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Journal articles on the topic 'KLFs factor'

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Published: 1 April 2023

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1

Huang, Zhongting, Haibin He, Feng Qiu, and Hailong Qian. "Expression and Prognosis Value of the KLF Family Members in Colorectal Cancer." Journal of Oncology 2022 (March 19, 2022): 1–13. http://dx.doi.org/10.1155/2022/6571272.

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Krüppel-like factors (KLFs) are some kind of transcriptional regulator that regulates a broad range of cellular functions and has been linked to the development of certain malignancies. KLF expression patterns and prognostic values in colorectal cancer (CRC) have, however, been investigated rarely. To investigate the differential expression, predictive value, and gene mutations of KLFs in CRC patients, we used various online analytic tools, including ONCOMINE, TCGA, cBioPortal, and the TIMER database. KLF2-6, KLF8-10, KLF12-15, and KLF17 mRNA expression levels were dramatically downregulated i
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2

Moi, Paolo, Loredana Porcu, Maria G. Marini та ін. "Differential Modulation of the β-Like Globin Genes by KLFs Isolated with a γ-Globin CACCC Bait." Blood 106, № 11 (2005): 3637. http://dx.doi.org/10.1182/blood.v106.11.3637.3637.

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Abstract The globin CACCC boxes are absolutely required for the appropriate regulation of the β-like globin genes. While the β-globin CACCC box binds EKLF/KLF1, a likely adult switching factor, analogous factors, interacting with the γ-globin gene and predicted to regulate the fetal stage of hemoglobin switching, have so far been elusive. By using yeast one hybrid assay, we have isolated four KLFs, KLF1, 2, 4, and 6, that bound the γ-CACCC bait. To establish their role in globin regulation and in the switching of hemoglobins, these factors were compared to four other KLFs already established o
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3

Sue, Nancy, Briony H. A. Jack, Sally A. Eaton, et al. "Targeted Disruption of the Basic Krüppel-Like Factor Gene (Klf3) Reveals a Role in Adipogenesis." Molecular and Cellular Biology 28, no. 12 (2008): 3967–78. http://dx.doi.org/10.1128/mcb.01942-07.

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ABSTRACT Krüppel-like factors (KLFs) recognize CACCC and GC-rich sequences in gene regulatory elements. Here, we describe the disruption of the murine basic Krüppel-like factor gene (Bklf or Klf3). Klf3 knockout mice have less white adipose tissue, and their fat pads contain smaller and fewer cells. Adipocyte differentiation is altered in murine embryonic fibroblasts from Klf3 knockouts. Klf3 expression was studied in the 3T3-L1 cellular system. Adipocyte differentiation is accompanied by a decline in Klf3 expression, and forced overexpression of Klf3 blocks 3T3-L1 differentiation. Klf3 repr
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4

Allen, Kristi L., Mukesh K. Jain, and Keith R. McCrae. "KLF2 and KLF4 Are Essential Mediators of the Anti-Thrombotic Effects of Statins in the Presence of Antiphospholipid/Anti-ß2GPI Antibodies,." Blood 118, no. 21 (2011): 3272. http://dx.doi.org/10.1182/blood.v118.21.3272.3272.

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Abstract Abstract 3272 Antiphospholipid syndrome (APS) is characterized by thrombosis and/or recurrent pregnancy loss in the presence of antiphospholipid antibodies (APLA). The majority of APLA are directed against phospholipid binding proteins, particularly β2GPI. Anti-ß2GPI antibodies activate endothelial cells and monocytes in a β2GPI-dependent manner through a pathway that involves NF-κB and leads to increased expression of adhesion molecules, tissue factor and proinflammatory cytokines. Krüppel-like factors (KLFs) regulate endothelial cell and monocyte responses to inflammatory stimuli;
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5

Natesampillai, Sekar, Jason Kerkvliet, Peter C. K. Leung, and Johannes D. Veldhuis. "Regulation of Kruppel-like factor 4, 9, and 13 genes and the steroidogenic genes LDLR, StAR, and CYP11A in ovarian granulosa cells." American Journal of Physiology-Endocrinology and Metabolism 294, no. 2 (2008): E385—E391. http://dx.doi.org/10.1152/ajpendo.00480.2007.

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Kruppel-like factors (KLFs) are important Sp1-like eukaryotic transcriptional proteins. The LDLR, StAR, and CYP11A genes exhibit GC-rich Sp1-like sites, which have the potential to bind KLFs in multiprotein complexes. We now report that KLF4, KLF9, and KLF13 transcripts are expressed in and regulate ovarian cells. KLF4 and 13, but not KLF9, mRNA expression was induced and then repressed over time ( P < 0.001). Combined LH and IGF-I stimulation increased KLF4 mRNA at 2 h ( P < 0.01), whereas LH decreased KLF13 mRNA at 6 h ( P < 0.05), and IGF-I reduced KLF13 at 24 h ( P < 0.01) comp
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6

Stratopoulos, Apostolos, Alexandra Kolliopoulou, Kariofyllis Karamperis та ін. "Genomic variants in members of the Krüppel-like factor gene family are associated with disease severity and hydroxyurea treatment efficacy in β-hemoglobinopathies patients". Pharmacogenomics 20, № 11 (2019): 791–801. http://dx.doi.org/10.2217/pgs-2019-0063.

