Relevant bibliographies by topics / KLFs factor

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Academic literature on the topic 'KLFs factor'

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Published: 1 April 2023

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Journal articles on the topic "KLFs factor"

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 in CRC tissues, but KLF1, KLF7, and KLF16 mRNA expression levels were significantly elevated in CRC tissues. According to the findings of Cox regression analysis, upregulation of KLF3, KLF5, and KLF6 and downregulation of KLF15 were linked with a better prognosis in CRC. For functional enrichment, our findings revealed that KLF members are involved in a variety of cancer-related biological processes. In colon cancer and rectal cancer, KLFs were also shown to be associated with a variety of immune cells. The findings of this research reveal that KLF family members’ mRNA expression levels are possible prognostic indicators for patients with CRC.
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Moi, Paolo, Loredana Porcu, Maria G. Marini, Isadora Asunis, Maria G. Loi, Tohru Ikuta, and Antonio Cao. "Differential Modulation of the β-Like Globin Genes by KLFs Isolated with a γ-Globin CACCC Bait." Blood 106, no. 11 (November 16, 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 or putative globin regulators, KLF3, 11, 13 and 16, mainly evaluating their ability to bind and transactivate the ε-, γ- and β-globin gene. γ-CACCC binding at variable intensities was confirmed in band shift assay for all four isolated KLFs, for KLF3 and, faintly, for KLF13. The ε- and β-CACCC were bound by the same factors with similar affinities with the exception of KLF3 and KLF13 that bound stronger to the β- and ε- than to the γ-CACCC box. On the other hand, KLF11 and 16 did not produce any specific complex in band shift assays with anyone of the globin CACCC boxes. More relevant differences were observed among the factors in the transactivation of single and dual luciferase reporters in both K562 and MEL cells. In these assays, most factors presented peculiar modulatory properties and specific promoter tropism. Several factors presented bidirectional activity displaying in the same time the capacity to stimulate and repress different globin promoters. KLF1 and 4 were the strongest stimulators of the β-globin promoter in both cell lines, whereas KLF2 activated the β-promoter only in K562 cells. KLF1 and especially KLF4 consistently repressed ε-globin expression especially in MEL cells. KLF3 behaved always as a general globin repressor in MEL cells, but acted as a weak stimulator of the γ- and ε-promoter in K562 cells. KLF4 was the strongest inhibitor of the ε-globin gene. KLF13 significantly stimulated the γ-promoter in both cell lines, whereas KLF3, 4 and 6 showed statistically significant stimulation only in MEL cells. By RT-PCR analysis we found that KLFs were highly variable in their tissue expression and that KLF1, 3 and 13 had the highest expression in erythroid tissues. Thus the level of tissue expression should ultimately determine which factors are really active in physiological conditions. Taken together our binding and expression studies suggest that several KLFs have the potential to modulate the activity of the globin genes and that the resulting globin expression will depend on the vectorial sum of the relative activities of the factors expressed at any given time of development. Furthermore, as some KLFs, like KLF1 and 4, exert opposite effects on fetal and adult globin genes, their role in hemoglobin switching may be direct and not only dependent on their ability to mediate promoter competition for the LCR.
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Sue, Nancy, Briony H. A. Jack, Sally A. Eaton, Richard C. M. Pearson, Alister P. W. Funnell, Jeremy Turner, Robert Czolij, et al. "Targeted Disruption of the Basic Krüppel-Like Factor Gene (Klf3) Reveals a Role in Adipogenesis." Molecular and Cellular Biology 28, no. 12 (April 7, 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 represses transcription by recruiting C-terminal binding protein (CtBP) corepressors. CtBPs bind NADH and may function as metabolic sensors. A Klf3 mutant that does not bind CtBP cannot block adipogenesis. Other KLFs, Klf2, Klf5, and Klf15, also regulate adipogenesis, and functional CACCC elements occur in key adipogenic genes, including in the C/ebpα promoter. We find that C/ebpα is derepressed in Klf3 and Ctbp knockout fibroblasts and adipocytes from Klf3 knockout mice. Chromatin immunoprecipitations confirm that Klf3 binds the C/ebpα promoter in vivo. These results implicate Klf3 and CtBP in controlling adipogenesis.
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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 (November 18, 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; increased expression of these transcription factors inhibits proinflammatory and procoagulant gene expression, and maintains vascular homeostasis. We recently reported that anti-ß2GPI antibodies decrease the expression of KLF2 and KLF4 in endothelial cells (Allen et al, Blood 2011), promoting endothelial cell activation. Subsequent studies demonstrate that these antibodies decrease expression of KLF2 in monocytes as well. Statins have been proposed as a potential alternative to anticoagulation for APS patients, and stimulate the expression of KLFs. We hypothesized that the ability of statins to block endothelial cell activation in response to anti-β2GPI antibodies was mediated by KLFs. Treatment of endothelial cells and monocytes with 100 nM fluvastatin, lovastatin, or simvastatin upregulated KLF2 and KLF4 mRNA, even in the presence of anti-ß2GPI antibodies. In parallel, statin treatment inhibited the anti-β2GPI antibody-mediated induction of E-selectin, VCAM-1, and TF mRNA in endothelial cells, and ICAM-1 and TF mRNA in human monocytes. To assess the dependence of these effects on KLF expression, endothelial cells were pretreated with KLF2 or KLF4 siRNA prior to treatment with statins. siRNA-mediated inhibition of KLF expression completely blocked the ability of statins to prevent anti-β2GPI antibody-induced endothelial cell activation, as measured by adhesion molecule and TF mRNA levels and expression of E-selectin on the endothelial cell surface. Taken together, these data demonstrate that KLFs are critical modulators of the effects of statins on endothelial cells, and that increased expression of KLFs may represent a mechanism by which these drugs inhibit the activation of endothelial cells and monocytes by APLA/anti-β2GPI antibodies. Disclosures: No relevant conflicts of interest to declare.
