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KLF1 encodes a hematopoietic-specific transcription factor that induces high-level expression of adult beta-globin and other erythroid genes. Additionally we are shipping KLF1 Kits (4) and KLF1 Proteins (4) and many more products for this protein.
Showing 10 out of 90 products:
Mouse (Murine) Monoclonal KLF1 Primary Antibody for ChIP, IP - ABIN2668639
Sengupta, Cohet, Morlé, Bieker: Distinct modes of gene regulation by a cell-specific transcriptional activator. in Proceedings of the National Academy of Sciences of the United States of America 2009
Show all 4 Pubmed References
Human Monoclonal KLF1 Primary Antibody for FACS, IHC - ABIN1724828
Zhou, Liu, Sun, Pawlik, Townes: KLF1 regulates BCL11A expression and gamma- to beta-globin gene switching. in Nature genetics 2010
Show all 2 Pubmed References
Human Polyclonal KLF1 Primary Antibody for ChIP, ELISA - ABIN249501
Pandya, Townes: Basic residues within the Kruppel zinc finger DNA binding domains are the critical nuclear localization determinants of EKLF/KLF-1. in The Journal of biological chemistry 2002
Human Polyclonal KLF1 Primary Antibody for WB - ABIN4228488
Wong, Hou, Tseng, Chien, Wu, Chen, Ho, Kyo, Teng: Krüppel-like transcription factor 4 contributes to maintenance of telomerase activity in stem cells. in Stem cells (Dayton, Ohio) 2010
Human Monoclonal KLF1 Primary Antibody for ELISA, WB - ABIN524111
Akgül, Lin, Ou Yang, Chen, Lu, Chen, Kikuchi, Chen, Tu: Garlic accelerates red blood cell turnover and splenic erythropoietic gene expression in mice: evidence for erythropoietin-independent erythropoiesis. in PLoS ONE 2011
NF-E2 (show NFE2 Antibodies), TAL1 (show TAL1 Antibodies) and KLF1, all activators play a primary role in HSs (show GFER Antibodies) formation in the LCR
Introduction of the British HPFH mutation into the fetal globin promoter in a human cell model causes elevated fetal globin expression. The British HPFH mutation creates a de novo binding site both in vitro and in vivo for the potent erythroid activator KLF1.
A hypothesis on possible liaisons between mutations in the gene encoding EKLF and resistance to pathogens is presented.
study reports a novel KLF1 mutation codon 211 A-->G (c.632 A>G) in a family with beta-hemoglobinopathy showing a considerable increase in the HbF level, thus supporting the role of KLF1 in hemoglobin switching
seven new alleles in the KLF1 gene, which are presumed to act dominantly to silence LU expression, were identified
The prevalence of the In(Lu) phenotype in the Japanese population was 0.02%, and we identified 13 known and 21 novel KLF1 alleles. The KLF1 mutations cause the reduced expression of the P1 antigen.
Our study highlighted two novel promoter KLF1 and 3'-region C/EBPalpha motifs in the phenylalanine hydroxylase (PAH) gene which decrease transcription in vitro and, thus, could be considered as PAH expression modifiers.
a broad range of hitherto unrelated human red cell disorders are caused by variants in KLF1, a master regulator of erythropoiesis, which were previously considered to be extremely rare causes of human genetic disease [review]
results suggest that KLF1 directly regulates the beta-globin gene, but probably has less direct impact on expression of the gamma-globin gene in fetal erythroblasts
A KLF1-targeted promoter-reporter assay showed that the two mutations reduce the expression of the HBB, BCL11A (show BCL11A Antibodies), and CD44 (show CD44 Antibodies) genes involved in erythropoiesis.
The semi-dominant neonatal anemia (Nan) mutation in the EKLF/KLF1 transcription factor leads to ectopic expression of proteins that are not normally expressed in the red blood cell, leading to systemic effects that exacerbate the intrinsic anemia in the adult and alter correct development in the early embryo.
Point mutations in the erythroid transcription factor, Klf1: one mutation, D11 generates a stop codon in the zinc finger domain and a homozygous null phenotype; another mutation, D45, generates an amino acid transversion (H350R) within a linker between zinc fingers two and three.
Data indicate that PIAS3 (protein inhibitor of activated STAT3 (show PIAS3 Antibodies)) interaction modulates EKLF (erythroid Kruppel-like factor) activity in a promoter-dependent and SUMO-independent manner.
Hemin-induced expression of PlGF (show PGF Antibodies) is abolished in EKLF-deficient erythroid cells but rescued by conditional expression of EKLF.
HIRA (show HIRA Antibodies) is not only critical for beta-globin (show HBB Antibodies) expression but is also required for activation of the erythropoietic regulators EKLF and GATA binding protein 1 (GATA1).
KLF1 and KLF2 (show KLF2 Antibodies) coordinately regulate embryonic erythroid precursor maturation through the regulation of multiple homeostasis-associated genes.
EKLF mRNA has exon skipping only in primary tissues. The splice variant is at a low level in embryonic and adult erythroid cells, and in terminal differentiation. The truncated protein partially encodes a non-erythroid Kruppel-like factor AA sequence.
Dok2 is able to control Klf1 expression by transcriptional regulation through directly binding to its promoter region.
EKLF plays a coordinating role between two different cell types whose interaction provides the optimal environment to generate a mature red blood cell
the regulatory mechanisms of the nuclear import of EKLF, which may also be utilized in the nuclear import of other factors
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.
Kruppel-like factor 1 (erythroid)
, Krueppel-like factor 1
, erythroid Kruppel-like factor
, erythroid krueppel-like transcription factor
, erythroid-specific transcription factor EKLF
, monoclonal antibody A3D8
, erythroid transcription factor
, neonatal anemia