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Aim: β-Type hemoglobinopathies are characterized by vast phenotypic diversity as far as disease severity is concerned, while differences have also been observed in hydroxyurea (HU) treatment efficacy. These differences are partly attributed to the residual expression of fetal hemoglobin (HbF) in adulthood. The Krüppel-like family of transcription factors (KLFs) are a set of zinc finger DNA-binding proteins which play a major role in HbF regulation. Here, we explored the possible association of variants in KLF gene family members with response to HU treatment efficacy and disease severity in β-
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7

Morris, Valerie A., Carrie Cummings, Brendan Korb, Sean M. Boaglio, and Vivian Oehler. "Krüppel-like Factors KLF4 and KLF2 Regulate microRNA-150 Expression in Myeloid Leukemias." Blood 124, no. 21 (2014): 874. http://dx.doi.org/10.1182/blood.v124.21.874.874.

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Abstract Background: Acute myeloid leukemia (AML) is characterized by increased self-renewal of leukemia stem/progenitor cells and failure of differentiation to mature myeloid cells. MicroRNAs (miRNAs) are small single stranded non-coding RNAs 19 to 24 nucleotides in length that regulate expression of tens to hundreds of genes via mRNA degradation or translational repression. MiRNA contributions to normal hematopoiesis have been described and deletion of key miRNA processing enzymes in murine and human cells suggests that miRNA loss contributes to the cancer phenotype and aberrant differentiat
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8

Goswami, Sandeep, Chandrani Sarkar, Wendy L. Frankel, Sujit Basu, and Debanjan Chakroborty. "Abstract 2415: Loss of Krüppel-like factor 4 facilitates disruption of epithelial barrier function in gastric cancer and promotes metastasis." Cancer Research 82, no. 12_Supplement (2022): 2415. http://dx.doi.org/10.1158/1538-7445.am2022-2415.

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Abstract Stomach or gastric cancer (GC) is one of the most common malignancies observed in men and women worldwide. It is also a leading cause of cancer-related deaths. The disease is potentially curable when diagnosed early with survival records of more than 90%. This number, however, sharply declines to less than 20% when diagnosed at advanced stages. Therefore identification of functional molecular markers that can predict the progression of the disease is of utmost importance as early diagnosis enhances the chances of successful therapeutic intervention. Krüppel-like Factors (KLFs) are a f
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9

Alder, Jonathan K., Robert W. Georgantas, Richard L. Hildreth, Xiaobing Yu, and Curt I. Civin. "Kruppel-Like Factor 4 Upregulates p21 and Downregulates Proliferation of Human and Mouse HSPCs, but Is Not Essential for Mouse HSPC Repopulation." Blood 108, no. 11 (2006): 1317. http://dx.doi.org/10.1182/blood.v108.11.1317.1317.

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Abstract Several Kruppel-like factor family members, including KLF1, KLF2, KLF3, and KLF6 have pivotal roles in hematopoiesis. Experiments in zebrafish have suggested that KLF4 may play a similar role. Here we found that enforced expression of KLF4 in hematopoietic cells induced cell cycle arrest without triggering apoptosis. Based on the high levels of expression of KLF4 in mouse and human hematopoietic stem-progenitor cells (HSPCs), we hypothesized and demonstrated that KLF4 regulates proliferation of these cells through regulation of p21cip1/waf1 (p21). Nevertheless, KLF4−/− mouse fetal liv
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10

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 (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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11

McConnell, Beth B., and Vincent W. Yang. "Mammalian Krüppel-Like Factors in Health and Diseases." Physiological Reviews 90, no. 4 (2010): 1337–81. http://dx.doi.org/10.1152/physrev.00058.2009.

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The Krüppel-like factor (KLF) family of transcription factors regulates diverse biological processes that include proliferation, differentiation, growth, development, survival, and responses to external stress. Seventeen mammalian KLFs have been identified, and numerous studies have been published that describe their basic biology and contribution to human diseases. KLF proteins have received much attention because of their involvement in the development and homeostasis of numerous organ systems. KLFs are critical regulators of physiological systems that include the cardiovascular, digestive,
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12

Allen, Kristi L., Mukesh K. Jain, and Keith R. McCrae. "Decreased Expression of KLF2 and KLF4 Induced by Antiphospholipid Antibodies Promotes NF-Kb-Mediated Endothelial Cell Activation and Is Modulated by CBP/p300." Blood 116, no. 21 (2010): 4315. http://dx.doi.org/10.1182/blood.v116.21.4315.4315.

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Abstract Abstract 4315 Antiphospholipid syndrome (APS) is characterized by thrombosis and/or pregnancy loss in the presence of antiphospholipid antibodies (APLA). These antibodies are directed primarily against phospholipid-bound β2-glycoprotein I (β2GPI). Anti-β2GPI antibodies activate endothelial cells, enhancing the expression of adhesion molecules and tissue factor, and the secretion of proinflammatory cytokines. Krüppel-like factors (KLF) regulate endothelial cell inflammatory responses. KLF2 and KLF4 mediate anti-atherosclerotic and anti-inflammatory effects in endothelial cells, and we
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13

Samak, Mostafa, Andreas Kues, Diana Kaltenborn, et al. "Dysregulation of Krüppel-Like Factor 2 and Myocyte Enhancer Factor 2D Drive Cardiac Microvascular Inflammation and Dysfunction in Diabetes." International Journal of Molecular Sciences 24, no. 3 (2023): 2482. http://dx.doi.org/10.3390/ijms24032482.

