Papers on
KLF11
The Mechanism and Function of Epigenetics in Uterine Leiomyoma Development.Al-Hendy et al., Augusta, United States. In Reprod Sci, Feb 2016
Several tumor suppressor genes, including Kruppel-like factor 11 (KLF11), deleted in lung and esophageal cancer 1 (DLEC1), keratin 19 (KRT19), and death-associated protein kinase 1 (DAPK1) also display higher hypermethylation levels in leiomyomas when compared to adjacent normal tissues.
Loss of neurogenesis in Hydra leads to compensatory regulation of neurogenic and neurotransmission genes in epithelial cells.Galliot et al., Genève, Switzerland. In Philos Trans R Soc Lond B Biol Sci, Feb 2016
By crossing these results with cell-type-specific transcriptomics, we identified epithelial genes up-regulated upon loss of neurogenesis: transcription factors (Dlx, Dlx1, DMBX1/Manacle, Ets1, Gli3, KLF11, LMX1A, ZNF436, Shox1), epitheliopeptides (Arminins, PW peptide), neurosignalling components (CAMK1D, DDCl2, Inx1), ligand-ion channel receptors (CHRNA1, NaC7), G-Protein Coupled Receptors and FMRFRL.
Molecular diagnosis of maturity-onset diabetes of the young (MODY) in Turkish children by using targeted next-generation sequencing.Böber et al., In J Pediatr Endocrinol Metab, Dec 2015
Molecular analyses of GCK, HNF1A, HNF4A, HNF1B, PDX1, NEUROD1, KLF11, CEL, PAX4, INS, and BLK genes were performed on genomic DNA by using next-generation sequencing.
Modulating the Genomic Programming of Adipocytes.Mandrup et al., Odense, Denmark. In Cold Spring Harb Symp Quant Biol, Nov 2015
These include genes encoding transcriptional regulators, such as Krüppel-like factor 11 (KLF11) that are essential for modulating the genomic program in white adipocytes to induce browning.
Browning of human adipocytes requires KLF11 and reprogramming of PPARγ superenhancers.Mandrup et al., Odense, Denmark. In Genes Dev, 2015
Based on such an association, we identified an evolutionarily conserved metabolic regulator, Kruppel-like factor 11 (KLF11), as a novel browning transcription factor in human adipocytes that is required for rosiglitazone-induced browning, including the increase in mitochondrial oxidative capacity.
Monoamine oxidases in major depressive disorder and alcoholism.Ou et al., Jackson, United States. In Drug Discov Ther, 2012
In recent studies, transcriptional regulation involves a repressor protein, R1, for MAO-A and an activator protein, KLF11 (a Krüppel-like factor; also referred to as transforming growth factor-beta early inducible gene 2, TIEG2), for both MAO-A and MAO-B, by binding to Sp/KLF sites in the core promoters of MAO and regulating MAO gene expression.