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Last update 08 May 2025

KLF1

Last update 08 May 2025

Basic Info

Synonyms

EKLF, Erythroid krueppel-like transcription factor, KLF1

+ [2]

Introduction

Transcription regulator of erythrocyte development that probably serves as a general switch factor during erythropoiesis. Is a dual regulator of fetal-to-adult globin switching. Binds to the CACCC box in the beta-globin gene promoter and acts as a preferential activator of this gene. Furthermore, it binds to the BCL11A promoter and activates expression of BCL11A, which in turn represses the HBG1 and HBG2 genes. This dual activity ensures that, in most adults, fetal hemoglobin levels are low. Able to activate CD44 and AQP1 promoters (PubMed:21055716). When sumoylated, acts as a transcriptional repressor by promoting interaction with CDH2/MI2beta and also represses megakaryocytic differentiation.

Drugs associated with KLF1

WO2023028294

Patent Mining

Target

KLF1

Mechanism-

Active Org.

Academia Sinica

Originator Org.

Academia Sinica

Active Indication

Nervous System Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with KLF1

100 Translational Medicine associated with KLF1

0 Patents (Medical) associated with KLF1

632

Literatures (Medical) associated with KLF1

01 Jun 2025·Transfusion and Apheresis Science

Precision diagnostics in Transfusion Medicine: Advancing accuracy in Bombay blood group typing through molecular methods

Article

Author: Chopra, Akshay ; Shastry, Shamee ; Liew, Yew-Wah ; Mohan, Ganesh ; Chenna, Deepika ; Millard, Glenda ; Madkaiker, Deep

BACKGROUNDIntegration of precision diagnosis in Immunohaematology and Transfusion Medicine has led to the development of more refined blood typing and crossmatching techniques, ensuring improved accuracy of blood group determination, thereby reducing the incidence of transfusion reactions and enhancing patient safety. It can also help resolve complex discrepancies noted in serological testing methods.STUDY DESIGN AND METHODSThe blood grouping of a 40 year old female patient done as a part of routine health check using column agglutination technology showed a O group phenotype with additional reaction with O cells in the serum group. Anti-H lectin study confirmed the absence of H antigen, with a Lewis Le(a+b-) phenotype, typing the patient as Classical Bombay phenotype. Further molecular workup was performed.RESULTSAn in-house designed panel enabling comprehensive genotyping for 45 blood group systems and transcription factors KLF1 and GATA1 was used. Sequencing covering the ABO gene predicted the presence of the ABO*O.01.01 and ABO*O.01.02 alleles and the group O phenotype. Combined results of the sequencing analysis identified ABO*O.01.01/*O.01.02, FUT1*01N.09/*01N.09 and FUT2*01/*01 with the predicted phenotype of H-deficient; secretor (para-Bombay). Oh-secretor shows the patient is genetically a ParaBombay since there is an active secretor gene, but phenotyped as Le(a+b-) due to the reduction in Lewis enzyme function by the FUT3 mutations. Hence the patient is classified as a paraBombay, even though the Lewis phenotype make the patient appeared to be a classical Bombay.CONCLUSIONIntegration of precision diagnostics into transfusion therapy improves transplant and transfusion safety.

01 Jun 2025·Comparative Biochemistry and Physiology Part D: Genomics and Proteomics

Comparative analysis of spleen structure, biochemical parameters, and transcriptome of adult and juvenile yellowfin tuna (Thunnus albacares) in the South China Sea

Article

Author: Guo, Zhiqiang ; Wang, Mei ; Zou, Ying ; Ji, Xu ; Yuan, Jigui ; Xiao, Juan ; Su, Xiameng ; Guan, Wanlin ; Li, Qian ; Lu, Zhiyuan

