Kruppel-Like Factor 1 (erythroid) (KLF1) ELISA Kits

Human Kruppel-Like Factor 1 (erythroid) (KLF1) Interaktionspartner

1. The two beta-TI patients were homozygous for a new mutation c.942delA in exon 3 of KLF1. Mutations in modifier genes can cause or affect thalassemia. Therefore, exact investigation of globin genes and modifiers such as KLF1 is necessary in areas where globin gene disorders are most prevalent to understand the reason of clinical and hematological symptoms of thalassemia and facilitate newborn screening or prenatal diagn...

2. Our results suggest that if there are mutations in KLF1 associated with erythroid malignancies, they are exceedingly rare.

3. KLF1 and KLF9 synergistically regulated erythroid differentiation through the PI3K-Akt and FoxO signaling pathways.

4. This case illustrates the E325K mutation in KLF1 presenting with severe anemia in infancy, persistently elevated fetal hemoglobin, and progressive improvement with age. This case of CDA because of KLF1 mutation highlights the common features and expected disease course of Congenital dyserythropoetic anemia type IV.

5. These results suggest that hypomethylation of the EKLF promoter has functional significance in the establishment and maintenance of erythroid-specific gene expression.

6. To the best of our knowledge, this is the first report of p.Ser102Pro (c.304T>C) in the KLF1 gene in beta-thalassemia patients with increased level of fetal hemoglobin

7. A Chinese family with KLF1 mutation causing mild beta-thalassemia

8. KLF1 gene variants are common in Chinese subjects with alpha-thal and increased Hb F levels, and KLF1 gene mutations decreased the red blood cell (RBC) indices in alpha-thal carriers as that in normal adults.

9. miR-326 suppresses EKLF expression directly by targeting its 3' UTR. In K562 cells, mir-326 overexpression reduced EKLF and increased gamma-globin production, while EKLF inhibition did the opposite.

10. KLF1 promoted metastasis and invasion via the PI3K/Akt signaling pathway in cervical cancer cells.

11. 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.

12. 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.

13. Changes in HbA2 and HbF in alpha thalassemia carriers with KLF1 mutation.

14. Reduction of KLF1 expression in beta(0)-thalassemia/HbE erythroblasts can increase HbF levels.

15. Alterations in high HbF levels may be associated with KLF1 gene mutations.

16. KLF1 enhancer sequence is frequently hypermethylated in juvenile myelomonocytic leukemia.

17. Findings suggest that the induction of an indel mutation in the Kruppel like factor 1 (KLF1) gene leading to a null allele.

18. 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.

19. Activation of KLF1 at day 10 of the differentiation process when hematopoietic progenitor cells were present, enhanced erythroid commitment and differentiation.

20. Hereditary persistence of fetal hemoglobin in two patients with KLF1 haploinsufficiency due to 19p13.2-p13.12/13 deletion

Mouse (Murine) Kruppel-Like Factor 1 (erythroid) (KLF1) Interaktionspartner

1. Study shows that embryos from KLF1 Nan variant have defects in erythroid maturation.

2. Mutant Nan-KLF1 leads to extensive and progressive transcriptome corruption in adult spleen erythroid precursors such that stress erythropoiesis is severely compromised.

3. Insight into the mechanism of Congenital Dyserythropoietic Anemia Type IV which is caused by a point mutation in the DNA-binding domain of KLF1. This mutation alters the DNA binding specificity of KLF1 and this leads to aberrant binding in vivo at a few thousand sites scattered across the genome.

4. data indicate that the cytotoxic effect of IFN-beta activation in CMEI contribute to the impairment of definitive erythropoiesis associated with Klf1 deprivation

5. Results provide new evidence to support a role for KLF1 in the erythroid/megakaryocyte switch, as well as indicating that transcription factor competition is an important regulation mechanism in eukaryotes in vivo.

6. KLF1 and KLF3 bind common as well as unique sites within the erythroid cell genome.

7. 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.

8. 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.

9. Data indicate that PIAS3 (protein inhibitor of activated STAT3) interaction modulates EKLF (erythroid Kruppel-like factor) activity in a promoter-dependent and SUMO-independent manner.

10. Hemin-induced expression of PlGF is abolished in EKLF-deficient erythroid cells but rescued by conditional expression of EKLF.

11. HIRA is not only critical for beta-globin expression but is also required for activation of the erythropoietic regulators EKLF and GATA binding protein 1 (GATA1).

12. KLF1 and KLF2 coordinately regulate embryonic erythroid precursor maturation through the regulation of multiple homeostasis-associated genes.

13. 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.

14. Dok2 is able to control Klf1 expression by transcriptional regulation through directly binding to its promoter region.

15. EKLF plays a coordinating role between two different cell types whose interaction provides the optimal environment to generate a mature red blood cell

16. the regulatory mechanisms of the nuclear import of EKLF, which may also be utilized in the nuclear import of other factors

17. Similar to its role at the beta-globin promoter, KLF1 induces factor recruitment and chromatin changes at the Alad1b promoter in a temporally-specific manner

18. data support an important role for the KLF1-BCL11A axis in erythroid maturation and developmental regulation of globin expression

19. KLF1 activates an extensive erythroid gene expression program.

20. EKLF increases PIT1 expression during RBC maturation by binding to its promoter in vivo.