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Journal articles on the topic 'Erythroid Kruppel-Like Factor'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Pandya, Kumar, David Donze, and Tim M. Townes. "Novel Transactivation Domain in Erythroid Kruppel-like Factor (EKLF)." Journal of Biological Chemistry 276, no. 11 (November 22, 2000): 8239–43. http://dx.doi.org/10.1074/jbc.m008457200.

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2

Perkins, Andrew. "Erythroid Kruppel like factor: from fishing expedition to gourmet meal." International Journal of Biochemistry & Cell Biology 31, no. 10 (October 1999): 1175–92. http://dx.doi.org/10.1016/s1357-2725(99)00083-7.

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3

Tallack, Michael R., Janelle R. Keys, and Andrew C. Perkins. "Erythroid Kruppel-like factor regulates the G1 Cdk inhibitor p18." Blood Cells, Molecules, and Diseases 38, no. 2 (March 2007): 168. http://dx.doi.org/10.1016/j.bcmd.2006.10.111.

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4

Gregory, RC, DJ Taxman, D. Seshasayee, MH Kensinger, JJ Bieker, and DM Wojchowski. "Functional interaction of GATA1 with erythroid Kruppel-like factor and Sp1 at defined erythroid promoters." Blood 87, no. 5 (March 1, 1996): 1793–801. http://dx.doi.org/10.1182/blood.v87.5.1793.1793.

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Abstract GATA and CACC elements commonly are codistributed within the regulatory domains of a variety of erythroid genes. Using Drosophila S2 cells, the actions of GATA1, Sp1, and erythroid Kruppel-like factor (EKLF) at these elements within model erythroid promoters have been assessed. For each promoter studied (erythroid pyruvate kinase, glycophorin B, and a murine betamaj globin-derived construct, GCT) Sp1 and EKLF each activated transcription despite differences in CACC element sequence, orientation, and positioning. However, GATA1 acted in apparent cooperativity with Sp1 at the pyruvate k

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5

Gregory, RC, DJ Taxman, D. Seshasayee, MH Kensinger, JJ Bieker, and DM Wojchowski. "Functional interaction of GATA1 with erythroid Kruppel-like factor and Sp1 at defined erythroid promoters." Blood 87, no. 5 (March 1, 1996): 1793–801. http://dx.doi.org/10.1182/blood.v87.5.1793.bloodjournal8751793.

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GATA and CACC elements commonly are codistributed within the regulatory domains of a variety of erythroid genes. Using Drosophila S2 cells, the actions of GATA1, Sp1, and erythroid Kruppel-like factor (EKLF) at these elements within model erythroid promoters have been assessed. For each promoter studied (erythroid pyruvate kinase, glycophorin B, and a murine betamaj globin-derived construct, GCT) Sp1 and EKLF each activated transcription despite differences in CACC element sequence, orientation, and positioning. However, GATA1 acted in apparent cooperativity with Sp1 at the pyruvate kinase pro

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6

Crossley, M., A. P. Tsang, J. J. Bieker, and S. H. Orkin. "Regulation of the erythroid Kruppel-like factor (EKLF) gene promoter by the erythroid transcription factor GATA-1." Journal of Biological Chemistry 269, no. 22 (June 1994): 15440–44. http://dx.doi.org/10.1016/s0021-9258(17)40698-3.

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7

Ilsley, Melissa, Kevin R. Gillinder, Graham Magor, Merlin Crossley, and Andrew C. Perkins. "Fine-Tuning Erythropoiesis By Competition Between Krüppel-like Factors for Promoters and Enhancers." Blood 128, no. 22 (December 2, 2016): 1036. http://dx.doi.org/10.1182/blood.v128.22.1036.1036.

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Abstract Krüppel-like factors (KLF) are a group of 17 transcription factors with highly conserved DNA-binding domains that contain three C-terminal C2H2-type zinc fingers and a variable N-terminal domain responsible for recruiting cofactors 1. KLFs participate in diverse roles in stem cell renewal, early patterning, organogenesis and tissue homeostasis. Krüppel-like factor 1 (KLF1) is an erythroid-specific KLF responsible for coordinating many aspects of terminal erythroid differentiation 2. It functions as a transcriptional activator by recruiting cofactors such as p300 and chromatin modifier

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8

Perkins, Andrew C., Janelle R. Keys, Denise J. Hodge, and Michael R. Tallack. "Erythroid Kruppel-Like Factor Regulates E2F4 and the G1 Cdk Inhibitor, p18." Blood 106, no. 11 (November 16, 2005): 1357. http://dx.doi.org/10.1182/blood.v106.11.1357.1357.

