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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Kruppel-like factor 1

EKLF, erythroid Kruppel-like factor, KLF1
This gene encodes a hematopoietic-specific transcription factor that induces high-level expression of adult beta-globin and other erythroid genes. The zinc-finger protein binds to the DNA sequence CCACACCCT found in the beta hemoglobin promoter. Heterozygous loss-of-function mutations in this gene result in the dominant In(Lu) blood phenotype. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: GATA-1, Beta-globin, CAN, CK7, NF-E2
Papers on EKLF
Reciprocal regulation of alternative lineages by Rgs18 and its transcriptional repressor Gfi1b.
Saleque et al., New York City, United States. In J Cell Sci, Feb 2016
These phenotypes reflect the differential impact of Rgs18 on signaling through p38 MAPK family proteins, and ERK1 and ERK2 (also known as MAPK3 and MAPK1, respectively) in the two lineages, which in turn alter the balance between the mutually antagonistic transcription factors Fli1 and Klf1.
[Relationship between macrophages and erythropoiesis].
Zhu et al., Tianjin, China. In Zhongguo Dang Dai Er Ke Za Zhi, Jan 2016
New research advances in Kruppel-like factor 1 (KLF1) provide new evidence for the important role of macrophages in erythroblastic islands.
Therapeutic fetal-globin inducers reduce transcriptional repression in hemoglobinopathy erythroid progenitors through distinct mechanisms.
Perrine et al., Boston, United States. In Blood Cells Mol Dis, Jan 2016
Cellular protein levels of BCL11A, LSD-1, and KLF1 were suppressed by the compounds.
Pomalidomide reverses γ-globin silencing through the transcriptional reprogramming of adult hematopoietic progenitors.
Blanc et al., United States. In Blood, Jan 2016
Further, the transcription networks involved in γ-globin repression were selectively and differentially affected by pomalidomide including BCL11A, SOX6, IKZF1, KLF1, and LSD1.
UFBP1, a Key Component of the Ufm1 Conjugation System, Is Essential for Ufmylation-Mediated Regulation of Erythroid Development.
Li et al., Wuhu, China. In Plos Genet, Nov 2015
In addition, loss of UFBP1 suppressed expression of erythroid transcription factors GATA-1 and KLF1 and blocked erythroid differentiation from CFU-Es (colony forming unit-erythroid) to proerythroblasts.
Krüppel-like factor 1: hematologic phenotypes associated with KLF1 gene mutations.
Eng et al., Hamilton, Canada. In Int J Lab Hematol, May 2015
Krüppel-like factor 1 (KLF1) is a pleiotropic erythroid transcription factor that is essential for hematopoiesis.
Erythroid-Specific Expression of LIN28A Is Sufficient for Robust Gamma-Globin Gene and Protein Expression in Adult Erythroblasts.
Miller et al., Bethesda, United States. In Plos One, 2014
For this purpose, lentiviral transduction vectors were produced with LIN28A expression driven by erythroid-specific gene promoter regions of the human KLF1 or SPTA1 genes.
Ldb1 complexes: the new master regulators of erythroid gene transcription.
Li et al., Bethesda, United States. In Trends Genet, 2014
Transcription profiling demonstrates that erythropoiesis is mainly controlled by a small group of lineage-restricted transcription factors [Gata binding protein 1 (Gata1), T cell acute lymphocytic leukemia 1 protein (Tal1), and Erythroid Kruppel-like factor (EKLF; henceforth referred to as Klf1)].
Primitive and definitive erythropoiesis in mammals.
Palis, Rochester, United States. In Front Physiol, 2013
Primitive and definitive erythropoiesis share central transcriptional regulators, including Gata1 and Klf1, but are also characterized by the differential expression and function of other regulators, including myb, Sox6, and Bcl11A.
Congenital dyserythropoietic anemias: molecular insights and diagnostic approach.
Tamary et al., Napoli, Italy. In Blood, 2013
CDA variants with mutations in erythroid transcription factor genes (KLF1 and GATA-1) have been recently identified.
The CACCC-binding protein KLF3/BKLF represses a subset of KLF1/EKLF target genes and is required for proper erythroid maturation in vivo.
Crossley et al., Sydney, Australia. In Mol Cell Biol, 2012
KLF3 is a feedback repressor that counters the activity of EKLF at selected target genes to achieve normal erythropoiesis
Kruppel-like factor 1 (KLF1), KLF2, and Myc control a regulatory network essential for embryonic erythropoiesis.
Trudel et al., Richmond, United States. In Mol Cell Biol, 2012
The expression of the Myc gene is synergistically regulated by KLF1 and KLF2, and both factors bind the Myc promoters.
Functional interactions between erythroid Krüppel-like factor (EKLF/KLF1) and protein phosphatase PPM1B/PP2Cβ.
Bieker et al., New York City, United States. In J Biol Chem, 2012
Studies show that Ppm1b plays a multilayered role in regulating the availability and optimal activity of the EKLF protein in erythroid cells.
A core erythroid transcriptional network is repressed by a master regulator of myelo-lymphoid differentiation.
Skoultchi et al., United States. In Proc Natl Acad Sci U S A, 2012
GATA-1, SCL, and Klf1 form an erythroid core transcriptional network by co-occupying >300 genes
Ten novel mutations in the erythroid transcription factor KLF1 gene associated with increased fetal hemoglobin levels in adults.
Henderson et al., Oxford, United Kingdom. In Haematologica, 2012
KLF1 mutations could make a significant contribution to Hb F variance in malarial regions where hemogobinopathies are common. A single altered KLF1 allele is sufficient to increase Hb F levels.
Putting a finger on the switch.
Bieker, In Nat Genet, 2010
Two new studies show that the KLF1 zinc finger protein uses direct and indirect means to regulate the final switch from fetal to adult globin expression and that monoallelic loss of KLF1 expression leads to persistence of fetal hemoglobin.
KLF1 regulates BCL11A expression and gamma- to beta-globin gene switching.
Townes et al., Birmingham, United States. In Nat Genet, 2010
KLF1 controls globin gene switching by directly activating beta-globin and indirectly repressing gamma-globin gene expression.
Haploinsufficiency for the erythroid transcription factor KLF1 causes hereditary persistence of fetal hemoglobin.
Philipsen et al., Malta. In Nat Genet, 2010
Haploinsufficiency for KLF1 causes hereditary persistence of fetal hemoglobin.
Preferential associations between co-regulated genes reveal a transcriptional interactome in erythroid cells.
Fraser et al., Cambridge, United Kingdom. In Nat Genet, 2010
Data show that the transcription factor Klf1 mediates preferential co-associations of Klf1-regulated genes at a limited number of specialized transcription factories.
Getting connected in the globin interactome.
Groudine et al., In Nat Genet, 2010
The alpha- and beta-globin loci associate with hundreds of active genes across the genome at transcription factories in erythroid cells, and specialized Klf1-containing transcription factories mediate the association of Klf1-regulated genes.
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