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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 (February 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) compared with untreated control. KLF9 was not regulated by either hormone. Transient transfection of KLF4, KLF9, and KLF13 suppressed LDLR/luc, StAR/luc, and CYP11A/luc by 80–90% ( P < 0.001). Histone-deacetylase (HDAC) inhibitors stimulated LDLR/luc five- to sixfold and StAR/luc and CYP11A/luc activity twofold ( P < 0.001) and partially reversed suppression by all three KLFs ( P < 0.001). Deletion of the zinc finger domain of KLF13 abrogated repression of LDLR/luc. Lentiviral overexpression of the KLF13 gene suppressed LDLR mRNA ( P < 0.001) and CYP11A mRNA ( P = 0.003) but increased StAR mRNA ( P = 0.007). Collectively, these data suggest that KLFs may recruit inhibitory complexes containing HDAC corepressors, thereby repressing LDLR and CYP11A transcription. Conversely, KLF13 may recruit unknown coactivators or stabilize StAR mRNA, thereby explaining enhancement of in situ StAR gene expression. These data introduce new potent gonadal transregulators of genes encoding proteins that mediate sterol uptake and steroid biosynthesis.
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Stratopoulos, Apostolos, Alexandra Kolliopoulou, Kariofyllis Karamperis, Anne John, Kyriaki Kydonopoulou, George Esftathiou, Argyro Sgourou, et al. "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, no. 11 (July 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-hemoglobinopathies patients. Materials & methods: Six tag single nucleotide polymorphisms, located in four KLF genes, namely KLF3, KLF4, KLF9 and KLF10, were analyzed in 110 β-thalassemia major patients (TDT), 18 nontransfusion dependent β-thalassemia patients (NTDT), 82 sickle cell disease/β-thalassemia compound heterozygous patients and 85 healthy individuals as controls. Results: Our findings show that a KLF4 genomic variant (rs2236599) is associated with HU treatment efficacy in sickle cell disease/β-thalassemia compound heterozygous patients and two KLF10 genomic variants (rs980112, rs3191333) are associated with persistent HbF levels in NTDT patients. Conclusion: Our findings provide evidence that genomic variants located in KLF10 gene may be considered as potential prognostic biomarkers of β-thalassemia clinical severity and an additional variant in KLF4 gene as a pharmacogenomic biomarker, predicting response to HU treatment.
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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 (December 6, 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 differentiation in leukemia. By combining observations of miRNA expression in normal hematopoietic progenitor cells and patient AML cells and high-throughput lentiviral expression library screening approaches in AML cell lines we have identified candidate miRNAs that contribute to altered proliferation and differentiation in AML cells. We have previously established 1) that miR-150 expression is decreased in a large subset of primary patient AML samples, in particular poor risk cytogenetic groups, 2) and that miR-150 re-expression induces myeloid differentiation and decreases cell proliferation of normal hematopoietic progenitor cells and AML cell lines and primary patient cells in part through downregulation of MYB expression. MiR-150 loss is relevant in other hematopoietic and solid tumor malignancies where re-expression inhibits cell proliferation, promotes apoptosis and induces reversal of endothelial to mesenchymal transition. Transcription factors are important regulators of myeloid differentiation and cell proliferation. Moreover, as highlighted by recent sequencing of the AML genome, alterations in myeloid transcription factors through mutation, gene rearrangement, and altered expression play a significant role in leukemogenesis. Consequently, we have focused on how myeloid transcription factors regulate miRNA expression, specifically for miR-150. Results: Using 5’RACE from healthy bone marrow RNA, we identified a major transcription start site at 214 basepairs upstream of the pre-miR-150 hairpin. We identified the minimal miR-150 promoter region as -266 to +259 basepairs from the major transcription start site using miR-150 promoter truncation luciferase constructs assayed in myeloid leukemia cell lines (THP-1, K562, and KG1a) and a lymphoid leukemia cell line (Jurkat). We identified DNA binding sites for the Krüppel-like factor (KLF) family of transcription factors that are necessary for miR-150 promoter activity using site-directed DNA mutagenesis of the luciferase reporters. KLFs regulate proliferation, differentiation, pluripotency, migration and inflammation. Depending on cell type and context, KLFs can function as tumor suppressors or oncogenes. To identify which KLF isoforms regulate miR-150 expression, we assayed the ability of KLFs 2, 3, 4, 5, 6, 7, 9, and 10 to induce miR-150 promoter activity using the luciferase reporters and endogenous miR-150 expression by quantitative PCR. KLF2 and KLF4 overexpression increased miR-150 promoter activity in luciferase assays 50-fold and 450-fold respectively in K562 cells. Furthermore, KLF2 and KLF4 induced endogenous miR-150 expression 20-fold and 100-fold respectively as detected by quantitative PCR in both THP-1 and K562 cells. Prior work has established that KLF2 and KLF4 regulate the differentiation of monocytes. We then confirmed that KLF2 and KLF4 overexpression promotes myeloid differentiation of THP-1 cells by flow cytometry and gene expression that was partially reversed by inhibition of miR-150 expression. Conclusions: Previous studies have determined that KLF2 and KLF4 expression are decreased or absent in a significant subset of AML cases. Our observations suggest that loss of KLF2 and KLF4 expression contributes to decreased miR-150 expression which in turn alters cell proliferation and differentiation. Other studies have implicated the cell cycle inhibitor p21WAF1/CIP1 and altered PPAR gamma signaling downstream of KLF4. Nonetheless, our mechanistic understanding is limited. Our work suggests that the loss of miR-150 and other miRNAs downstream of these transcription factors also contributes. Understanding the interactions between KLFs, miR-150 and other miRNAs has broader significance as KLF2 and KLF4 expression is altered in other hematopoietic and solid tumors. Disclosures No relevant conflicts of interest to declare.
