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Germline deletion of Krüppel-like factor 14 does not increase risk of diet-induced metabolic syndrome in male C57BL/6 mice

ABSTRACT: Germline deletion of Krüppel-like factor 14 does not increase risk of diet-induced metabolic syndrome in male C57BL/6 mice

PROVIDER: PRJNA721979 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14239600.fastq.gz	Fastqsanger.gz
	SRR14239601.fastq.gz	Fastqsanger.gz
	SRR14239602.fastq.gz	Fastqsanger.gz
	SRR14239603.fastq.gz	Fastqsanger.gz
	SRR14239604.fastq.gz	Fastqsanger.gz

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Germline deletion of Krüppel-like factor 14 does not increase risk of diet-induced metabolic syndrome in male C57BL/6 mice

Project description:The transcription factor Krüppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model.

2021-04-15 | GSE172090 | GEO

Germline deletion of Kruppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice.

Project description:ObjectiveThe transcription factor Krüppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model.MethodsMale whole body Klf14 KO mice were fed a chow or high fat diet (HFD) and diet induced phenotypes were analyzed. Additionally, tissue-specific expression of Klf14 was determined using RT-PCR, RNA sequencing, immunoblotting and whole mount lacZ staining. Finally, the consequences of KLF14 loss-of-function were studied using RNA sequencing in tissues with relatively high Klf14 expression levels.ResultsKLF14 loss-of-function did not affect HFD-induced weight gain or insulin resistance. Fasting plasma concentrations of glucose, insulin, cholesterol, HDL-C and ApoA-I were also comparable between Klf14+/+ and Klf14-/- mice on chow and HFD. We found that in mice expression of Klf14 was the highest in the anterior pituitary (adenohypophysis), lower but detectable in white adipose tissue and undetectable in liver. Loss of KLF14 function impacted on the pituitary transcriptome with extracellular matrix organization as the primary affected pathway and a predicted link to glucocorticoid receptor signaling.ConclusionsWhole body loss of KLF14 function in male mice does not result in metabolic abnormalities as assessed under chow and HFD conditions. Mostly likely there is redundancy for the role of KLF14 in the mouse and a diverging function in humans.

| S-EPMC8607354 | biostudies-literature

Sequencing of proteomic pan-β-hydroxybutyrylation in female germline stem cells

Project description:Metformin increase the number of FGSCs in mouse ovary, and the increased pan-β-hydroxylbutylated protein modification level in vitro FGSCs was detected by WB. There are the Mass spectrum original data of proteomic examination about pan-β-hydroxybutyrylation sites in female germline stem cells after merformin treatment

2022-11-11 | PXD038090 |

Germline BRCA1 mutations increase prostate cancer risk.

Project description:BackgroundProstate cancer (PrCa) is one of the most common cancers affecting men but its aetiology is poorly understood. Family history of PrCa, particularly at a young age, is a strong risk factor. There have been previous reports of increased PrCa risk in male BRCA1 mutation carriers in female breast cancer families, but there is a controversy as to whether this risk is substantiated. We sought to evaluate the role of germline BRCA1 mutations in PrCa predisposition by performing a candidate gene study in a large UK population sample set.MethodsWe screened 913 cases aged 36–86 years for germline BRCA1 mutation, with the study enriched for cases with an early age of onset. We analysed the entire coding region of the BRCA1 gene using Sanger sequencing. Multiplex ligation-dependent probe amplification was also used to assess the frequency of large rearrangements in 460 cases.ResultsWe identified 4 deleterious mutations and 45 unclassified variants (UV). The frequency of deleterious BRCA1 mutation in this study is 0.45%; three of the mutation carriers were affected at age 65 years and one developed PrCa at 69 years. Using previously estimated population carrier frequencies, deleterious BRCA1 mutations confer a relative risk of PrCa of ~3.75-fold, (95% confidence interval 1.02–9.6) translating to a 8.6% cumulative risk by age 65.ConclusionThis study shows evidence for an increased risk of PrCa in men who harbour germline mutations in BRCA1. This could have a significant impact on possible screening strategies and targeted treatments.

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Megasphaera elsdenii 14-14

Project description:Megasphaera elsdenii 14-14 Genome Sequence

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Krüppel-like factor 3 KO and rescue expression data in murine embyronic fibroblasts

Project description:Krüppel-like factor 3 (KLF3) is a transcriptional repressor that has roles in adipogenesis, B-cell maturation and erythropoiesis (for review see Pearson et al., 2012). We profiled gene expression in murine embryonic fibroblasts (MEFs) where Klf3 had been knocked-out and where the same cell had been rescued with Klf3 using microarrays. Klf3 KO murine embryonic fibroblast cell lines were produced from Klf3 KO mice. These cells were rescued with epitope tagged Klf3 (Klf3-V5) using retroviral delivery (murine stem cell virus). Stable clones were selected uner puromycin seletion and total RNA was taken for array

2013-10-17 | E-GEOD-44744 | biostudies-arrayexpress

Krüppel-like factor 4 regulates T cell function

Project description:Krüppel-like factor 4 (Klf4), a transcription factor mediating context-dependent activation or repression, plays a key role in maintaining pluripotency of stem cells and in regulating cell differentiation. However, the precise function of Klf4 in T cell development and differentiation is largely unknown. Here we showed that Klf4 was highly expressed in thymocyte subsets and mature T cells, and was rapidly down-regulated in mature T cells after activation. In T cell-specific Klf4 conditional knockout mice, we observed a modest reduction of thymocytes (27%). This was due partly to the loss of Klf4 repression of Cdkn1b expression in thymocytes resulting in decreased proliferation of DN thymocytes. Together, these findings identify Klf4 as a critical regulator in T cell development. Klf4fl/fl mice (Katz et al., 2002) were crossed with CD4-Cre mice (Lee et al., 2001) to generate Klf4fl/fl-CD4-Cre+ (Klf4 conditional knockout in T cells) and Klf4fl/fl-CD4-Cre- (control) mice. Mice used for experiments were between 8 and 10 weeks old. Total RNA was extracted from freshly isolated DP+SP4 thymocytes from 3 KO mice and 3 control mice. RNA samples were labeled and hybridized to Illumina Sentrix MouseRef-8 v2 bead arrays.

2011-06-24 | E-GEOD-24880 | biostudies-arrayexpress

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