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Relevant bibliographies by topics / KLFs factor

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Journal articles

Academic literature on the topic 'KLFs factor'

Author: Grafiati

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 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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