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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 (June 15, 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 family of evolutionarily conserved transcriptional regulators with zinc finger DNA binding domains. KLFs have been shown to play important roles both in normal development as well as in disease progression. In cancers, KLFs have been reported to regulate diverse cellular processes like cell growth, proliferation and differentiation. Of the 17 KLFs identified to date, KLF4 and KLF 5 show significantly altered expression in GC tissues compared to normal gastric tissues (TCGA sample analysis of gene expression pattern for KLFs). WhileKLF5 typically pro-proliferative and acts as a tumor promoter, KLF4 has been both oncogenic and tumor-suppressive. KLF4 downregulation is associated with a poor prognosis in GC. However, the specific role of KLF4 in GC progression has not been fully elucidated. Using human GC tissues, orthotropic gastric tumors developed in athymic nude mice, and in vitro functional assays, we hereby report that loss of KLF4 in GC disrupts tight junction stability of epithelial cells. Loss of KLF4 expression correlates with altered expression of tight junction proteins such as claudins and ZO1 in GC. Altered expression of these proteins results in disruption of epithelial barrier integrity leading to cell detachment and metastasis. Therefore, our work indicates that loss of KLF4 observed in GC may promote cell metastasis and can serve as a prognostic marker for GC metastasis. The knowledge generated from this study not only imparts insight into the pathogenesis of GC metastasis but also will be helpful in the development of newer treatment strategies in the future. Citation Format: Sandeep Goswami, Chandrani Sarkar, Wendy L. Frankel, Sujit Basu, Debanjan Chakroborty. Loss of Krüppel-like factor 4 facilitates disruption of epithelial barrier function in gastric cancer and promotes metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2415.
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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 (November 16, 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 liver cells had normal numbers of all mature lineages and provided radioprotection, similar to wild type (wt) controls. Furthermore, in long-term competitive repopulation assays, KLF4−/− mouse HSPCs demonstrated hematopoietic potency equivalent to wt. We found that KLF2 is expressed at higher levels than KLF4 in mouse HSPCs and is a more potent activator of p21, suggesting that KLF2 (and/or other KLF family members) may play a compensatory role in KLF4−/− HSPCs. Thus, although is not essential for their normal development and function, KLF4 expression is sufficient to induce p21-mediated cell cycle arrest in hematopoietic cells.
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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 modifiers such as Brg1 via N-terminal transactivation domains 3. Krüppel-like factor 3 (KLF3) acts as a transcriptional repressor via recruitment of C-terminal binding proteins 4. In erythropoiesis, KLF1 directly activates KLF3 via an erythroid-specific promoter 5. Some KLF1 target genes are upregulated in Klf3-/- fetal liver suggesting possible competition between the two factors for promoter/enhancer occupancy. We generated three independent clones of the erythroid cell line, J2E, by retroviral transduction of a tamoxifen-inducible version of Klf3 (Klf3-ERTM) as previously described 6. Using next-generation sequencing of newly synthesised RNA (4sU-labeling), we show KLF3 induction leads to immediate repression of a set of ~580 genes; a subset of these (54) are also directly induced by KLF1 in K1-ER cells, suggesting antagonistic regulation. Indeed, ChIP-seq revealed KLF1 and KLF3 bind many of the same regulatory sites within the erythroid cell genome. KLF3 also binds an independent set of promoters which are not bound by KLF1, suggesting it also plays a KLF1-independent role in maintenance of gene repression. By de novo motif discovery we confirm KLF3 binds preferably to a extended CACCC motif, R-CCM-CRC-CCN, so the DNA-binding specificity in vivo is indistinguishable from the KLF1 binding specificity 7, and is independent of co-operating DNA-binding proteins or cofactors. Using Q-PCR of KLF1 ChIPed DNA in J2E-Klf3ER cells, we show that overexpression of KLF3 directly displaces KLF1 from many key target sites such as the E2f2 enhancer and this leads to down regulation of gene expression. This is the first proof that KLF1 and KLF3 directly compete for key promoters and enhancers which drive erythroid cell proliferation and differentiation. We propose KLF3 acts to 'fine-tune' transcription in erythropoiesis by repressing genes activated by KLF1 and that this negative feedback system is necessary for precise control over the generation of erythrocytes. It also works independently of KLF1 perhaps via competition for binding with other KLF/SP factors. References: 1. van Vliet J, Crofts LA, Quinlan KG, Czolij R, Perkins AC, Crossley M. Human KLF17 is a new member of the Sp/KLF family of transcription factors. Genomics. 2006;87(4):474-482. 2. Tallack MR, Magor GW, Dartigues B, et al. Novel roles for KLF1 in erythropoiesis revealed by mRNA-seq. Genome Res. 2012. 3. Perkins A, Xu X, Higgs DR, et al. "Kruppeling" erythropoiesis: an unexpected broad spectrum of human red blood cell disorders due to KLF1 variants unveiled by genomic sequencing. Blood. 2016. 4. Dewi V, Kwok A, Lee S, et al. Phosphorylation of Kruppel-like factor 3 (KLF3/BKLF) and C-terminal binding protein 2 (CtBP2) by homeodomain-interacting protein kinase 2 (HIPK2) modulates KLF3 DNA binding and activity. J Biol Chem. 2015;290(13):8591-8605. 5. Funnell AP, Maloney CA, Thompson LJ, et al. Erythroid Kruppel-like factor directly activates the basic Kruppel-like factor gene in erythroid cells. Mol Cell Biol. 2007;27(7):2777-2790. 6. Coghill E, Eccleston S, Fox V, et al. Erythroid Kruppel-like factor (EKLF) coordinates erythroid cell proliferation and hemoglobinization in cell lines derived from EKLF null mice. Blood. 2001;97(6):1861-1868. 7. Tallack MR, Whitington T, Yuen WS, et al. A global role for KLF1 in erythropoiesis revealed by ChIP-seq in primary erythroid cells. Genome Res. 2010;20(8):1052-1063. Disclosures Perkins: Novartis Oncology: Honoraria, Membership on an entity's Board of Directors or advisory committees; Bristol-Myers Squibb: Honoraria.
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Dissertations / Theses on the topic "KLFs factor"