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Abstract Erythroid Kruppel-Like Factor (EKLF) is a zinc finger transcription factor which is essential for β-globin gene expression. Knockout mice die from anemia at E15, but restoration of globin chain imbalance does not rescue anemia or increase survival. Cell lines derived from EKLF null mice undergo proliferation arrest upon reactivation of a conditional EKLF-ER fusion protein, suggesting a role in cell cycle control. A transcriptional profiling experiment comparing the global gene expression in EKLF null and wild type fetal liver identified many differentially expressed genes, a number of

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9

Donze, David, Tim M. Townes, and James J. Bieker. "Role of Erythroid Kruppel-like Factor in Human - to -Globin Gene Switching." Journal of Biological Chemistry 270, no. 4 (January 27, 1995): 1955–59. http://dx.doi.org/10.1074/jbc.270.4.1955.

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10

Tallack, Michael R., Janelle R. Keys, and Andrew C. Perkins. "Erythroid Kruppel-like Factor Regulates the G1 Cyclin Dependent Kinase Inhibitor p18INK4c." Journal of Molecular Biology 369, no. 2 (June 2007): 313–21. http://dx.doi.org/10.1016/j.jmb.2007.02.109.

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11

Zhu, Jianqiongz, Kyung Chin, Wulin Aerbajinai, Cecelia D. Trainor, Gao Perter та Griffin P. Rodgers. "Recombinant Erythroid Kruppel-Like Factor Fused to GATA1 up-Regulates δ-Globin Expression In Erythroid Cells." Blood 116, № 21 (19 листопада 2010): 3752. http://dx.doi.org/10.1182/blood.v116.21.3752.3752.

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Abstract Abstract 3752 The β-hemoglobinopathies sickle cell disease and β-thalassemia are among the most common human genetic disorders worldwide. Hemoglobin A2 (HbA2, α2δ2) and fetal hemoglobin (HbF, a2γ2) both inhibit the polymerization of hemoglobin S that results in erythrocyte sickling. Expression of erythroid Kruppel-like factor (EKLF) and GATA1 is critical for transitioning hemoglobin from HbF to hemoglobin A (HbA, α2β2) and HbA2. The lower levels of δ-globin expression compared with β-globin expression seen in adulthood are likely due to the absence of an EKLF-binding motif in the δ-gl

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12

Pilon, Andre M., Subramanian S. Ajay, Swathi Ashok Kumar, Laurie A. Steiner, Praveen F. Cherukuri, Stephen Wincovitch, Stacie M. Anderson, et al. "Genome-wide ChIP-Seq reveals a dramatic shift in the binding of the transcription factor erythroid Kruppel-like factor during erythrocyte differentiation." Blood 118, no. 17 (October 27, 2011): e139-e148. http://dx.doi.org/10.1182/blood-2011-05-355107.

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Abstract Erythropoiesis is dependent on the activity of transcription factors, including the erythroid-specific erythroid Kruppel-like factor (EKLF). ChIP followed by massively parallel sequencing (ChIP-Seq) is a powerful, unbiased method to map trans-factor occupancy. We used ChIP-Seq to study the interactome of EKLF in mouse erythroid progenitor cells and more differentiated erythroblasts. We correlated these results with the nuclear distribution of EKLF, RNA-Seq analysis of the transcriptome, and the occupancy of other erythroid transcription factors. In progenitor cells, EKLF is found pred

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13

Zhu, Jianqiong, Kyung Chin, Wulin Aerbajinai, Cecelia Trainor, Peter Gao, and Griffin P. Rodgers. "Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells." Blood 117, no. 11 (March 17, 2011): 3045–52. http://dx.doi.org/10.1182/blood-2010-07-294751.

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Abstract The β-hemoglobinopathies sickle cell disease and β-thalassemia are among the most common human genetic disorders worldwide. Hemoglobin A2 (HbA2, α2δ2) and fetal hemoglobin (HbF, α2γ2) both inhibit the polymerization of hemoglobin S, which results in erythrocyte sickling. Expression of erythroid Kruppel-like factor (EKLF) and GATA1 is critical for transitioning hemoglobin from HbF to hemoglobin A (HbA, α2β2) and HbA2. The lower levels of δ-globin expression compared with β-globin expression seen in adulthood are likely due to the absence of an EKLF-binding motif in the δ-globin proxima

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14

Yien, Yvette Y., та James J. Bieker. "Functional Interactions between Erythroid Kruppel-like Factor (EKLF/KLF1) and Protein Phosphatase PPM1B/PP2Cβ". Journal of Biological Chemistry 287, № 19 (5 березня 2012): 15193–204. http://dx.doi.org/10.1074/jbc.m112.350496.