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Cardiovascular complications are the main cause of morbidity and mortality from diabetes. Herein, vascular inflammation is a major pathological manifestation. We previously characterized the cardiac microvascular inflammatory phenotype in diabetic patients and highlighted micro-RNA 92a (miR-92a) as a driver of endothelial dysfunction. In this article, we further dissect the molecular underlying of these findings by addressing anti-inflammatory Krüppel-like factors 2 and 4 (KLF2 and KLF4). We show that KLF2 dysregulation in diabetes correlates with greater monocyte adhesion as well as migratory
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14

Cao, Zhuoxiao, Xinghui Sun, Basak Icli, Akm Khyrul Wara, and Mark W. Feinberg. "Role of Krüppel-like factors in leukocyte development, function, and disease." Blood 116, no. 22 (2010): 4404–14. http://dx.doi.org/10.1182/blood-2010-05-285353.

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Abstract The Krüppel-like transcription factor (KLF) family participates in diverse aspects of cellular growth, development, differentiation, and activation. Recently, several groups have identified new connections between the function of these factors and leukocyte responses in health and disease. Gene targeting of individual KLFs in mice has uncovered novel and unexpected physiologic roles among myeloid and lymphocyte cell lineage maturation, particularly in the bone marrow niche and blood. In addition, several KLF family members are downstream targets of stimuli and signaling pathways criti
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15

Simmen, R. C. M., J. M. P. Pabona, M. C. Velarde, C. Simmons, O. Rahal, and F. A. Simmen. "The emerging role of Krüppel-like factors in endocrine-responsive cancers of female reproductive tissues." Journal of Endocrinology 204, no. 3 (2009): 223–31. http://dx.doi.org/10.1677/joe-09-0329.

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Krüppel-like factors (KLFs), of which there are currently 17 known protein members, belong to the specificity protein (Sp) family of transcription factors and are characterized by the presence of Cys2/His2 zinc finger motifs in their carboxy-terminal domains that confer preferential binding to GC/GT-rich sequences in gene promoter and enhancer regions. While previously regarded to simply function as silencers of Sp1 transactivity, many KLFs are now shown to be relevant to human cancers by their newly identified abilities to mediate crosstalk with signaling pathways involved in the control of c
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16

Basu, Priyadarshi, Tina K. Lung, Wafaa Lemsaddek та ін. "EKLF and KLF2 have compensatory roles in embryonic β-globin gene expression and primitive erythropoiesis". Blood 110, № 9 (2007): 3417–25. http://dx.doi.org/10.1182/blood-2006-11-057307.

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Abstract The Krüppel-like C2/H2 zinc finger transcription factors (KLFs) control development and differentiation. Erythroid Krüppel-like factor (EKLF or KLF1) regulates adult β-globin gene expression and is necessary for normal definitive erythropoiesis. KLF2 is required for normal embryonic Ey- and βh1-, but not adult βglobin, gene expression in mice. Both EKLF and KLF2 play roles in primitive erythroid cell development. To investigate potential interactions between these genes, EKLF/KLF2 double-mutant embryos were analyzed. EKLF−/−KLF2−/− mice appear anemic at embryonic day 10.5 (E10.5) and
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17

Basu, Priyadarshi, Pamela E. Morris, Jack L. Haar та ін. "KLF2 is essential for primitive erythropoiesis and regulates the human and murine embryonic β-like globin genes in vivo". Blood 106, № 7 (2005): 2566–71. http://dx.doi.org/10.1182/blood-2005-02-0674.

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AbstractThe Krüppel-like factors (KLFs) are a family of C2/H2 zinc finger DNA-binding proteins that are important in controlling developmental programs. Erythroid Krüppel-like factor (EKLF or KLF1) positively regulates the β-globin gene in definitive erythroid cells. KLF2 (LKLF) is closely related to EKLF and is expressed in erythroid cells. KLF2-/- mice die between embryonic day 12.5 (E12.5) and E14.5, because of severe intraembryonic hemorrhaging. They also display growth retardation and anemia. We investigated the expression of the β-like globin genes in KLF2 knockout mice. Our results sh
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18

Salmon, Jessica M., Casie Leigh Reed, Maddyson Bender, et al. "KLF3 Represses the Inflammatory Response in Macrophages." Blood 136, Supplement 1 (2020): 36. http://dx.doi.org/10.1182/blood-2020-142373.

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Krüppel-like factors (KLFs) are a family of transcription factors that play essential roles in the development and differentiation of the hematopoietic system. These transcription factors possess highly conserved C-terminal zinc-finger motifs, which enable their binding to GC-rich, or CACC-box, motifs in promoter and enhancer regions of target genes. The N-terminal domains of these proteins are more varied and mediate the recruitment of various co-factors, which can form a complex with either activator or repressor function. Acting primarily as a gene repressor through its recruitment of CtBPs
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19

Tallack, Michael, Thomas Whitington, Brooke Gardiner, et al. "Klf1 Regulatory Networks in Primary Erythroid Cells." Blood 114, no. 22 (2009): 1462. http://dx.doi.org/10.1182/blood.v114.22.1462.1462.