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Alhashem, Yousef. "ROLES OF KRÜPPEL LIKE FACTORS KLF1, KLF2, AND KLF4 IN EMBRYONIC BETA-GLOBIN GENE EXPRESSION." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1880.

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Krüppel like factors (KLFs) are a family of 17 proteins whose main function is gene regulation by binding to DNA elements in the promoters of various genes. KLF transcription factors recognize CACCC-elements and act as activators or repressors of the gene expression. Among the 17 family members, KLF1, KLF2, and KLF4 share high homology to each other. KLF1 is the founding member of the family and is an erythroid-specific protein. KLF2 is expressed in erythroid, endothelial, and other cells. KLF4 is expressed in endothelial, smooth muscle, and other cells. In this thesis, the functions of these KLFs were reviewed in the context of subjects related to erythropoiesis and cardiovascular development. A mouse model lacking KLF1, KLF2, and KLF4 was used to investigate whether these genes have overlapping functions in regulating the embryonic β-globin genes during early embryogenesis. Quantitative RT-PCR assays were used to measure the expression level of Ey- and βh1- globin mRNA at embryonic day 9.5 (E9.5). It was found that KLF1-/-KLF2-/- and KLF1-/-KLF2-/-KLF4-/- embryos express significantly decreased amounts of Ey- and βh1-globin genes when compared to WT and KLF4-/- embryos. There were no significant changes in the levels of Ey- and βh1-globin mRNA between KLF1-/-KLF2-/- and KLF1-/-KLF2-/-KLF4-/- embryos. It was demonstrated here that KLF1 does not regulate KLF2 in mouse erythroid cells at E10.5.
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Williams, Helen. "Investigation of the metabolic functions of Klf3 and Klf8 using mouse models." Thesis, The University of Sydney, 2011. https://hdl.handle.net/2123/28935.