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15

Coghill, Elise, Sarah Eccleston, Vanessa Fox, Loretta Cerruti, Clark Brown, John Cunningham, Stephen Jane, and Andrew Perkins. "Erythroid Kruppel-like factor (EKLF) coordinates erythroid cell proliferation and hemoglobinization in cell lines derived from EKLF null mice." Blood 97, no. 6 (March 15, 2001): 1861–68. http://dx.doi.org/10.1182/blood.v97.6.1861.

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Erythroid Kruppel-like factor (EKLF) is a transcription factor of the C2H2 zinc-finger class that is essential for definitive erythropoiesis. We generated immortal erythroid cell lines from EKLF−/− fetal liver progenitor cells that harbor a single copy of the entire human β-globin locus and then reintroduced EKLF as a tamoxifen-inducible, EKLF–mutant estrogen receptor (EKLF-ER™) fusion protein. Addition of tamoxifen resulted in enhanced differentiation and hemoglobinization, coupled with reduced proliferation. Human β-globin gene expression increased significantly, whereas γ-globin transcripts

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16

Mas, C., M. Lussier-Price, S. Soni, T. Morse, G. Arseneault, P. Di Lello, J. Lafrance-Vanasse, J. J. Bieker, and J. G. Omichinski. "Structural and functional characterization of an atypical activation domain in erythroid Kruppel-like factor (EKLF)." Proceedings of the National Academy of Sciences 108, no. 26 (June 13, 2011): 10484–89. http://dx.doi.org/10.1073/pnas.1017029108.

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17

Zhang, W., and J. J. Bieker. "Acetylation and modulation of erythroid Kruppel-like factor (EKLF) activity by interaction with histone acetyltransferases." Proceedings of the National Academy of Sciences 95, no. 17 (August 18, 1998): 9855–60. http://dx.doi.org/10.1073/pnas.95.17.9855.

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18

Keys, Janelle R., Michael R. Tallack, Denise J. Hodge, Simon O. Cridland, Rakesh David, and Andrew C. Perkins. "Genomic organisation and regulation of murine alpha haemoglobin stabilising protein by erythroid Kruppel-like factor." British Journal of Haematology 136, no. 1 (January 2007): 150–57. http://dx.doi.org/10.1111/j.1365-2141.2006.06381.x.

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19

Luo, Qi, Xiaojing Ma, Sharon M. Wahl, James J. Bieker, Merlin Crossley, and Luis J. Montaner. "Activation and Repression of Interleukin-12 p40 Transcription by Erythroid Kruppel-like Factor in Macrophages." Journal of Biological Chemistry 279, no. 18 (February 19, 2004): 18451–56. http://dx.doi.org/10.1074/jbc.m400320200.

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20

Manwani, Deepa, Mariann Galdass та James J. Bieker. "Altered Regulation of β like Globin Genes by a Redesigned Erythroid Transcription Factor." Blood 104, № 11 (16 листопада 2004): 1212. http://dx.doi.org/10.1182/blood.v104.11.1212.1212.

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Abstract The well characterized switch during ontogeny of globin gene expression from embryonic/ fetal to adult type is a result of a complex interplay between cis and trans acting regulatory elements at the beta globin locus. Trans acting elements include tissue specific transcription factors that bind specific motifs within the beta globin gene cluster with high specificity. Erythroid Kruppel like factor (EKLF) is one such erythroid specific, zinc finger transcription factor that is critical for the activation of the beta globin promoter and for consolidating the switch from gamma to beta gl

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21

Shyu, Yu-Chiau, Shau-Ching Wen, Tung-Liang Lee, Xin Chen, Chia-Tse Hsu, Hsin Chen, Ruei-Lin Chen, Jau-Lang Hwang, and Che-Kun James Shen. "Chromatin-binding in vivo of the erythroid kruppel-like factor, EKLF, in the murine globin loci." Cell Research 16, no. 4 (April 2006): 347–55. http://dx.doi.org/10.1038/sj.cr.7310045.

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22

Lee, J. S., C. H. Lee, and J. H. Chung. "The beta -globin promoter is important for recruitment of erythroid Kruppel-like factor to the locus control region in erythroid cells." Proceedings of the National Academy of Sciences 96, no. 18 (August 31, 1999): 10051–55. http://dx.doi.org/10.1073/pnas.96.18.10051.

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23

Siatecka, M., K. E. Sahr, S. G. Andersen, M. Mezei, J. J. Bieker, and L. L. Peters. "Severe anemia in the Nan mutant mouse caused by sequence-selective disruption of erythroid Kruppel-like factor." Proceedings of the National Academy of Sciences 107, no. 34 (August 9, 2010): 15151–56. http://dx.doi.org/10.1073/pnas.1004996107.