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Abstract Abstract 1462 Poster Board I-485 Klf1/Eklf regulates a diverse suite of genes to direct erythroid cell differentiation from bi-potent progenitors. To determine the local cis-regulatory contexts and transcription factor networks in which Klf1 works, we performed Klf1 ChIP-seq using the SOLiD deep sequencing platform. We mapped more than 10 million unique 35mer tags and found ∼1500 sites in the genome of primary fetal liver erythroid cells are occupied by endogenous Klf1. Many reside within well characterised erythroid gene promoters (e.g. b-globin) or enhancers (e.g. E2f2 intron 1), bu
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20

Xiong, Qunli, Zhiwei Zhang, Yang Yang, et al. "Krüppel-like Factor 6 Suppresses the Progression of Pancreatic Cancer by Upregulating Activating Transcription Factor 3." Journal of Clinical Medicine 12, no. 1 (2022): 200. http://dx.doi.org/10.3390/jcm12010200.

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Background: As a member of the Krüppel-like factor (KLFs) family, Krüppel-like factor 6 (KLF6) plays a critical role in regulating key cellular functions. Presently, scholars have proved the important role of KLF6 in the tumorigenesis of certain cancers through a large number of experiments. However, gaps still remain in our knowledge of the role of KLF6 in pancreatic cancer (PAAD). Therefore, this paper mainly investigates the role of KLF6 in the progression of pancreatic cancer. Methods: The expression pattern of KLF6 in pancreatic cancer was explored in pancreatic cancer tissues and cell li
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21

Hiroi, Toyoko, Clayton B. Deming, Haige Zhao, et al. "Bortezomib Improves Endothelial Thromboresistance Via Induction of KLF Transcription Factors." Blood 112, no. 11 (2008): 1890. http://dx.doi.org/10.1182/blood.v112.11.1890.1890.

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Abstract Background: Patients with multiple myeloma (MM) are at high risk for venothromboembolic events (VTE). Recent studies, however, suggest that MM patients treated with bortezomib, an approved proteasome inhibitor with potent NF-kB inhibitory effects, appear to have a lower risk of VTE compared to those treated with other therapies. We hypothesize that this could be due to a beneficial effect of bortezomib on endothelial thromboresistance. Methods and Results: Human umbilical vein endothelial cells (HUVECs) were incubated with bortezomib for 20 hours and changes in the expression of a pan
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22

Itakura, Meiji, Masato Shingoji, and Toshihiko Iizasa. "Expressions of KLF2 and chemokine receptor CCR7 in pulmonary adenocarcinoma." Journal of Clinical Oncology 30, no. 15_suppl (2012): e21054-e21054. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e21054.

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e21054 Background: Chemokines and chemokine receptors not only have the powerful ability in cancer metastasis and tumorigenesis, but also act as anti-tumorgenic ability. Lung Krueppel-like factor (LKLF, KLF2) is a member of the family of the Krueppel-like factors (KLFs). KLF2 was initially described as a lung-specific transcription factor. KLF2 is reported to regulate some malignant cells. We examined and evaluated the effect of KLF2 on pulmonary adenocarcinoma and the relationship of their mRNA expression with CCR7, EGFR and p53 genetical mutations in pulmonary adenocarcinoma. Methods: 120 pa
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23

Laub, Friedrich, Lei Lei, Hideaki Sumiyoshi, et al. "Transcription Factor KLF7 Is Important for Neuronal Morphogenesis in Selected Regions of the Nervous System." Molecular and Cellular Biology 25, no. 13 (2005): 5699–711. http://dx.doi.org/10.1128/mcb.25.13.5699-5711.2005.

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ABSTRACT The Krüppel-like transcription factors (KLFs) are important regulators of cell proliferation and differentiation in several different organ systems. The mouse Klf7 gene is strongly active in postmitotic neuroblasts of the developing nervous system, and the corresponding protein stimulates transcription of the cyclin-dependent kinase inhibitor p21 waf/cip gene. Here we report that loss of KLF7 activity in mice leads to neonatal lethality and a complex phenotype which is associated with deficits in neurite outgrowth and axonal misprojection at selected anatomical locations of the nervo
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24

Wu, Kaikai, Zhiying Jia, Qi’ai Wang, Zhenlin Wei, Zunchun Zhou, and Xiaolin Liu. "Identification, expression analysis, and the regulating function on C/EBPs of KLF10 in Dalian purple sea urchin, Strongylocentrotus nudus." Genome 60, no. 10 (2017): 837–49. http://dx.doi.org/10.1139/gen-2017-0033.

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Accumulating evidence indicates that Krüppel-like factors (KLFs) play important roles in fat biology via the regulation of CCAAT/enhancer binding proteins (C/EBPs). However, KLFs and C/EBPs have not been identified from Strongylocentrotus nudus, and their roles in this species are not clear. In this study, the full-length cDNA of S. nudus KLF10 (SnKLF10) and three cDNA fragments of S. nudus C/EBPs (SnC/EBPs) were obtained. Examination of tissue distribution and expression patterns during gonadal development implied that SnKLF10 and SnC/EBPs play important roles in gonadal lipogenesis. The pres
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25

Sangwung, Panjamaporn, Guangjin Zhou, Yuan Lu, et al. "Regulation of endothelial hemoglobin alpha expression by Kruppel-like factors." Vascular Medicine 22, no. 5 (2017): 363–69. http://dx.doi.org/10.1177/1358863x17722211.

