China 
Africa 
Explore chapters and articles related to this topic
Biochemical Markers in Ophthalmology
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Abdus Samad Ansari, Pirro G. Hysi
Variations in DNAm caused by heritable factors (i.e., increased or decreased methylation of a genomic region due to the presence of cis-regulatory SNPs) are significantly less tissue-specific [92]. It is therefore possible to use DNAm information from a large number of samples acquired from peripheral tissues to investigate mechanisms through which genomic markers associated with certain phenotypic traits exert their effect and produce clinical phenotypes. There are several bioinformatic tools that can assess if certain GWAS associations to a phenotype are mediated through changes of methylation levels at a particular locus, even if these changes occur much earlier in life and before the disease manifests clinically. For example, a recent GWAS has identified several polymorphisms of the genomic DNA sequence that are associated with keratoconus, many of which appear to affect cell differentiation. A causal inference analysis correlated the observed association of these SNPs with keratoconus with the level of association of the same SNPs with methylation changes observed in the peripheral blood of other, independent samples. The results suggested that SNPs located in certain regions associated with keratoconus caused changes in the methylation levels of the KLF4 and KLF5 gene promoters and enhancers, whose altered activity contributed to the development of keratoconus [103].
Increasing the Sensitivity of Adipocytes and Skeletal Muscle Cells to Insulin
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
In adipocytes, peroxisome proliferator-activated receptor-γ promotes triglycerides storage by increasing the expression of fatty acid-binding protein, acyl-CoA-binding protein, lipoprotein lipase and fatty acid translocase.78,79 Cucurbitacin B at concentration of 300 nM abrogated accumulation in 3T3-L1 preadipocytes in vitro together with reduced expression of peroxisome proliferator-activated receptor-γ, fatty acid-binding protein, CCAAT/enhancer-binding protein-α, adiponectin, and fatty acid translocase.80 This cucurbitane-type steroid at a concentration of 300 nM in 3T3-L1 adipocytes halved the phosphorylation of STAT3 repressed CCAAT/enhancer-binding protein-δ and cyclin D1 and increased KLF5.80 In multipotent C3H10T1/2 cells, this cucurbitane at a dose of 200 nM lowered CCAAT/enhancer-binding protein-δ, mitigated cyclin D1, and boosted KLF5.80 Likewise, cucurbitacin I at a concentration of 300 nM lowered peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding protein-α, and fatty acid translocase in 3T3-L1 preadipocytes.80 Adipogenesis is regulated by a balance of positive and negative regulators.81 In preadipocytes, the negative regulators of adipogenesis such as CCAAT/enhancer-binding protein-γ, C/EBP homologous protein, and Kruppel-like factor are predominantly expressed. Positive regulators such as CCAAT/enhancer-binding protein-δ, sterol regulatory element binding protein-1c, and KLF5 have low expression levels.81,82
KLF5-mediated aquaporin 3 activated autophagy to facilitate cisplatin resistance of gastric cancer
Published in Immunopharmacology and Immunotoxicology, 2023
Xudong Dai, Yong Chen, Ning Chen, Jin Dou, Haiwen Zhuang, Jian Wang, Xin Zhao, Xiaoyu Zhang, Haijian Zhao
To further explore the mechanism underlying the effects of AQP3 on the resistance of GC to CDDP, bioinformatics analysis was performed and the potential targeting relationship between KLF5 and AQP3 was predicted, with the succeeding dual-luciferase reporter and ChIP assays revealing that KLF5 could positively modulate the transcription of AQP3 in CDDP-resistant GC cells. KLF5, a zinc-finger transcription factor, mediates essential functions in diverse cellular processes including invasion, proliferation and apoptosis [40,41]. Mechanically, KLF5 specifically binds to the promoter regions of its target genes to activate or restrain their transcription [42]. In addition, several reports have revealed the oncogenic role of KLF5 in GC [43–45]. In our study, it was worth noting that the KLF5 knockdown reversed overexpressed AQP3-induced effects on the autophagy, viability, invasion, migration and EMT in CDDP-resistant GC cells, which implied that KLF5-mediated AQP3 activated autophagy to facilitate CDDP resistance in GC.
KLF16 suppresses human glioma cell proliferation and tumourigenicity by targeting TFAM
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Xiangrong Chen, Shun Li, Yumin Ke, Shukai Wu, Tianzao Huang, Weipeng Hu, Huangde Fu, Xieli Guo
Krüppel-like factor (KLF) members, including KLFs 1–17, are zinc finger-containing transcription factors that play crucial roles in the regulation of differentiation and development as well as biological processes central to the development of malignancies [7,8]. Numerous evidence indicates a significant role for this family of transcription factors in carcinogenesis, acting as oncogenes and/or tumour suppressors under distinct cellular contexts [7,8]. Typically, KLF5 promotes proliferation of human breast, bladder and pancreatic cancer cells [9–11]. KLF6 is frequently lost in many cancers by somatic mutation, loss of heterozygosity or promoter methylation [12–14]. KLF4 suppresses tumour growth in multiple cancers, including gastric, colorectal, hepatocellular and lung carcinomas [15–18], but promotes cell cycle progression in pancreatic cancer [19]. Moreover, KLF9 regulates the transactivation of progesterone-responsive promoters and has been found to be downregulated in endometrial carcinoma and colorectal cancer [20–23], suggesting that KLF9 downregulation might be linked to cancer development. Therefore, a better understanding of the expression pattern and biological role of KLF9 in glioma progression may provide clues for novel targets for therapeutic intervention.
Heart failure risk estimation based on novel biomarkers
Published in Expert Review of Molecular Diagnostics, 2021
Feven Ataklte, Ramachandran S. Vasan
The study by Di et al, investigated the KLF5 gene. Similar to ISL1, KLF5 gene also encodes a key transcription factor required for cardiac structural and functional remodeling. The KLF5 gene was sequenced in 234 probands affected with DCM, and a heterozygous KLF5 mutation, NM_001730.5: c.1100 T > A; p.(Leu367*), was identified in a proband. The mutated KLF5 lost transcriptional activity and abrogated the synergistic activity KLF5 had with NFKB1, another transcription factor that has been linked to DCM. This KLF5 mutant was later shown to co-segregate with DCM in the family. Therefore, the authors concluded that genetically compromised KLF5 predisposes to DCM in carriers of this mutation [114].