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Obesity is a disease characterised by an excess of white adipose tissue. It leads to increased risk of several associated disorders including cardiovascular disease and type 2 diabetes mellitus. The number of people who are obese is increasing worldwide and as such much research is conducted on obesity and associated disorders. The use of animal models in the study of obesity allows understanding of involvement of specific genes in fat formation and related processes. This can be used to identify targets for prevention or treatment of obesity. Kriippel—like factors are a family of transcription factors that have been implicated in a number of roles, one of which is metabolism. The Klf3'/' mouse has decreased adipose tissue but the metabolic implications of this had not been determined. Klf8 has high homology to Klf3 in the zinc finger region and was suspected to have a role in metabolism and fat formation. A metabolic role for Klf8 had not been investigated. In this thesis, the metabolic profiles of Klf3— and Klf8—deficient mice were examined. Klf3'/' male mice were found to be resistant to diet-induced weight gain. They maintained lower WAT mass and smaller adipocytes. In addition, these mice had reduced hepatic steatosis and improved glucose tolerance and circulating hormone levels. Klf88W male and Klf8+/g’ female mice had no clear phenotype suggesting Klf8 either has roles in areas other than metabolism, or that functional redundancy occurs, thus compensating for the decreased Klf8. These studies show that Klf3 could potentially be targeted for treatments of obesity as mice lacking this protein are lean, resistant to diet-induced obesity and appear metabolically healthy.
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Crutchfield, Gerald L. "Kruppel-Like Transcription Factor 6 & 7 mRNAs (KLF6 & KLF7) Expression in the Developing Zebrafish." University of Akron / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=akron1572200378181869.

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Curtis, Benjamin. "KLF2/KLF4 Double Knock-out Mouse Embryos Show Cranial Bleeding with Endothelial Disruption of the Primary Head Vein." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2216.

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Krüppel-like factors (KLFs) are a family of 3 Cys2/His2 zinc finger transcription factors with a diverse set of roles in cellular differentiation, cell cycle regulation, tumor suppression, erythropoiesis, angiogenesis, and other processes. During embryonic development, KLF2 has a role in vessel maturation. Adult conditional KLF4 knockout mouse embryos have thickened arterial intima follow vascular injury. Breeding KLF2+/- and KLF4+/- mice resulted in the generation of KLF2/KLF4 double knockout (DKO) embryos. KLF2/KLF4 DKO embryos died by E10.5 with cranial bleeding. Using immunohistochemistry, embryo whole-mounts were examined for differences in gross vascularization between wild-type (WT), KLF2-/- and KLF2/KLF4 (DKO embryonic day 9.5 (E9.5) embryos. No obvious gross capillary abnormalities were noted in E9.5 KLF2/KLF4 DKOs, although the posterior cardinal vein appeared to narrow rostral to caudal in KLF2-/- and KLF2/KLF4 DKO embryos. Light and electronic microscopy were employed to investigate potential structural and ultrastructural phenotypes in KLF2/KLF4 DKO embryos. Microscopy confirmed hemorrhaging near and endothelial breaks in the primary head vein (PHV) in E9.5 KLF2/KLF4 DKOs (n=8) and E10.5 KLF2-/-KLF4+/- embryos (n=1). Electron micrographs illustrated a disrupted endothelium in KLF2/KLF4 DKOs with endothelial cells having filopodia-like projections. Surprisingly, KLF2-/- embryos had the presence of wider medial PHV endothelial gaps compared to WT at the electron micrograph level. Density counts revealed a 15% reduction in midline cranial mesenchyme at the level of hemorrhaging in KLF2/KLF4 DKOs compared to KLF2-/- (n=3). An in-situ hybridization localized KLF2 RNA expression to the endothelium of the PHV. A quantitative reverse transcriptase polymerase chain reaction assay revealed that the eNOS expression is synergistically regulated by KLF2 and KLF4, as a shared downstream target. It is proposed that KLF2 and KLF4 share in the regulation of multiple gene targets, leading to early death by E10.5.
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Alhashem, Yousef N. "REGULATION OF THE MOUSE AND HUMAN β-GLOBIN GENES BY KRÜPPEL LIKE TRANSCRIPTION FACTORS KLF1 AND KLF2." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2927.