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Hemoglobin subunit alpha (HBA) expression in endothelial cells (ECs) has recently been shown to control vascular tone and function. We sought to elucidate the transcriptional regulation of HBA expression in the EC. Gain of KLF2 or KLF4 function studies led to significant induction of HBA in ECs. An opposite effect was observed in ECs isolated from animals with endothelial-specific ablation of Klf2, Klf4 or both. Promoter reporter assays demonstrated that KLF2/KLF4 transactivated the hemoglobin alpha promoter, an effect that was abrogated following mutation of all four putative KLF-binding site
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Allen, Kristi L., Anne Hamik, Mukesh K. Jain, and Keith R. McCrae. "Endothelial cell activation by antiphospholipid antibodies is modulated by Krüppel-like transcription factors." Blood 117, no. 23 (2011): 6383–91. http://dx.doi.org/10.1182/blood-2010-10-313072.

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Abstract Antiphospholipid syndrome is characterized by thrombosis and/or recurrent pregnancy loss in the presence of antiphospholipid antibodies (APLAs). The majority of APLAs are directed against phospholipid-binding proteins, particularly β2-glycoprotein I (β2GPI). Anti-β2GPI antibodies activate endothelial cells in a β2GPI-dependent manner through a pathway that involves NF-κB. Krüppel-like factors (KLFs) play a critical role in regulating the endothelial response to inflammatory stimuli. We hypothesized that activation of endothelial cells by APLA/anti-β2GPI antibodies might be associated
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27

Kuneš, Pavel, Zdeňka Holubcová, and Jan Krejsek. "Occurrence and Significance of the Nuclear Transcription Factor Krüppel-Like Factor 4 (KLF4) in the Vessel Wall." Acta Medica (Hradec Kralove, Czech Republic) 52, no. 4 (2009): 135–39. http://dx.doi.org/10.14712/18059694.2016.119.

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Practically all mammalian cells including human can switch, according to micro- or macroenvironmental conditions, from states of cellular quiescence to inflammatory activation and vice versa. Along with recent knowledge, cellular quiescence is not a passive, but a highly active state with broad engagement of the cell synthetic and secretory machinery. Inflammatory activation is a beneficial process in cases of infection; however, if its control fails, it may degrade into autoimmune diseases or cancer growth. Control over cellular quiescence is exerted predominantly by a set of zincfinger trans
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28

Perkins, Andrew C., and Melissa R. Gardiner. "Zebrafish KLF4 Is Essential for Primitive Haematopoiesis." Blood 106, no. 11 (2005): 1746. http://dx.doi.org/10.1182/blood.v106.11.1746.1746.

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Abstract Gene knockout studies of Krüppel-like factors (KLFs) in mice have demonstrated key roles in organogenesis. EKLF (Klf1) plays an essential role in definitive erythropoiesis and b-globin gene expression, but primitive (yolk sac) erythropoiesis and embryonic globin gene expression are essentially normal. Since expression of embryonic globin genes is dependent upon proximal CACC box elements, additional KLFs must function during the embryonic wave of erythropoiesis. A number of KLFs have been described in zebrafish. One of these, zKLF4, the homologue of neptune, a Xenopus Laevis KLF expr
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29

Sousa, Luis, Ines Pankonien, Luka A. Clarke, Iris Silva, Karl Kunzelmann, and Margarida D. Amaral. "KLF4 Acts as a wt-CFTR Suppressor through an AKT-Mediated Pathway." Cells 9, no. 7 (2020): 1607. http://dx.doi.org/10.3390/cells9071607.

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Cystic Fibrosis (CF) is caused by >2000 mutations in the CF transmembrane conductance regulator (CFTR) gene, but one mutation—F508del—occurs in ~80% of patients worldwide. Besides its main function as an anion channel, the CFTR protein has been implicated in epithelial differentiation, tissue regeneration, and, when dysfunctional, cancer. However, the mechanisms that regulate such relationships are not fully elucidated. Krüppel-like factors (KLFs) are a family of transcription factors (TFs) playing central roles in development, stem cell differentiation, and proliferation. Herein, we hypoth
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30

Fernandez-Zapico, Martin E., Gwen A. Lomberk, Shoichiro Tsuji, et al. "A functional family-wide screening of SP/KLF proteins identifies a subset of suppressors of KRAS-mediated cell growth." Biochemical Journal 435, no. 2 (2011): 529–37. http://dx.doi.org/10.1042/bj20100773.

