KFL1 is known to modulate BCL11A expression and can increase human γ-globin/β-globin expression ratios. Furthermore, KFL1 haploinsufficiency can cause hereditary persistence of fetal hemoglobin. Rabbit Anti-KLF1 antibody recognizes bovine, pig, human, mouse, and rat KLF1.
Immunogen
Synthetic peptide directed towards the middle region of human KLF1
Application
Rabbit Anti-KLF1 antibody can be used for western blot assays at 1μg/ml.
Biochem/physiol Actions
KLF1 is a transcription factor, originally identified in this laboratory, which plays a crucial role as a transcriptional activator at the adult beta-globin locus.
Sequence
Synthetic peptide located within the following region: PKALALQPVYPGPGAGSSGGYFPRTGLSVPAASGAPYGLLSGYPAMYPAP
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Hereditary persistence of fetal hemoglobin (HPFH) is characterized by persistent high levels of fetal hemoglobin (HbF) in adults. Several contributory factors, both genetic and environmental, have been identified but others remain elusive. HPFH was found in 10 of 27 members
We show that knockdown of KLF1 in human and mouse adult erythroid progenitors markedly reduces BCL11A levels and increases human gamma-globin/beta-globin expression ratios. These results suggest that KLF1 controls globin gene switching by directly activating beta-globin and indirectly repressing gamma-globin
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