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KLF14 encodes a member of the Kruppel-like family of transcription factors. Zusätzlich bieten wir Ihnen KLF14 Antikörper (27) und KLF14 Kits (17) und viele weitere Produktgruppen zu diesem Protein an.
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KIF14 was upregulated in colorectal cancer (CRC) tissues and promoted tumor cell proliferation. Study is the first to comprehensively demonstrate the expression profile and functional roles of KIF14 in CRC and reveal that downregulated miR-200c expression may contribute to increased KIF14 expression.
SNPs at the CETP, HNF4A and KLF14 locus are associated with HDL-C levels and type 2 diabetes (in female participants).
KLF14 plays an important role in increasing glucose uptake and insulin sensitivity by the activation of PI3-kinase/Akt signaling pathway in vitro.
KLF14 transcription is significantly downregulated, whereas Plk4 transcription is upregulated in multiple types of cancers, and there exists an inverse correlation between KLF14 and Plk4 protein expression in human breast and colon cancers.
Transduction of HepG2 cells with human KLF14 showed that KLF14 is a regulator of APOA1 expression.
The risk allele C of rs151290 in KCNQ1 and risk allele G of rs972283 in KLF14 were both associated with increased risk of T2DM in a global population.
This is the first description of the activity and mechanisms underlying the function of KLF14 as an activator protein and novel regulator of lipid signaling.
The objective of the present study was to detect the association of the rs4731702 single nucleotide polymorphism (SNP) and serum lipid levels in the Guangxi Mulao and Han populations.
we show that the type 2 diabetes and high-density lipoprotein cholesterol-associated cis-acting expression quantitative trait locus (eQTL) of the maternally expressed transcription factor KLF14 acts as a master trans regulator of adipose gene expression
KLF14 gene is imprinted, with preferential expression from the maternal allele.
the TGFbeta pathway activation leads to recruitment of a KLF14-mSin3A-HDAC2 repressor complex to the TGFbetaRII promoter, as well as the remodeling of chromatin to increase histone marks that associate with transcriptional silencing.
these data provide proof of concept that deregulation of KLF14/PLK1 cascade plays a key role in thrombin-induced endothelial dysfunction in type 2 diabetes mellitus
DNA methylation at Klf14 regulated mRNA expressions, which were downstream and inflammation genes in the adipose tissue. The methylation level of KLF14 supposed to predict inflammatory change in the adipose tissue as epigenetic biomarker in the whole blood.
Klf14 is not expressed in adult liver and its deletion does not affect plasma HDL-cholesterol concentration and other diet-induced obesity phenotypes in male mice. Klf14 is highly expressed in mouse adenohypophysis and KLF14 loss of function impacts on the pituitary transcriptome.
These data demonstrate an important role for KLF14 expression in atherosclerotic lesion formation.
KLF14 reduction serves as a mechanism leading to centrosome amplification and tumorigenesis. On the other hand, forced expression of KLF14 leads to mitotic catastrophe.
KLF14 is dysregulated in the liver of 2 dyslipidemia mouse models. KLF14 regulates plasma HDL-C levels and cholesterol efflux capacity by modulating hepatic ApoA-I production. Hepatic-specific Klf14 deletion in mice decreased circulating HDL-C levels.
The presence of progesterone induced the gene expression of egr-1 and also KLF14, indicating that this steroid channels the signaling pathway into a non-canonical mechanism.
KLF14 gene is intronless, and is monoallelically expressed from the maternal allele in both human and mouse.
This gene encodes a member of the Kruppel-like family of transcription factors. The gene exhibits imprinted expression from the maternal allele in embryonic and extra-embryonic tissues. Expression of this gene is induced by TGF-beta, and the protein represses TGF-beta receptor II expression. The protein functions as part of a transcriptional co-repressor complex that also contains the transcriptional regulator SIN3A and histone deacetylase 2.
BTE-binding protein 5
, Krueppel-like factor 14
, basic transcription element-binding protein 5
, transcription factor BTEB5
, LOW QUALITY PROTEIN: Krueppel-like factor 14