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24

Siatecka, Miroslawa, Shefali Soni, Antanas Planutis, and James J. Bieker. "Transcriptional Activity of Erythroid Kruppel-like Factor (EKLF/KLF1) Modulated by PIAS3 (Protein Inhibitor of Activated STAT3)." Journal of Biological Chemistry 290, no. 15 (February 24, 2015): 9929–40. http://dx.doi.org/10.1074/jbc.m114.610246.

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25

Gillinder, Kevin R., Graham Magor, Charles Bell, Melissa D. Ilsley, Stephen Huang, and Andrew Perkins. "KLF1 Acts As a Pioneer Transcription Factor to Open Chromatin and Facilitate Recruitment of GATA1." Blood 132, Supplement 1 (November 29, 2018): 501. http://dx.doi.org/10.1182/blood-2018-99-119608.

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Abstract Only a small subset of transcription factors (TFs) can act as pioneer factors; i.e. those that can 'open' otherwise 'closed' chromatin to facilitate assembly of TF complexes and co-factors to enable transcription. The KLF/SP family of TFs bind to a 9-10 bp consensus motif in DNA to activate or repress target gene expression. We have studied the potential for KLF1, which is essential for erythropoiesis, to provide a pioneering function in erythroid progentior cells. Previous ChIP-seq studies have shown KLF1 binds a few thousand enhancers and promoters to activate erythroid cell gene ex

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26

Hodge, Denise, Elise Coghill, Janelle Keys, Tina Maguire, Belinda Hartmann, Alasdair McDowall, Mitchell Weiss, Sean Grimmond, and Andrew Perkins. "A global role for EKLF in definitive and primitive erythropoiesis." Blood 107, no. 8 (April 15, 2006): 3359–70. http://dx.doi.org/10.1182/blood-2005-07-2888.

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Abstract Erythroid Kruppel-like factor (EKLF, KLF1) plays an important role in definitive erythropoiesis and β-globin gene regulation but failure to rectify lethal fetal anemia upon correction of globin chain imbalance suggested additional critical EKLF target genes. We employed expression profiling of EKLF-null fetal liver and EKLF-null erythroid cell lines containing an inducible EKLF-estrogen receptor (EKLF-ER) fusion construct to search for such targets. An overlapping list of EKLF-regulated genes from the 2 systems included α-hemoglobin stabilizing protein (AHSP), cytoskeletal proteins, h

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27

Yokomizo, Tomomasa, Kazuteru Hasegawa, Hiroyuki Ishitobi, Motomi Osato, Masatsugu Ema, Yoshiaki Ito, Masayuki Yamamoto, and Satoru Takahashi. "Runx1 is involved in primitive erythropoiesis in the mouse." Blood 111, no. 8 (April 15, 2008): 4075–80. http://dx.doi.org/10.1182/blood-2007-05-091637.

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Abstract Targeted disruption of the Runx1/ AML1 gene in mice has demonstrated that it is required for the emergence of definitive hematopoietic cells but that it is not essential for the formation of primitive erythrocytes. These findings led to the conclusion that Runx1 is a stage-specific transcription factor acting only during definitive hematopoiesis. However, the zebrafish and Xenopus homologs of Runx1 have been shown to play roles in primitive hematopoiesis, suggesting that mouse Runx1 might also be involved in the development of primitive lineages. In this study, we show that primitive

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28

Parga, Juan A., Ana I. Rodriguez-Perez, Maria Garcia-Garrote, Jannette Rodriguez-Pallares, and Jose L. Labandeira-Garcia. "NRF2 Activation and Downstream Effects: Focus on Parkinson’s Disease and Brain Angiotensin." Antioxidants 10, no. 11 (October 20, 2021): 1649. http://dx.doi.org/10.3390/antiox10111649.

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Reactive oxygen species (ROS) are signalling molecules used to regulate cellular metabolism and homeostasis. However, excessive ROS production causes oxidative stress, one of the main mechanisms associated with the origin and progression of neurodegenerative disorders such as Parkinson’s disease. NRF2 (Nuclear Factor-Erythroid 2 Like 2) is a transcription factor that orchestrates the cellular response to oxidative stress. The regulation of NRF2 signalling has been shown to be a promising strategy to modulate the progression of the neurodegeneration associated to Parkinson’s disease. The NRF2 p

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29

Sengupta, Ananya, Ghanshyam Upadhyay, Asif Chowdhury, and Shireen Saleque. "Regulation Of Erythro-Megakaryocytic Lineage Bifurcation By The Gfi1b Gene Target Rgs18." Blood 122, no. 21 (November 15, 2013): 1191. http://dx.doi.org/10.1182/blood.v122.21.1191.1191.

