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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 Proteins (6) and KLF1 Kits (5) and many more products for this protein.
Showing 10 out of 82 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 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
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
3 new mutations were found KLF1*90A (p.Trp30Ter), KLF*911A (p.Thr304Lys), and KLF1*304C,318G (p. Ser102Pro, Tyr106Ter) in 2 unrelated individuals. 2 others had c.954dupG (p.Arg319Glufs*34), that is, KLF1*BGM06. A child with unexplained anemia had c.973G>A (p.Glu325Lys), associated with congenital dyserythropoietic anemia. The common c.304T>C was found in 2 of 7 samples and 60 of 100 blood donors.
4 individuals who were Lua and Lub negative were identified from 5420 unrelated blood donors. KLF1 allele with c.199delA and c.304T>C in Exon 2 was identified in one individual, which caused a frameshift at AA67 and formed a new premature stop codon at nucleotide position 708 p.(Gly68AlafsTer236). One KLF1 allele with c.304T>C and c.604G>A was found in another, which resulted which resulted in p.Ser102Pro and p.Gly202A.
Changes in HbA2 (show HBa2 Antibodies) and HbF in alpha thalassemia carriers with KLF1 mutation.
Reduction of KLF1 expression in beta(0)-thalassemia/HbE (show HBe1 Antibodies) erythroblasts can increase HbF levels.
Alterations in high HbF levels may be associated with KLF1 gene mutations.
KLF1 enhancer sequence is frequently hypermethylated in juvenile myelomonocytic leukemia.
Findings suggest that the induction of an indel mutation in the Kruppel like factor 1 (KLF1) gene leading to a null allele.
KLF1 is an important genetic factor associated with increased Hb F and in combination with other modifying factors could explain the phenotypic variation of Hb F expression in this common hemoglobinopathy.
Activation of KLF1 at day 10 of the differentiation process when hematopoietic progenitor cells were present, enhanced erythroid commitment and differentiation.
Hereditary persistence of fetal hemoglobin (show HBB Antibodies) in two patients with KLF1 haploinsufficiency due to 19p13.2-p13.12/13 deletion
KLF1 and KLF3 (show KLF3 Antibodies) bind common as well as unique sites within the erythroid cell genome.
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
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