As one of the top predators in the ocean, yellowfin tuna possesses physiological characteristics that are highly adapted to its high-speed swimming habits, such as high cardiac output and efficient oxygen uptake and transportation systems, which enable it to swim rapidly various diverse layers of the water for feeding activities. These physiological characteristics are intricately associated with the efficient hematopoietic function of its spleen, which plays a crucial role in maintaining its long-distance migration and sustained physical activity in particular. However, there are fewer studies on the developmental biology and function of the spleen in this species. In order to investigate the changes in spleen structure and function during the development of yellowfin tuna, this study compared the histological characteristics, biochemical indexes and transcriptome profiles of the spleen in adult and juvenile yellowfin tuna from the South China Sea. Hematoxylin and eosin (H&E), Masson, and reticular fiber staining revealed that the proportion of white pulp and the mean number of blood sinus in the spleen of adult fish were significantly less than those in juvenile fish (p < 0.05), while the relative area of red pulp displayed no significant difference between the two groups. In addition, the contents of granulocyte-macrophage colony-stimulating factor, erythropoietin, thrombopoietin, and stromal cell-derived factor 1 were significantly lower in the spleen of adult fish than in juvenile fish (p < 0.001), while the contents of bone morphogenetic protein 2 and transforming growth factor β1 were significantly increased in juvenile fish spleens (p < 0.001). Comparative transcriptome analysis revealed that there were 1255 differentially expressed genes (DEGs) between adult and juvenile fish, of which 477 were upregulated and 778 were down-regulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that these DEGs were mainly related to embryonic hematopoiesis, the development of blood and lymphoid organs, and the HIF-1 signaling pathway. Key DEGs associated with hematopoietic function were further identified, such as pik3r3b, gata1a, klf1, epor, and lmo2. In conclusion, this study offers a comprehensive comparison of spleen histology, cytokine activities related to hematopoiesis and cell development, and transcriptomic differences between adult and juvenile yellowfin tuna. These findings provide valuable insights into the spleen hematopoietic development mechanism of decoding yellowfin tuna and other tuna species.

06 Apr 2025·Human Molecular Genetics

A replication study of novel fetal hemoglobin-associated genetic variants in sickle cell disease-only cohorts

Article

Author: Kutlar, Abdullah ; Lo, Ken Sin ; Moutereau, Stéphane ; Ilboudo, Yann ; Marshall, Kwesi ; Reid, Marvin ; Bartolucci, Pablo ; Ashley-Koch, Allison E ; Galactéros, Frédéric ; Joly, Philippe ; Brosseau, Nicolas ; Belhaj, Hicham ; Telen, Marilyn J ; Lettre, Guillaume

AbstractSickle cell disease (SCD) is the most common monogenic disease in the world and is caused by mutations in the β-globin gene (HBB). Notably, SCD is characterized by extreme clinical heterogeneity. Inter-individual variation in fetal hemoglobin (HbF) levels strongly contributes to this patient-to-patient variability, with high HbF levels associated with decreased morbidity and mortality. Genetic association studies have identified and replicated HbF levels-associated variants at three loci: BCL11A, HBS1L-MYB, and HBB. In SCD patients, genetic variation at these three loci accounts for ~ 50% of HbF heritability. Genome-wide association studies (GWAS) in non-anemic and SCD patients of multiple ancestries have identified 20 new HbF-associated variants. However, these genetic associations have yet to be replicated in independent SCD cohorts. Here, we validated the association between HbF levels and variants at five of these new loci (ASB3, BACH2, PFAS, ZBTB7A, and KLF1) in up to 3740 SCD patients. By combining CRISPR inhibition and single-cell transcriptomics, we also showed that sequences near non-coding genetic variants at BACH2 (rs4707609) and KLF1 (rs2242514, rs10404876) can control the production of the β-globin genes in erythroid HUDEP-2 cells. Finally, we analyzed whole-exome sequence data from 1354 SCD patients but could not identify rare genetic variants of large effect on HbF levels. Together, our results confirm five new HbF-associated loci that can be functionally studied to develop new strategies to induce HbF expression in SCD patients.

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KLF1

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