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Abstract The molecular basis for the divergence of the erythroid (red blood cell) and megakaryocyte (platelet) lineages from a common bipotent MEP (megakaryocyte-erythroid progenitor) remains undefined. We now demonstrate that Rgs18 (regulator of G protein signaling 18), a GAP (GTPase activating protein) factor and a transcriptional gene target of the Gfi1b transcriptional repressor complex, likely arbitrates this critical lineage decision downstream of Gfi1b. Rgs18 was identified in a chromatin immunoprecipitation (ChIP on chip) screen for Gfi1b/LSD1/Rcor1 targets in erythroid cells. Accordin

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30

Bianchi, Elisa, Roberta Zini, Simona Salati, Elena Tenedini, Ruggiero Norfo, Enrico Tagliafico, Rossella Manfredini, and Sergio Ferrari. "c-myb supports erythropoiesis through the transactivation of KLF1 and LMO2 expression." Blood 116, no. 22 (November 25, 2010): e99-e110. http://dx.doi.org/10.1182/blood-2009-08-238311.

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The c-myb transcription factor is highly expressed in immature hematopoietic cells and down-regulated during differentiation. To define its role during the hematopoietic lineage commitment, we silenced c-myb in human CD34+ hematopoietic stem/progenitor cells. Noteworthy, c-myb silencing increased the commitment capacity toward the macrophage and megakaryocyte lineages, whereas erythroid differentiation was impaired, as demonstrated by clonogenic assay, morphologic and immunophenotypic data. Gene expression profiling and computational analysis of promoter regions of genes modulated in c-myb–sil

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31

Perkins, Andrew C., Elise Coghill, Tina Maguire, Belinda Hartmann, Alasdair McDowall, Mitchell Weiss, Sean Grimmond, Janelle Keys, and Denise Hodge. "A Global Role for EKLF in Definitive and Primitive Erythropoiesis." Blood 106, no. 11 (November 16, 2005): 1745. http://dx.doi.org/10.1182/blood.v106.11.1745.1745.

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Abstract Erythroid Kruppel-like factor (EKLF or Klf1) is an erythroid specific C2H2 zinc-finger transcription factor which is essential for definitive erythropoiesis and β-globin gene expression. The absence of EKLF results in fatal anaemia but correction of globin chain imbalance does result in rescue, suggesting the existence of additional EKLF target genes. The aim of this study was to search for such genes by expression profiling. We performed profiling on fetal livers from wild-type versus EKLF null litter mates, and also EKLF null erythroid cell lines containing an inducible EKLF-ERTM fu

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32

Perrine, Susan P., Rishikesh Mankidy, Michael S. Boosalis, James J. Bieker та Douglas V. Faller. "EKLF Is Recruited to the γ-Globin Gene Promoter as a Co-Activator and Is Required for γ-Globin Gene Induction by Short-Chain Fatty Acids." Blood 110, № 11 (16 листопада 2007): 1771. http://dx.doi.org/10.1182/blood.v110.11.1771.1771.

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Abstract The erythroid Kruppel-like factor, EKLF, is an essential transcription factor for mammalian β-type globin gene switching, and specifically activates transcription of the adult β-globin gene through binding of its zinc finger domain to the β-globin promoter. We report now that EKLF is also required for activation of the γ-globin gene by short-chain fatty acid (SCFA) derivatives. We found that specific knockdown of EKLF levels by siRNA prevents SCFA induced-expression of an integrated γ-globin promoter in a stably-expressed mLCRβprRluc AγprFluc cassette, and prevents induction of the en

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33

Tewari, R. "Erythroid Kruppel-like factor (EKLF) is active in primitive and definitive erythroid cells and is required for the function of 5'HS3 of the beta -globin locus control region." EMBO Journal 17, no. 8 (April 15, 1998): 2334–41. http://dx.doi.org/10.1093/emboj/17.8.2334.

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34

Perkins, A. C., K. R. Peterson, G. Stamatoyannopoulos, H. E. Witkowska та S. H. Orkin. "Fetal expression of a human Aγ globin transgene rescues globin chain imbalance but not hemolysis in EKLF null mouse embryos". Blood 95, № 5 (1 березня 2000): 1827–33. http://dx.doi.org/10.1182/blood.v95.5.1827.004k10_1827_1833.

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Mice lacking the erythroid Kruppel-like factor (EKLF) die in utero at embryonic day 15 (E15) from severe anemia. EKLF−/− embryos display a marked deficit in β-globin gene expression. To test whether β-globin deficiency was solely responsible for the anemia and intrauterine death, we corrected the globin chain imbalance in EKLF−/− embryos by breeding with a strain of mice that express high levels of human γ-globin. Despite efficient production of hybrid m2-hγ2 hemoglobin in the fetal livers of EKLF−/− animals, hemolysis was not corrected and survival was not prolonged. We concluded that defici

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35

Miki, T., N. Kawamata, S. Hirosawa, and N. Aoki. "Gene involved in the 3q27 translocation associated with B-cell lymphoma, BCL5, encodes a Kruppel-like zinc-finger protein." Blood 83, no. 1 (January 1, 1994): 26–32. http://dx.doi.org/10.1182/blood.v83.1.26.26.