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Krüppel-like factors KLF1 and KLF2 are closely related transcription factors with three zinc finger domains in their carboxy-termini. KLF1 (erythroid Krüppel-like factor, or EKLF) plays essential roles in embryonic and adult erythropoiesis. KLF2 is a positive regulator of the mouse and human embryonic β- globin genes. KLF1 and KLF2 have overlapping roles in embryonic erythropoiesis, as demonstrated using single and double knockout (KO) mouse models. Ablation of the KLF1 or KLF2 gene causes embryonic lethality, and double KO embryos are more anemic and die sooner than either single KO. We have shown that KLF1 and KLF2 positively regulate the human ϵ- (embryonic) and γ-globin (fetal) genes during embryonic erythropoiesis. Chromatin immunoprecipitation assays (ChIP) show that KLF1 and KLF2 bind to the promoters of the human ϵ- and γ-globin genes, the mouse embryonic Ey- and βh1-globin genes, and also to the β-globin locus control region (LCR) in mouse embryonic erythroid cells. ChIP assays show that KLF1 but not KLF2 ablation results in abnormal histone modifications in the β-globin locus in mouse embryonic erythroid cells. H3K9Ac and H3K4me3, which correlate with open chromatin and active transcription, are both reduced in KLF1-/- primitive erythroid cells. Human CD34+ hematopoietic stem cells obtained from umbilical cord blood were in vitro differentiated along the erythroid lineage. ChIP assays indicate that both KLF1 and KLF2 bind to the promoter of γ-globin gene in this fetal erythroid model. KLF1 knockdown in these cells affects mainly adult β- globin gene expression. However, the decrease in β- globin gene expression in KLF1 knockdown also affects the ratio of γ- to β- globin in these cells. H3K9Ac and H3K4me3 were decreased only at the β- globin gene which coincides with lower recruitment of RNA polymerase II and its active form, RNA polymerase II phospho-serine 2. In conclusion, we showed using mouse primitive erythroid cells and cord blood definitive cells that KLF1 and KLF2 coordinate the regulation of the mouse and human β- globin genes by direct binding to the promoters and LCR in the β- globin locus. In conclusion, cord blood hematopoietic cells could serve as a complimentary system in addition to the transgenic mouse models to study the regulation of γ- globin gene expression.
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Vinjamur, Divya. "The Roles of Krüppel-like Transcription Factors KLF1 and KLF2 in Mouse Embryonic and Human Fetal Erythropoiesis." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/630.