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SP/KLF (Specificity protein/Krüppel-like factor) transcription factors comprise an emerging group of proteins that may behave as tumour suppressors. Incidentally, many cancers that display alterations in certain KLF proteins are also associated with a high incidence of KRAS (V-Ki-ras2 Kirsten rat sarcoma viral oncogene homologue) mutations. Therefore in the present paper we investigate whether SP/KLF proteins suppress KRAS-mediated cell growth, and more importantly, the potential mechanisms underlying these effects. Using a comprehensive family-wide screening of the 24 SP/KLF members, we disco
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31

Kalra, Inderdeep S., Md M. Alam та Betty S. Pace. "Transcriptional Regulation of γ-Globin Gene Expression by KLF4". Blood 116, № 21 (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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32

Burns, Audrea, Chun-Shik Park, Takeshi Yamada, Monica Puppi, Lei Lei, and Daniel Lacroazza. "The role of KLF7 in hematopoiesis and lymphopoiesis (160.2)." Journal of Immunology 186, no. 1_Supplement (2011): 160.2. http://dx.doi.org/10.4049/jimmunol.186.supp.160.2.

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Abstract Krüppel-like factors (KLFs) are transcription factors that possess important roles in cell development and differentiation through the regulation of proliferation. Similar to KLF4, KLF7 regulates genes that control cell cycle arrest, specifically increasing p21 expression and downregulating cyclin D1. Based on our previous findings that KLF4 is important in hematopoiesis and negatively regulates CD8+ T cell proliferation, we hypothesize that KLF7 may also be important in hematopoiesis and T cell function. To test this hypothesis, qRT-PCR analysis of lineage negative, progenitor, and
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33

Kotlyarov, Stanislav, and Anna Kotlyarova. "Participation of Krüppel-like Factors in Atherogenesis." Metabolites 13, no. 3 (2023): 448. http://dx.doi.org/10.3390/metabo13030448.

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Atherosclerosis is an important problem in modern medicine, the keys to understanding many aspects of which are still not available to clinicians. Atherosclerosis develops as a result of a complex chain of events in which many cells of the vascular wall and peripheral blood flow are involved. Endothelial cells, which line the vascular wall in a monolayer, play an important role in vascular biology. A growing body of evidence strengthens the understanding of the multifaceted functions of endothelial cells, which not only organize the barrier between blood flow and tissues but also act as regula
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34

Moi, Paolo, Giuseppina Maria Marini, Loredana Porcu та ін. "Regulation of the Human α-Globin Genes by GKLF." Blood 112, № 11 (2008): 1867. http://dx.doi.org/10.1182/blood.v112.11.1867.1867.

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Abstract EKLF and related Krueppel-like factors (KLFs) are variably implicated in the regulation of the β- and β-like globin genes. Prompted by the observation that four KLF sites are distributed in the human α-globin promoter, we investigated if any of the β-globin cluster regulating KLFs could also act to modulate the expression of the α-globin genes. We found that, among the globin regulating KLFs (EKLF, LKLF, BKLF, GKLF, KLF6, FKLF and FKLF2), only GKLF and BKLF bound specifically to three out of four KLF sites. In K562 cells, over-expressed GKLF transactivated at high levels a α-globin-lu
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35

Li, Jun-Chen, Qiu-Han Chen, Rui Jian, et al. "The Partial Role of KLF4 and KLF5 in Gastrointestinal Tumors." Gastroenterology Research and Practice 2021 (July 27, 2021): 1–13. http://dx.doi.org/10.1155/2021/2425356.

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Background. KLF4 and KLF5 are members of the KLF transcription factor family, which play an important role in many gastrointestinal tumors. To gain a deeper insight into its function and role, bioinformatics was used to analyze the function and role of KLF4 and KLF5 in gastrointestinal tumors. Methods. Data were collected from several online databases. Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN database analysis, Kaplan-Meier Plotter analysis, LOGpc system, the Pathology Atlas, and the STRING website were used to analyze the data. We download relevant data from TCGA and the
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36

Ulfhammer, Erik, Pia Larsson, Mia Magnusson, Lena Karlsson, Niklas Bergh, and Sverker Jern. "Dependence of Proximal GC Boxes and Binding Transcription Factors in the Regulation of Basal and Valproic Acid-Induced Expression of t-PA." International Journal of Vascular Medicine 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/7928681.

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Objective.Endothelial tissue-type plasminogen activator (t-PA) release is a pivotal response to protect the circulation from occluding thrombosis. We have shown that the t-PA gene is epigenetically regulated and greatly induced by the histone deacetylase (HDAC) inhibitor valproic acid (VPA). We now investigated involvement of known t-PA promoter regulatory elements and evaluated dependence of potential interacting transcription factors/cofactors.Methods.A reporter vector with an insert, separately mutated at either the t-PA promoter CRE or GC box II or GC box III elements, was transfected into
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37

Goldstein, Bree G., Hann-Hsiang Chao, Yizeng Yang, Yuliya A. Yermolina, John W. Tobias, and Jonathan P. Katz. "Overexpression of Krüppel-like factor 5 in esophageal epithelia in vivo leads to increased proliferation in basal but not suprabasal cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 6 (2007): G1784—G1792. http://dx.doi.org/10.1152/ajpgi.00541.2006.

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Krüppel-like factor 5 ( Klf5; also called IKLF or BTEB2), a zinc-finger transcription factor with proproliferative and transforming properties in vitro, is expressed in proliferating cells of gastrointestinal tract epithelia, including in basal cells of the esophagus. Thus, Klf5 is an excellent candidate to regulate esophageal epithelial proliferation in vivo. Nonetheless, the function of Klf5 in esophageal epithelial homeostasis and tumorigenesis in vivo has not previously been determined. Here, we used the ED- L2 promoter of the Epstein-Barr virus to express Klf5 throughout esophageal epithe
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38

Abe, Makoto, Naoya Saeki, Yuki Ikeda, and Shinsuke Ohba. "Kruppel-like Factors in Skeletal Physiology and Pathologies." International Journal of Molecular Sciences 23, no. 23 (2022): 15174. http://dx.doi.org/10.3390/ijms232315174.