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Abstract Chromosomal translocations involving band 3q27 are the recently described nonrandom cytogenetic abnormalities in B-cell malignancies. We have previously cloned the breakpoint region of 3q27, designated as the BCL5 locus, from the B-cell line carrying the t(3;22). The cDNA for the BCL5 gene was cloned from the human liver cDNA library. The nucleotide sequencing analysis showed that the BCL5 gene encodes a potential transcription factor containing six repeats of the Cys2-His2 zinc-finger motif resembling the Drosophila segmentation gene Kruppel. The calculated molecular weight was 78.8

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36

Miki, T., N. Kawamata, S. Hirosawa, and N. Aoki. "Gene involved in the 3q27 translocation associated with B-cell lymphoma, BCL5, encodes a Kruppel-like zinc-finger protein." Blood 83, no. 1 (January 1, 1994): 26–32. http://dx.doi.org/10.1182/blood.v83.1.26.bloodjournal83126.

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Chromosomal translocations involving band 3q27 are the recently described nonrandom cytogenetic abnormalities in B-cell malignancies. We have previously cloned the breakpoint region of 3q27, designated as the BCL5 locus, from the B-cell line carrying the t(3;22). The cDNA for the BCL5 gene was cloned from the human liver cDNA library. The nucleotide sequencing analysis showed that the BCL5 gene encodes a potential transcription factor containing six repeats of the Cys2-His2 zinc-finger motif resembling the Drosophila segmentation gene Kruppel. The calculated molecular weight was 78.8 kD, which

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37

Xu, Zhixiong, Xianzhang Meng, Ying Cai, and Stephen J. Brandt. "Recruitment of mSin3A and Histone Deacetylase 2 (HDAC2) by the Chromatin Remodeling Protein BRG1 Mediates Transcriptional Repression in Erythroid Progenitors." Blood 104, no. 11 (November 16, 2004): 1601. http://dx.doi.org/10.1182/blood.v104.11.1601.1601.

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Abstract The Swi/Snf chromatin remodeling complexes are critical for activating or repressing transcription of specific genes and require one of two homologous ATPases, Brg1 and Brm. Although Brg1 is also known to be involved in ß-globin gene transcription and a recent report showed that Brg1-containing complexes could be recruited to the ß-globin promoter and its locus control region (LCR), the exact roles of Brg1 in erythroid gene expression and differentiation have not been directly investigated. We previously showed that Brg1, but not Brm, is recruited to the Protein 4.2 (P4.2) promoter by

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38

Kapetanaki, Maria G., Deva Sharma, Oluwabukola T. Gbotosho, Valerie Schrott, Frances Weidart, Solomon Fiifi Ofori-Acquah, Grant C. Bullock, and Gregory J. Kato. "The Oxidant Response Transcription Factor NRF2 Mediates Heme Activation of Placenta Growth Factor Expression in Erythroid Cells, a Contributor to Pulmonary Hypertension in Sickle Cell Disease." Blood 126, no. 23 (December 3, 2015): 403. http://dx.doi.org/10.1182/blood.v126.23.403.403.

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Abstract Patients with sickle cell disease (SCD) have elevated plasma levels of placenta growth factor (PlGF) which promotes expression of the pulmonary vasoconstrictor endothelin-1 (ET-1) contributing to pulmonary hypertension, an important age-related and life-limiting complication of SCD. In SCD patients, markers of high iron burden are associated with the highest PlGF levels, leading us to hypothesize a mechanistic link between excessive iron and the induction of the PlGF protein. We have published evidence that heme-bound iron stimulates the PlGF promoter up to 400-fold in human K562 cell

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Wang, Xunde, Gregory J. Kato, and Laurel Mendelsohn. "Iron Containing Compound Stimulates Expression of Pulmonary Hypertension Promoting Factor PlGF." Blood 118, no. 21 (November 18, 2011): 900. http://dx.doi.org/10.1182/blood.v118.21.900.900.