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Hemoglobinopathies are some of the most common monogenic disorders in the world, affecting millions of people and representing a growing burden on health systems worldwide. Although the pathophysiology of sickle cell anemia and beta-thalassemia, two of the most common hemoglobinopathies, have been the focus of much research over the last century, patients affected by these diseases still lack a widely applicable and easily available cure. Sickle cell anemia and beta-thalassemia are caused by defects in the structure and production of the beta-globin chains that, along with the alpha-globin chains make up the heterotetrameric hemoglobin molecule. Studies geared towards re-expression of the silenced fetal gamma-globin gene in adult erythroid cells as a therapeutic strategy to alleviate the symptoms of beta-globin deficiencies have met with some success for the treatment of sickle cell anemia but not for beta-thalassemia. A better understanding of normal gamma-globin gene regulation will undoubtedly advance the development of more effective therapeutic strategies. Because many of the potential targets that may be modulated to achieve gamma-globin re-expression also have functions in erythroid cells other than regulating the gamma-globin gene, it is imperative to understand their role in all aspects of erythropoiesis before they are used for therapy. The current study focuses on the role of two Krüppel-like transcription factors, KLF1 and KLF2, which have known roles in the processes of primitive and definitive erythropoiesis as well as globin gene regulation. The regulation of primitive erythropoiesis by KLF1 and KLF2 is studied using the mouse as a model system because it is not possible to study primitive erythropoiesis in humans. Previous studies have shown that KLF1 and KLF2 are essential for and have overlapping roles in primitive erythropoiesis. Simultaneous ablation of KLF1 and KLF2 results in a severely anemic embryonic phenotype that is not evident in KLF1 or KLF2 single knockout embryos. In this study, we show that this anemia is caused by a paucity of blood cells, and exacerbated by diminished beta-like globin gene expression. The anemia phenotype is dose-dependent, and interestingly, can be ameliorated by a single copy of the KLF2, but not the KLF1 gene. The roles of KLF1 and KLF2 in maintaining both normal peripheral blood cell numbers and globin mRNA amounts are erythroid cell-specific. It was discovered that KLF2 has an essential function in erythroid precursor maintenance. KLF1 can partially compensate for KLF2 in this role, but is uniquely crucial for erythroid precursor proliferation, through its regulation of G1- to S-phase cell cycle transition. A more drastic impairment of primitive erythroid colony formation from embryonic progenitor cells occurs with simultaneous deficiency of KLF1 and KLF2, than with loss of a single factor. The regulation of human beta-like globin gene expression is studied using a recently developed in vitro system for the production of erythroid cells from umbilical cord blood hematopoietic precursor cells, representing a more “fetal” model of globin gene expression. Previous studies have shown that KLF1 binds to the promoters of the gamma- and beta-globin genes, while KLF2 binds to the promoter of the gamma-globin gene in cord blood-derived erythroid cells. Studies using transgenic mice carrying the entire human beta-globin locus had indicated that KLF1 and KLF2 positively regulate gamma-globin expression in mouse embryonic erythroid cells. We demonstrate in this study that KLF1 appears to have dual roles in the regulation of gamma-globin expression in human cord blood-derived definitive erythroid cells. Partial depletion of KLF1 causes elevated gamma-globin expression, while nearly complete depletion of KLF1 results in a down-regulation of gamma-globin expression. Of particular interest was the observation that KLF2 positively regulates gamma-globin expression in cord blood-derived erythroid cells. Surprisingly, KLF2 also positively regulates beta-globin expression in these cells. If regulation of gamma-globin by KLF2 proves to be a direct effect, KLF2 will join a very small group of factors known to directly activate gamma-globin expression.
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Pandya, Ashka Y. "Structural and functional analysis of KLF4." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/pandya.pdf.

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Jiang, Wen. "KLF4 and retinoid receptor signaling in cancer." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009r/jiang.pdf.

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Liu, Zhaoli. "KLF4 regulates notch1 expression and signaling during epithelial transformation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2006. https://www.mhsl.uab.edu/dt/2008r/liu.pdf.

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Saum, Keith L. "Targeting Endothelial Kruppel-like Factor 2 (KLF2) in Arteriovenous Fistula Maturation Failure." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1530269382206163.

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Book chapters on the topic "KLFs factor"

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Moehle, Christopher W., and Gary K. Owens. "Krüppel-like Factors KLF2, KLF4, and KLF5: Central Regulators of Smooth Muscle Function." In The Biology of Krüppel-like Factors, 185–204. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-87775-2_15.

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Yoshida, Tadashi. "Krüppel-Like Factor 4 (KLF4)." In Encyclopedia of Signaling Molecules, 2777–81. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101673.

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Yoshida, Tadashi. "Krüppel-Like Factor 4 (KLF4)." In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101673-1.

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DiFeo, Analisa, Goutham Narla, and John A. Martignetti. "Krüppel-like Factors KLF6 and KLF6-SV1 in the Diagnosis and Treatment of Cancer." In The Biology of Krüppel-like Factors, 223–44. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-87775-2_17.

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Tillu, Himanshu, and Ganji Purnachandra Nagaraju. "YY1 and KLF4: Their Role in Gastrointestinal Malignancies." In Role of Transcription Factors in Gastrointestinal Malignancies, 5–17. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6728-0_2.

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Bieker, James J. "Expanded Role for EKLF/KLF1 Within the Hematopoietic Lineage." In The Biology of Krüppel-like Factors, 83–93. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-87775-2_6.

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Nagai, Ryozo, Takayuki Shindo, Ichiro Manabe, Toru Suzuki, Kennichi Aizawa, Saku Miyamoto, Shinsuke Muto, Keiko Kawai-Kowase, and Masahiko Kurabayashi. "KLF5/BTEB2, a Krüppel-like Transcription Factor, Regulates Smooth Muscle Phenotypic Modulation." In Signal Transduction and Cardiac Hypertrophy, 417–23. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7_30.

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Moser, C., A. Mori, S. A. Lang, C. Hackl, H. J. Schlitt, E. K. Geissler, and O. Stöltzing. "Expression and regulation of Krüppel-like factor 5 (KLF5) in human pancreatic cancer cells: a new molecular target?" In Deutsche Gesellschaft für Chirurgie, 21–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_9.