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Kruppel-like factors (KLFs) belong to a large group of zinc finger-containing transcription factors with amino acid sequences resembling the Drosophila gap gene Krüppel. Since the first report of molecular cloning of the KLF family gene, the number of KLFs has increased rapidly. Currently, 17 murine and human KLFs are known to play crucial roles in the regulation of transcription, cell proliferation, cellular differentiation, stem cell maintenance, and tissue and organ pathogenesis. Recent evidence has shown that many KLF family molecules affect skeletal cells and regulate their differentiatio
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39

Perkins, Andrew C., Dinushka Gunaratnam, Melissa R. Gardiner, and Kathleen C. Robinson. "Klf12 Is Required for Vessel Organization in Zebrafish Embryos." Blood 106, no. 11 (2005): 3695. http://dx.doi.org/10.1182/blood.v106.11.3695.3695.

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Abstract The process of forming a lumenised vessel from an angioblast cord is a crucial part of both vasculogenesis and angiogenesis. The Krüppel like factors (klfs) are a family of zinc finger transcription factors which play important roles in many aspects of differentiation. Klf2 knockout mice die in utero from haemorrhaging due to arterial wall defects. Due to the similarity of vascular and haematopoietic systems to those of mammals, the zebrafish was chosen as a model in which to study the function of klf12, the only zebrafish representative of the repressor subfamily of mammalian klfs w
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40

Syafruddin, Saiful E., M. Aiman Mohtar, Wan Fahmi Wan Mohamad Nazarie, and Teck Yew Low. "Two Sides of the Same Coin: The Roles of KLF6 in Physiology and Pathophysiology." Biomolecules 10, no. 10 (2020): 1378. http://dx.doi.org/10.3390/biom10101378.

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The Krüppel-like factors (KLFs) family of proteins control several key biological processes that include proliferation, differentiation, metabolism, apoptosis and inflammation. Dysregulation of KLF functions have been shown to disrupt cellular homeostasis and contribute to disease development. KLF6 is a relevant example; a range of functional and expression assays suggested that the dysregulation of KLF6 contributes to the onset of cancer, inflammation-associated diseases as well as cardiovascular diseases. KLF6 expression is either suppressed or elevated depending on the disease, and this is
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41

Morris, Valerie A., Carrie L. Cummings, Brendan Korb, Sean Boaglio, and Vivian G. Oehler. "Deregulated KLF4 Expression in Myeloid Leukemias Alters Cell Proliferation and Differentiation through MicroRNA and Gene Targets." Molecular and Cellular Biology 36, no. 4 (2015): 559–73. http://dx.doi.org/10.1128/mcb.00712-15.

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Acute myeloid leukemia (AML) is characterized by increased proliferation and blocked differentiation of hematopoietic progenitors mediated, in part, by altered myeloid transcription factor expression. Decreased Krüppel-like factor 4 (KLF4) expression has been observed in AML, but how decreased KLF4 contributes to AML pathogenesis is largely unknown. We demonstrate decreased KLF4 expression in AML patient samples with various cytogenetic aberrations, confirm that KLF4 overexpression promotes myeloid differentiation and inhibits cell proliferation in AML cell lines, and identify new targets of K
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42

Yang, Xuexian O., Raymond T. Doty, Justin S. Hicks та Dennis M. Willerford. "Regulation of T-cell receptor Dβ1 promoter by KLF5 through reiterated GC-rich motifs". Blood 101, № 11 (2003): 4492–99. http://dx.doi.org/10.1182/blood-2002-08-2579.

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Abstract Rearrangement of T-cell receptor (TCR) and immunoglobulin genes by a common V(D)J recombination machinery is regulated by developmentally specific chromatin changes at the target locus, a process associated with transcription. At the TCRβ locus, the Eβ enhancer and the Dβ1 promoter regulate germline transcription originating near the TCR Dβ1 gene segment. The Dβ1 promoter contains 3 GC-rich motifs that bind a common set of nuclear proteins from pro–T-cell lines. Mutations that diminish the binding of nuclear proteins also diminish the activity of the Dβ1 promoter in transcriptional re
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43

Kalra, Inderdeep S., Wei Li, Shalini Muralidhar та Betty Pace. "Role of KLF4 and KLF12 in γ-Globin Gene Regulation." Blood 114, № 22 (2009): 4075. http://dx.doi.org/10.1182/blood.v114.22.4075.4075.

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Abstract Abstract 4075 Poster Board III-1010 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 gene promoters. The CACCC element is critical for the developmental regulation of the human γ-globin and β-globin genes and studies are being done to ferret out various factors that bind this region and modulate gene activity. We recently identified two Kruppel-like factors, KLF4 and KLF12 whose expression levels decreased based on microarray-based gene profiling, concomitantly with decreased γ-globin
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44

Xu, Bing, Xiangmeng Wang, Peng Li, et al. "KLF4 induces apoptosis in T-ALL through the BCL2/BCLXL pathway." Blood 122, no. 21 (2013): 4902. http://dx.doi.org/10.1182/blood.v122.21.4902.4902.