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Abstract Abstract 900 We have previously reported elevated plasma levels of placental growth factor (PlGF) and endothelin-1 (ET-1) in patients with sickle cell disease with high estimated pulmonary artery systolic pressure, a marker of pulmonary hypertension, and gene transfer experiments in mice document that PlGF stimulates ET-1 expression and pulmonary hypertension. Among other markers, PlGF in SCD subjects is correlated with markers of excessive iron burden, including serum ferritin and transferrin, markers that have been previously associated with pulmonary hypertension in SCD in many stu

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Pilon, Andre M., Subramanian S. Ajay, Hatice Ozel Abaan, Elliott H. Margulies, Patrick G. Gallagher, and David M. Bodine. "Genome-Wide ChIP-Seq Reveals a Dramatic Shift in the EKLF Binding Profile Between Erythroid Progenitors and Erythroblasts." Blood 114, no. 22 (November 20, 2009): 565. http://dx.doi.org/10.1182/blood.v114.22.565.565.

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Abstract Abstract 565 Erythroid Kruppel-Like Factor (EKLF; KLF1) is the founding member of the Kruppel family of C2H2 zinc finger transcription factors. First identified as an activator of the beta-globin locus, EKLF facilitates chromatin remodeling and transcriptional activation of target genes, at least in part through recognition of a 9-base consensus motif (NCNCNCCCN). By comparing the transcriptional profiles of E13.5 wild type and Eklf-/- mice, we demonstrated that the lethal failure to complete definitive erythropoiesis in the fetal liver (FL) was due in part to dysregulation of an EKLF

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Goodwin, Andrew J., Jane M. McInerney, Michelle A. Glander, Oded Pomerantz та Christopher H. Lowrey. "In VivoFormation of a Human β-Globin Locus Control Region Core Element Requires Binding Sites for Multiple Factors Including GATA-1, NF-E2, Erythroid Kruppel-like Factor, and Sp1". Journal of Biological Chemistry 276, № 29 (13 квітня 2001): 26883–92. http://dx.doi.org/10.1074/jbc.m008410200.

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Gao, Xiang, Shuangpeng Jiang, Zhangzhen Du, Angtin Ke, Qingwei Liang, and Xu Li. "KLF2 Protects against Osteoarthritis by Repressing Oxidative Response through Activation of Nrf2/ARE Signaling In Vitro and In Vivo." Oxidative Medicine and Cellular Longevity 2019 (November 19, 2019): 1–18. http://dx.doi.org/10.1155/2019/8564681.

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Osteoarthritis (OA) is a multifactorial and inflammatory disease characterized by cartilage destruction that can cause disability among aging patients. There is currently no effective treatment that can arrest or reverse OA progression. Kruppel-like factor 2 (KLF2), a member of the zinc finger family, has emerged as a transcription factor involved in a wide variety of inflammatory diseases. Here, we identified that KLF2 expression is downregulated in IL-1β-treated human chondrocytes and OA cartilage. Genetic and pharmacological overexpression of KLF2 suppressed IL-1β-induced apoptosis and matr

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Perrine, Susan P., Rishikesh Mankidy, Michael S. Boosalis, James J. Bieker та Douglas V. Faller. "Erythroid Kruppel-like factor (EKLF) is recruited to theγ-globingene promoter as a co-activator and is required forγ-globingene induction by short-chain fatty acid derivatives". European Journal of Haematology 82, № 6 (червень 2009): 466–76. http://dx.doi.org/10.1111/j.1600-0609.2009.01234.x.

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Pilon, Andre M., Elliott H. Margulies, Hatice Ozel Abaan, Amy Werner Allen, Tim M. Townes, Abbie M. Frederick, Dewang Zhou, Patrick G. Gallagher, and David M. Bodine. "Genome-Wide Analysis of EKLF Occupancy in Erythroid Chromatin Reveals 5′, 3′ and Intragenic Binding Sites in EKLF Target Genes." Blood 112, no. 11 (November 16, 2008): 283. http://dx.doi.org/10.1182/blood.v112.11.283.283.

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Abstract Erythroid Kruppel-Like Factor (EKLF; KLF1) is the founding member of the Kruppel family of transcription factors, with 3 C2H2 zinc-fingers that bind a 9-base consensus sequence (NCNCNCCCN). The functions of EKLF, first identified as an activator of the beta-globin locus, include gene activation and chromatin remodeling. Our knowledge of genes regulated by EKLF is limited, as EKLF-deficient mice die by embryonic day 15 (E15), due to a severe anemia. Analysis of E13.5 wild type and EKLF-deficient fetal liver (FL) erythroid cells revealed that EKLF-deficient cells fail to complete termin

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Bruns, Ingmar, Ulrich Steidl, Guido Kobbe, Roland Fenk, Slawomir Kliszewski, Sabrina Pechtel, Rainer Haas, and Ralf Kronenwett. "Distinct Gene Expression Pattern of CD34+ Stem and Progenitor Cells Mobilized by Pegfilgrastim after Cytotoxic Therapy in Multiple Myeloma in Comparison to G-CSF." Blood 106, no. 11 (November 16, 2005): 5191. http://dx.doi.org/10.1182/blood.v106.11.5191.5191.

