To determine how the Caenorhabditis elegans RNA binding protein ADR-1 regulates tissue-specific gene expression, we profiled the binding targets of ADR-1 in neural cells and assessed the effects of ADR-1 RNA binding on neural gene expression. We identified a cohort of neural transcripts that facilitate lipid synthesis and are directly regulated by ADR-1 RNA binding. To identify cellular factors that influence ADR-1 binding, a forward genetic screen was performed, revealing that the serine/threonine protein kinase, glycogen synthase kinase-3 (GSK-3), inhibits ADR-1 binding to the cohort. Further investigation revealed that RNA binding protein VIG-1, promotes ADR-1 binding to the cohort in a GSK-3-dependent manner. Together, we reveal that interplay between kinases and RNA binding proteins regulates expression of lipid metabolism genes within neural cells, potentially impacting stress resistance and longevity.

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The kinase GSK-3 alters the repertoire of RNA binding proteins present on lipid metabolism transcripts leading to altered expression in the C. elegans nervous system

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Regulation of lipid metabolism gene expression in the C. elegans nervous system occurs via altering the repertoire of RNA binding proteins present on specific transcripts

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GSK-3A and GSK-3B knockdown in AML cell lines

Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3AM-bM-^@M-^Sspecific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML. The AML cell lines, MOLM-14, U937, THP-1 and HL-60, were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), and two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).

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Project description:GSK-615 was used to treat ES2, SUM159, and A549 cells, and RNA-seq was used to look at how the compound changed gene expression in general. We aimed to predict probable TFs activated with GSK-615 treatment by focusing on the overlapping differentially expressed genes across the three cell lines impacted by GSK-615 in order to find common molecular changes across the three cancer cell lines. The Integrated System for Motif Activity Response Analysis (ISMARA) was then used to look at the DNA-binding motifs of these genes and find the TFs that were present.

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Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3A–specific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML.

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Project description:Mutations in KRAS occur in a variety of tumors of epithelial origin, driving the oncogenic phenotype.The NF-kB transcription factor pathway is important for oncogenic RAS to transform cells and to drive tumorigenesis in animal models. Recently TAK1, an upstream regulator of IKK which controls canonical NF-kB, was shown to be important for chemoresistance in pancreatic cancer and for regulating KRAS+ colorectal cancer cell growth and survival. Here we show that GSK-3alpha is upregulated by KRAS leading to interaction with TAK1 to stabilize the TAK1/TAB complex to promote IKK activity. Additionally, GSK-3alpha is required for promoting critical non-canonical NF-kB signaling in pancreatic cancer cells. Pharmacologic inhibition of GSK-3 suppresses growth of human pancreatic tumor explants, consistent with loss of expression of genes such as c-myc and TERT. These data identify GSK-3alpha as a key downstream effector of oncogenic RAS via its ability to coordinately regulate distinct NF-kB signaling pathways GSK-3 inhibition at 2 and 8 hours

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Gene expression profiles in GSK-3beta Ser9Ala knock-in mouse heart

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