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Kruppel-like factor 11

The protein encoded by this gene is a zinc finger transcription factor that binds to SP1-like sequences in epsilon- and gamma-globin gene promoters. This binding inhibits cell growth and causes apoptosis. Defects in this gene are a cause of maturity-onset diabetes of the young type 7 (MODY7). Three transcript variants encoding two different isoforms have been found for this gene. [provided by RefSeq, Apr 2010] (from NCBI)
Top mentioned proteins: SP1, TIEG, V1a, CAN, Insulin
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.
C2H2 zinc finger proteins of the SP/KLF, Wilms tumor, EGR, Huckebein, and Klumpfuss families in metazoans and beyond.
Grishin et al., Dallas, United States. In Gene, Dec 2015
The last ancestor of jawed vertebrates was inferred to have at least 18 KLFs (group A: KLF1/2/4/17, group B: KLF3/8/12; group C: KLF5/5l; group D: KLF6/7; group E: KLF9/13/16; group F: KLF10/KLF11; group G: KLF15/15l) and 10 SPs (group A: SP1/2/3/4; group B: SP5/5l; group C: SP6/7/8/9), since they were found in both cartilaginous and boned fishes.
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.
Phenotypic Characterization of Mice Carrying Homozygous Deletion of KLF11, a Gene in Which Mutations Cause Human Neonatal and MODY VII Diabetes.
Urrutia et al., Montevideo, Uruguay. In Endocrinology, Oct 2015
Here, we report that Klf11-/- mice have decreased circulating insulin levels, alterations in the control of blood glucose and body weight, as well as serum dyslipidemia, but do not develop diabetes.
Promoter DNA methylation is associated with KLF11 expression in epithelial ovarian cancer.
Zhao et al., Tianjin, China. In Genes Chromosomes Cancer, Jul 2015
As a transforming growth factor-β (TGF-β)-inducible gene, the expression of Krüppel-like transcription factor 11 (KLF11) is altered in several types of cancer.
MicroRNA-30 Protects Against Carbon Tetrachloride-induced Liver Fibrosis by Attenuating Transforming Growth Factor Beta Signaling in Hepatic Stellate Cells.
Zhang et al., Nanjing, China. In Toxicol Sci, Jul 2015
Krüppel-like factor 11 (KLF11) is an early response transcription factor that potentiates TGF-β/Smad signaling by suppressing the transcription of inhibitory Smad7.
Chronic Social Stress and Ethanol Increase Expression of KLF11, a Cell Death Mediator, in Rat Brain.
Wang et al., Jackson, United States. In Neurotox Res, Jul 2015
Studies in animal models related to depression or alcoholism reveal that the expression of Krüppel-like factor 11 (KLF11, also called TIEG2) is elevated in frontal cortex, which suggests that KLF11 may play a role in stress- or ethanol-induced psychiatric conditions.
Evidence revealing deregulation of the KLF11-MAO A pathway in association with chronic stress and depressive disorders.
Wang et al., Jackson, United States. In Neuropsychopharmacology, May 2015
In the current study, we compared the protein levels of a MAO A-transcriptional activator, Kruppel-like factor 11 (KLF11 , also recognized as transforming growth factor-beta-inducible early gene 2) between the brains of 18 human subjects with MDD and 18 control subjects.
All trans retinoic acid (ATRA) mediated modulation of N-methyl D-aspartate receptor (NMDAR) and Kruppel like factor 11 (KLF11) expressions in the mitigation of ethanol induced alterations in the brain.
Indira et al., Thiruvananthapuram, India. In Neurochem Int, Apr 2015
Chronic exposure to ethanol leads to upregulation of N-methyl D-aspartate receptors (NMDAR) and also activates Kruppel like factor 11 (KLF11) mediated death cascade and thereby neurodegeneration.
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.
Mechanistic role for a novel glucocorticoid-KLF11 (TIEG2) protein pathway in stress-induced monoamine oxidase A expression.
Ou et al., Jackson, United States. In J Biol Chem, 2012
KLF11 is an MAO A regulator and is produced in response to neuronal stress, which transcriptionally activates MAO A.
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.
Sequence-specific recruitment of heterochromatin protein 1 via interaction with Krüppel-like factor 11, a human transcription factor involved in tumor suppression and metabolic diseases.
Urrutia et al., Rochester, United States. In J Biol Chem, 2012
A PXVXL HP1-interacting domain identified at position 487-491 of KLF11 mediates the binding of HP1alpha and KLF11 in vitro and in cultured cells.
Krüppel-like factor 11 differentially couples to histone acetyltransferase and histone methyltransferase chromatin remodeling pathways to transcriptionally regulate dopamine D2 receptor in neuronal cells.
Urrutia et al., Rochester, United States. In J Biol Chem, 2012
Here we report the characterization of two antagonistic, chromatin-mediated mechanisms by which KLF11 regulated the transcription of the dopamine D2 receptor.
Klf10 and Klf11 as mediators of TGF-beta superfamily signaling.
Krieglstein et al., Freiburg, Germany. In Cell Tissue Res, 2012
Klf10 and Klf11 belong to the family of Sp1/Krüppel-like zinc finger transcription factors that play important roles in a variety of cell types and tissues.
Disruption of a novel Kruppel-like transcription factor p300-regulated pathway for insulin biosynthesis revealed by studies of the c.-331 INS mutation found in neonatal diabetes mellitus.
Urrutia et al., Lille, France. In J Biol Chem, 2011
an important role for KLF11 in the regulation of INS transcription via the novel c.-331 KLF site.
Transcriptional regulation of a brown adipocyte-specific gene, UCP1, by KLF11 and KLF15.
Huh et al., Okayama, Japan. In Biochem Biophys Res Commun, 2010
KLF11, but not KLF15, was essential for UCP1 expression during brown adipocyte differentiation of muBM3.1.
TGFbeta regulated gene expression by Smads and Sp1/KLF-like transcription factors in cancer.
Ellenrieder, Marburg an der Lahn, Germany. In Anticancer Res, 2008
These studies have led to the identification of a novel family of TGFbeta-inducible Sp1/KLF-(Krüppel-like factors) like transcription factors (KLF10 and KLF11) which play remarkable roles in TGFbeta mediated cell growth control and differentiation.
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