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Nagai, Ryozo, Takayuki Shindo, Ichiro Manabe, Toru Suzuki, and Masahiko Kurabayashi. "KLF5/BTEB2, A Krüppel-like Zinc-finger Type Transcription Factor, Mediates Both Smooth Muscle Cell Activation And Cardiac Hypertrophy." In Advances in Experimental Medicine and Biology, 57–66. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9029-7_5.

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Erpenbeck, John, Lutz Rosenstiel, Sven Grote, and Werner Sauter. "Key Leadership Factors KLF." In Handbuch Kompetenzmessung, 478–99. Schäffer-Poeschel, 2017. http://dx.doi.org/10.34156/9783791035123-478.

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Conference papers on the topic "KLFs factor"

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Fritz, Jason S., Anne Hamik, and Mukesh Jain. "The Transcription Factor Krüppel-like Factor 4 (KLF4) Modulates Endothelial Permeability." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1038.

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Pitch, Michelle A., Beth A. Russell, and Geoffrey L. Greene. "Abstract 67: Characterization of the role of KLF9 transcription factor in breast cancer estrogen response." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-67.

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Tilman, Jessica, Peter Barnes, and Louise Donnelly. "Reduced expression of the transcription factor KLF4 in COPD macrophages is associated with dysfunctional differentiation." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3905.

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Schreck, Johannes, Carolin Ploeger, Thorben Huth, RaisatunNisa Sugiyanto, Stefan Pusch, KaiBreuhahnPeter Schirmacher, Benjamin Goeppert, and Stephanie Rössler. "Analysis of SH2D4A promoter activity reveals positive regulation by inflammatory cytokines via transcription factor KLF4." In 39. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0042-1760031.

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Zhao, Dong, Han-Qiu Zheng, Zhongmei Zhou, and Ceshi Chen. "Abstract 3155: The SCFFBW7E3 ubiquitin ligase targets Krüppel-like factor 5 (KLF5) for proteolysis in breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3155.

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Chen, Ceshi, Junying Qin, and Zhongmei Zhou. "Abstract 4967: The BAP1 deubiquitinase promotes triple-negative breast cancer partially by stabilizing the KLF5 transcription factor." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4967.

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Ying, Mingyao, Yingying Sang, Yunqing Li, Hugo Guerrero-Cazares, Alfredo Quinones-Hinojosa, Angelo L. Vescovi, Charles G. Eberhart, Shuli Xia, and John Laterra. "Abstract 3296: KLF9, a differentiation-associated transcription factor, suppresses Notch1 signaling and inhibits glioblastoma-initiating stem cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3296.

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Zhi, Xu, Dong Zhao, Zhongmei Zhou, Rong Liu, and Ceshi Chen. "Abstract LB-137: YAP promotes breast cell proliferation and survival partially through stabilizing the KLF5 transcription factor." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-137.

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Singh, Ankur, Shalu Suri, Ted T. Lee, Jamie M. Chilton, Steve L. Stice, Hang Lu, Todd C. McDevitt, and Andrés J. Garcia. "Adhesive Signature-Based, Label-Free Isolation of Human Pluripotent Stem Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80044.

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Generation of human induced pluripotent stem cells (hiPSCs) from fibroblasts and other somatic cells represents a highly promising strategy to produce auto- and allo-genic cell sources for therapeutic approaches as well as novel models of human development and disease1. Reprogramming protocols involve transduction of the Yamanaka factors Oct3/4, Sox2, Klf4, and c-Myc into the parental somatic cells, followed by culturing the transduced cells on mouse embryonic fibroblast (MEF) or human fibroblast feeder layers, and subsequent mechanical dissociation of pluripotent cell-like colonies for propagation on feeder layers1, 2. The presence of residual parental and feeder-layer cells introduces experimental variability, pathogenic contamination, and promotes immunogenicity3. Similar to human embryonic stem cells (hESCs), reprogrammed hiPSCs suffer from the unavoidable problem of spontaneous differentiation due to sub-optimal feeder cultures4, growth factors5, and the feeder-free substrate6. Spontaneously differentiated (SD)-hiPSCs display reduced pluripotency and often contaminate hiPSC cultures, resulting in overgrowth of cultures and compromising the quality of residual pluripotent stem cells5. Therefore, the ability to rapidly and efficiently isolate undifferentiated hiPSCs from the parental somatic cells, feeder-layer cells, and spontaneously differentiated cells is a crucial step that remains a bottleneck in all human pluripotent stem cell research.
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Penke, L. R. K., H. Ouchi, C. Draijer, B. Hu, J. Speth, S. H. Phan, and M. Peters-Golden. "Kruppel-Like Factor 4 (KLF4): A Brake on Fibroblast Activation and A Target for Pharmacologic Induction in Pulmonary Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5881.

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