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Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia

ABSTRACT: Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia

PROVIDER: PRJNA533070 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8906500.fastq.gz	Fastqsanger.gz
	SRR8906510.fastq.gz	Fastqsanger.gz
	SRR8906501.fastq.gz	Fastqsanger.gz
	SRR8906511.fastq.gz	Fastqsanger.gz
	SRR8906502.fastq.gz	Fastqsanger.gz

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Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia [ChIP-Seq]

Project description:Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia [ChIP-Seq]

| PRJNA533061 | ENA

Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia [RNA-Seq]

Project description:Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia [RNA-Seq]

| PRJNA533192 | ENA

Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia

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

2019-11-01 | GSE129863 | GEO

Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia [ChIP-Seq]

Project description:Genome-wide binding/occupancy profiling by high throughput sequencing

2019-11-01 | GSE129861 | GEO

Chemical Inhibition of Salt-Inducible Kinase as Therapeutic Strategy in Acute Myeloid Leukemia [RNA-Seq]

Project description:Transcriptome analysis by high throughput sequencing

2019-11-01 | GSE129862 | GEO

Stimulation of fracture mineralization by salt-inducible kinase inhibitors

Project description:Stimulation of fracture mineralization by salt-inducible kinase inhibitors

| PRJNA1105911 | ENA

Stimulation of fracture mineralization by salt-inducible kinase inhibitors

Project description:Over 6.8 million fractures are reported annually in the US, accounting for 20% of all musculoskeletal injuries. Approximately 10% of fractures will experience delayed- or non-union. Parathyroid hormone (PTH) analogs and anabolic osteoporosis therapeutics can stimulate fracture repair in animal models and patients with chronic nonunion. Previous studies have demonstrated that small molecule salt inducible kinase (SIK) inhibitors mimic PTH action in vitro and in vivo. Therefore, we hypothesize that YKL-05-099, a small molecule SIK inhibitor, will accelerate fracture callus osteogenesis.

2024-09-01 | GSE266115 | GEO

Chemical genetics strategy to profile kinase target engagement reveals role of FES in neutrophil phagocytosis via SYK activation

Project description:Chemical genetics strategy to profile kinase target engagement reveals role of FES in neutrophil phagocytosis via SYK activation

| PRJNA608435 | ENA

Sympathetic inputs regulate adaptive thermogenesis in brown adipose tissue through cAMP-Salt inducible kinase axis

Project description:Various physiological stimuli, such as cold environment, diet, and hormones, trigger brown adipose tissue (BAT) to produce heat through sympathetic nervous system (SNS)- and -adrenergic receptors (ARs). The AR stimulation increases intracellular cAMP levels through heterotrimeric G proteins and adenylate cyclases, but the processes by which cAMP modulates brown adipocyte function are not fully understood. Here we described that specific ablation of cAMP production in brown adipocytes led to reduced lipolysis, mitochondrial biogenesis, uncoupling protein 1 (Ucp1) expression, and consequently defective adaptive thermogenesis. Elevated cAMP signaling by sympathetic activation inhibited Salt-inducible kinase 2 (Sik2) through protein kinase A (PKA)-mediated phosphorylation in brown adipose tissue. Inhibition of SIKs enhanced Ucp1 expression in differentiated brown adipocytes and Sik2 knockout mice exhibited enhanced adaptive thermogenesis at thermoneutrality in an Ucp1-dependent manner. Taken together, our data indicate that suppressing Sik2 by PKA-mediated phosphorylation is a requisite for SNS-induced Ucp1 expression and adaptive thermogenesis in BAT, and targeting Sik2 may present a novel therapeutic strategy to ramp up BAT thermogenic activity in humans.

2018-07-12 | PXD009262 | Pride

Development of Chemical Probes for Investigation of Salt-Inducible Kinase Function in Vivo.

Project description:Salt-inducible kinases (SIKs) are promising therapeutic targets for modulating cytokine responses during innate immune activation. The study of SIK inhibition in animal models of disease has been limited by the lack of selective small-molecule probes suitable for modulating SIK function in vivo. We used the pan-SIK inhibitor HG-9-91-01 as a starting point to develop improved analogs, yielding a novel probe 5 (YKL-05-099) that displays increased selectivity for SIKs versus other kinases and enhanced pharmacokinetic properties. Well-tolerated doses of YKL-05-099 achieve free serum concentrations above its IC50 for SIK2 inhibition for >16 h and reduce phosphorylation of a known SIK substrate in vivo. While in vivo active doses of YKL-05-099 recapitulate the effects of SIK inhibition on inflammatory cytokine responses, they did not induce metabolic abnormalities observed in Sik2 knockout mice. These results identify YKL-05-099 as a useful probe to investigate SIK function in vivo and further support the development of SIK inhibitors for treatment of inflammatory disorders.

| S-EPMC4992440 | biostudies-literature

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