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Abstract Background: Current regimens for peripheral blood stem cell (PBSC) mobilization in patients with multiple myeloma are based on daily subcutaneous injections of G-CSF starting shortly after cytotoxic therapy. Recently a polyethylenglycole (PEG)-conjugated G-CSF (pegfilgrastim) has been introduced which has a substantially longer half-life than the original formula. Here, we compared the molecular phenotypes of CD34+ stem and progenitor cells mobilized by G-CSF with those mobilized by pegfilgrastim. Study design and Methods: We examined immunomagnetically enriched CD34+ cells from leuka

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Macari, Elizabeth R., та Christopher H. Lowrey. "Simvastatin and tBHQ Act Synergistically to Increase γ-Globin Gene Expression Through the Transcription Factors KLF2 and NRF2". Blood 118, № 21 (18 листопада 2011): 2149. http://dx.doi.org/10.1182/blood.v118.21.2149.2149.

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Abstract Abstract 2149 While increased fetal hemoglobin (HbF) levels have proven therapeutic benefit for people with sickle cell disease and β-thalassemia, none of the current HbF inducing agents have the optimal combination of safety, efficacy and ease of use that would make them applicable to most hemoglobinopathy patients. In an effort to develop new strategies for HbF induction, we have recently shown that drugs that activate the NF-E2 related factor 2 (NRF2)/antioxidant response signaling pathway stimulate HbF production in primary human erythroid cells. This discovery prompted us to inve

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Peralta, Raechel, Audrey Low, Aneeza Kim, Sue Murray, Shuling Guo, Sue Freier, Tim M. Townes та Gene Hung. "Targeting BCL11A and KLF1 For The Treatment Of Sickle Cell Disease and β-Thalassemia In Vitro using Antisense Oligonucleotides". Blood 122, № 21 (15 листопада 2013): 1022. http://dx.doi.org/10.1182/blood.v122.21.1022.1022.

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Abstract Sickle cell anemia (SCD) is a hereditary blood disorder in which red blood cells (RBC) become sickle-shaped and block blood vessels, leading to painful vaso-occlusive episodes. Sickling occurs because of a point-mutation in the β-globin gene of hemoglobin. Fetal hemoglobin (HbF, α2γ2) is the main oxygen transport protein with greater oxygen binding affinity in the fetus during the last months of embryonic development and the first few months of life after birth. HbF inhibits sickling by interfering with the polymerization of hemoglobin S. Higher HbF levels in SCD correlate with better

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Kalra, Inderdeep S., Md M. Alam та Betty S. Pace. "Transcriptional Regulation of γ-Globin Gene Expression by KLF4". Blood 116, № 21 (19 листопада 2010): 645. http://dx.doi.org/10.1182/blood.v116.21.645.645.

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Abstract Abstract 645 Kruppel-like factors (KLFs) are a family of Cys2His2 zinc-finger DNA binding proteins that regulate gene expression through CACCC/GC/GT box binding in various gene promoters. The CACCC element is also critical for developmental regulation of the human γ-globin and β-globin genes; therefore studies to identify transcription factors that bind the CACCC element to alter gene expression are desirable. By microarray-based gene profiling, we identified two Kruppel-like factors, KLF4 and KLF12 whose expression levels decreased simultaneously with γ-globin silencing during in vit

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Lee, J. S., H. Ngo, D. Kim, and J. H. Chung. "Erythroid Kruppel-like factor is recruited to the CACCC box in the beta -globin promoter but not to the CACCC box in the gamma -globin promoter: The role of the neighboring promoter elements." Proceedings of the National Academy of Sciences 97, no. 6 (March 7, 2000): 2468–73. http://dx.doi.org/10.1073/pnas.040476297.

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Mitchell, W. Beau, Merlin Nithya Gnanapragasam, Julie A. Jaffray, James J. Bieker, and Deepa Manwani. "Case Report of Erythroid Transcription Factor EKLF Mutation Causing a Rare Form of Congenital Dyserythropoetic Anemia in a Patient of Taiwanese Origin." Blood 118, no. 21 (November 18, 2011): 2154. http://dx.doi.org/10.1182/blood.v118.21.2154.2154.

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Abstract Abstract 2154 Congenital dyserythropoietic anemias (CDA) are a rare, inherited form of blood disorders characterized by dyserythropoiesis in the bone marrow, anemia, jaundice and splenomegaly. There are three major types of CDAs, although rarer variants have been identified. We describe a patient with an unusual type of CDA, of which only four other cases have been reported. Our patient had severe hemolytic anemia, increased fetal hemoglobin and abnormal bone marrow pathology inconsistent with previously described forms of CDA. On further study he was also found to have a mutation in

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