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HBP1 inhibits the development of type 2 diabetes mellitus through transcriptional activation of the IGFBP1 gene

ABSTRACT: HBP1 inhibits the development of type 2 diabetes mellitus through transcriptional activation of the IGFBP1 gene

PROVIDER: PRJNA883746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21691489_1.fastq.gz	Fastqsanger.gz
	SRR21691489_2.fastq.gz	Fastqsanger.gz
	SRR21691490_1.fastq.gz	Fastqsanger.gz
	SRR21691490_2.fastq.gz	Fastqsanger.gz
	SRR21691491_1.fastq.gz	Fastqsanger.gz

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HBP1 inhibits the development of type 2 diabetes mellitus through transcriptional activation of the IGFBP1 gene

Project description:Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease that is highly prevalent worldwide and characterized by glucose and lipid metabolism disorders. However, the pathogenic mechanisms have not been fully established. Here, we found that HMG-box transcription factor 1 (HBP1) is involved in T2DM and that its deficiency in mice aggravates the features of diabetes. In addition, we undertook screening by RNA sequencing and found that HBP1 activates the transcription of the insulin-like growth factor binding protein 1 (IGFBP1) gene. Moreover, Insulin and palmitic acid reduced HBP1 protein expression and inhibited its binding to the IGFBP1 promoter. Furthermore, HBP1 reduced the serum free insulin-like growth factor 1 (IGF-1) concentration through IGFBP1 and inhibited the PI3K/AKT signaling pathway. This forms an insulin/HBP1/IGFBP1 negative feedback regulatory loop to dynamically regulate blood glucose and insulin concentrations. These findings have elucidated a mechanism whereby HBP1 and its negative feedback regulatory loop influence the development of T2DM, thereby providing a new theoretical basis and potential therapeutic target for T2DM.

2022-09-26 | GSE214089 | GEO

Methylation of HBP1 by PRMT1 inhibits its tumor-suppressive function through regulating 2 GSN-mediated actin cytoskeleton remodeling

Project description:HBP1 is a sequence-specific transcription factor which acts as a tumor inhibitor. HBP1 exerts tumor-suppressive function through regulating the expression of many genes during cell metabolism and cell cycle process. Posttranslational modification of HBP1 is crucial for its function. In this study, we found that HBP1 was methylated at R378 by PRMT1, which decreased 16 HBP1 protein stability by promoting its ubiquitination and proteasome-mediated degradation. PRMT1-mediated methylation of HBP1 could alleviate the repressive effects of HBP1 on tumor metastasis and growth through regulation of GSN expression. GSN was identified as a novel target gene of HBP1. Methylation of HBP1 promoted actin cytoskeleton remodeling and tumor progression by downregulating GSN levels. The methylated HBP1-GSN axis was also associated with the clinical outcomes of cancer patients. Targeting methylated HBP1-GSN axis may provide a therapeutic strategy for cancer. Significance: This investigation elucidated the mechanism of how methylation of HBP1 at R378 inhibits its tumor-suppressive function and promotes actin cytoskeleton remodeling, thus providing the strategy for targeting HBP1 during cancer treatment.

2022-06-19 | GSE205932 | GEO

Diabetes Mellitus Type 1 miRnome

Project description:Diabetes Mellitus Type 1 miRnome

| PRJEB51173 | ENA

Type 2 Diabetes mellitus: mRNA and miRNA profiling

Project description:This SuperSeries is composed of the following subset Series: GSE21321: Blood microRNA profiles and upregulation of hsa-miR-144 in males with type 2 diabetes mellitus. GSE26167: MicroRNA 144 impairs insulin signaling by inhibiting the expression of insulin receptor substrate 1 in Type 2 Diabetes mellitus Refer to individual Series

2010-12-18 | E-GEOD-26168 | biostudies-arrayexpress

Single-cell transcriptome profiling reveals the suppressive role of retinal neurons in microglia activation under diabetes mellitus

Project description:Diabetic retinopathy, as one of the common complications of diabetes mellitus, is the leading cause of blindness in working-age population. The disease is characterized by damage to retinal vasculature, which is associated with the activation of retina microglial and chronic neurodegeneration. Previous studies have identified the effects of activated microglial on the retinal neurons, but how the microglial activation is regulated by the others is largely unknown. Here, we performed scRNA-seq on the retina of non-human primates with diabetes mellitus, and identified cell-type-specific molecular changes of the six major cell types. By identifying the ligand-receptor expression patterns among different cells, we established the interactome of the whole retina. The data showed that TNF-α signal mediated the activation of microglial through an autocrine manner. We found Muller and amacrine acted through SPP1 signaling and cone acted through TGFβ signaling, to inhibit the genes related to microglial activation. Our study is the first to profile cell-specific molecular changes and the cell-cell interactome of retina under diabetes mellitus, paving a way to dissect the cellular and molecular mechanisms underlying early-stage diabetic retinopathy.

2021-08-05 | GSE168908 | GEO

Post-transplant diabetes mellitus after kidney transplantation

Project description:Diabetes mellitus (DM) after transplantation remains a crucial clinical problem in kidney transplantation. To obtain insights into molecular mechanisms underlying the development of post-transplant diabetes mellitus (PTDM) and its early impact on glomerular structures, here we comparatively analyze the proteome of histologically normal appearing glomeruli from patients with PTDM from normoglycemic (NG) transplant recipients, and from recipients with pre-existing type 2 DM (PTDM)

2023-10-24 | PXD042188 | Pride

Serum microRNA profile of human type 1 diabetes mellitus

Project description:To evaluate whether serum micoRNAs can be biomarkers for diagnosis of type 1 diabetes mellitus, we analyzed the serum microRNA expression profiles in 6 patients with new-onset type 1 diabetes mellitus and 6 age- and gender-matched healthy controls. A difference was observed in 31 miRNAs between the patients and controls (fold change ≥ 2, P < 0.05)

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DNA methylation and gestational diabetes mellitus

Project description:DNA methylation and gestational diabetes mellitus

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RNAseq between gestational diabetes mellitus and healthy control groups

Project description:tsRNA profiles of gestational diabetes mellitus and healthy control groups were generated by deep sequencing using Illumina NextSeq 500.

2024-05-12 | GSE267259 | GEO

Transcriptional profile of peripheral blood mononuclear cells from Gestational Diabetes Mellitus Patients

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