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Abstract KLF4, also known as GKLF (gut KLF), is a member of the KLF zinc finger-containing transcription factor family. Klf4 together with Oct4, Sox2, and c-Mycare widely referred to as ‘Yamanaka factors’ because mouse somatic cells can be reprogrammed into pluripotent stem cells following their ectopic expression. The transcription factor Kruppel-like factor 4 (KLF4) may induce tumorigenesis or suppress tumor growth in a tissue-dependent manner. In T cell leukemia and pre-B cell lymphoma cells, KLF4 acts as a tumor suppressor. We found that over expression of KLF4 induced human acute T cell l
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45

Schuettpelz, Laura, Felipe Giuste, Priya Gopalan, and Daniel Link. "Kruppel Like Factor 7 Suppresses Hematopoietic Stem and Progenitor Cell Function." Blood 118, no. 21 (2011): 2356. http://dx.doi.org/10.1182/blood.v118.21.2356.2356.

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Abstract Abstract 2356 Kruppel like factor 7 (KLF7) expression is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia (Flotho, et al; Blood 2007). In addition, KLF7 overexpression is associated with Imatinib-resistant CML (Cammarata, et al; Clinical Leukemia 2007). The kruppel like factor (KLF) family of transcription factors are involved in regulating cellular growth and differentiation in multiple tissue types. KLF7 is important for neurogenesis, and mice lacking KLF7 die perinatally with severe neurologic defects (Laub, et al; Mol Cell Biol 2005). While no spe
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46

Funnell, Alister P. W., Christopher A. Maloney, Lucinda J. Thompson, et al. "Erythroid Krüppel-Like Factor Directly Activates the Basic Krüppel-Like Factor Gene in Erythroid Cells." Molecular and Cellular Biology 27, no. 7 (2007): 2777–90. http://dx.doi.org/10.1128/mcb.01658-06.

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ABSTRACT The Sp/Krüppel-like factor (Sp/Klf) family is comprised of around 25 zinc finger transcription factors that recognize CACCC boxes and GC-rich elements. We have investigated basic Krüppel-like factor (Bklf/Klf3) and show that in erythroid tissues its expression is highly dependent on another family member, erythroid Krüppel-like factor (Eklf/Klf1). We observe that Bklf mRNA is significantly reduced in erythroid tissues from Eklf-null murine embryos. We find that Bklf is driven primarily by two promoters, a ubiquitously active GC-rich upstream promoter, 1a, and an erythroid downstrea
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47

Leisegang, Matthias S., Sofia-Iris Bibli, Stefan Günther, et al. "Pleiotropic effects of laminar flow and statins depend on the Krüppel-like factor-induced lncRNA MANTIS." European Heart Journal 40, no. 30 (2019): 2523–33. http://dx.doi.org/10.1093/eurheartj/ehz393.

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Abstract Aims To assess the functional relevance and therapeutic potential of the pro-angiogenic long non-coding RNA MANTIS in vascular disease development. Methods and results RNA sequencing, CRISPR activation, overexpression, and RNAi demonstrated that MANTIS, especially its Alu-element, limits endothelial ICAM-1 expression in different types of endothelial cells. Loss of MANTIS increased endothelial monocyte adhesion in an ICAM-1-dependent manner. MANTIS reduced the binding of the SWI/SNF chromatin remodelling factor BRG1 at the ICAM-1 promoter. The expression of MANTIS was induced by lamin
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48

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 (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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49

Zinghirino, Federica, Xena Giada Pappalardo, Angela Messina, Francesca Guarino, and Vito De Pinto. "Is the Secret of VDAC Isoforms in Their Gene Regulation? Characterization of Human VDAC Genes Expression Profile, Promoter Activity, and Transcriptional Regulators." International Journal of Molecular Sciences 21, no. 19 (2020): 7388. http://dx.doi.org/10.3390/ijms21197388.

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VDACs (voltage-dependent anion-selective channels) are pore-forming proteins of the outer mitochondrial membrane, whose permeability is primarily due to VDACs’ presence. In higher eukaryotes, three isoforms are raised during the evolution: they have the same exon–intron organization, and the proteins show the same channel-forming activity. We provide a comprehensive analysis of the three human VDAC genes (VDAC1–3), their expression profiles, promoter activity, and potential transcriptional regulators. VDAC isoforms are broadly but also specifically expressed in various human tissues at differe
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50

Mallipattu, Sandeep K., Chelsea C. Estrada, and John C. He. "The critical role of Krüppel-like factors in kidney disease." American Journal of Physiology-Renal Physiology 312, no. 2 (2017): F259—F265. http://dx.doi.org/10.1152/ajprenal.00550.2016.

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Krüppel-like factors (KLFs) are a family of zinc-finger transcription factors critical to mammalian embryonic development, regeneration, and human disease. There is emerging evidence that KLFs play a vital role in key physiological processes in the kidney, ranging from maintenance of glomerular filtration barrier to tubulointerstitial inflammation to progression of kidney fibrosis. Seventeen members of the KLF family have been identified, and several have been well characterized in the kidney. Although they may share some overlap in their downstream targets, their structure and function remain
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