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Journal articles on the topic 'FOX1'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

Deng, Xiaodong, and Mats Eriksson. "Two Iron-Responsive Promoter Elements Control Expression of FOX1 in Chlamydomonas reinhardtii." Eukaryotic Cell 6, no. 11 (2007): 2163–67. http://dx.doi.org/10.1128/ec.00324-07.

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ABSTRACT FOX1 encodes an iron deficiency-induced ferroxidase involved in a high-affinity iron uptake system. Mutagenesis analysis of the FOX1 promoter identified two separate iron-responsive elements, FeRE1 (CACACG) and FeRE2 (CACGCG), between positions −87 and −82 and between positions −65 and −60, respectively, and both are needed for induced FOX1 expression under conditions of iron deficiency.

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Chen, Jen-Chih, Scott I. Hsieh, Janette Kropat, and Sabeeha S. Merchant. "A Ferroxidase Encoded by FOX1 Contributes to Iron Assimilation under Conditions of Poor Iron Nutrition in Chlamydomonas." Eukaryotic Cell 7, no. 3 (2008): 541–45. http://dx.doi.org/10.1128/ec.00463-07.

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ABSTRACT When the abundance of the FOX1 gene product is reduced, Chlamydomonas cells grow poorly in iron-deficient medium, but not in iron-replete medium, suggesting that FOX1-dependent iron uptake is a high-affinity pathway. Alternative pathways for iron assimilation, such as those involving ZIP family transporters IRT1 and IRT2, may be operational.

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Allen, Michael D., José A. del Campo, Janette Kropat, and Sabeeha S. Merchant. "FEA1, FEA2, and FRE1, Encoding Two Homologous Secreted Proteins and a Candidate Ferrireductase, Are Expressed Coordinately with FOX1 and FTR1 in Iron-Deficient Chlamydomonas reinhardtii." Eukaryotic Cell 6, no. 10 (2007): 1841–52. http://dx.doi.org/10.1128/ec.00205-07.

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ABSTRACT Previously, we had identified FOX1 and FTR1 as iron deficiency-inducible components of a high-affinity copper-dependent iron uptake pathway in Chlamydomonas. In this work, we survey the version 3.0 draft genome to identify a ferrireductase, FRE1, and two ZIP family proteins, IRT1 and IRT2, as candidate ferrous transporters based on their increased expression in iron-deficient versus iron-replete cells. In a parallel proteomic approach, we identified FEA1 and FEA2 as the major proteins secreted by iron-deficient Chlamydomonas reinhardtii. The recovery of FEA1 and FEA2 from the medium o

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Terzulli, Alaina, and Daniel J. Kosman. "Analysis of the High-Affinity Iron Uptake System at the Chlamydomonas reinhardtii Plasma Membrane." Eukaryotic Cell 9, no. 5 (2010): 815–26. http://dx.doi.org/10.1128/ec.00310-09.

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ABSTRACT Multicopper ferroxidases play a vital role in iron metabolism in bacteria, fungi, algae, and mammals. Saccharomyces cerevisiae utilizes a channeling mechanism to couple the ferroxidase activity of Fet3p to Fe3+ transport into the cell by Ftr1p. In contrast, the mechanisms by which mammals couple the ferroxidase reaction to iron trafficking is unclear. The human ferroxidases ceruloplasmin and hephaestin are twice the size of Fet3p and interact with proteins that are not expressed in fungi. Chlamydomonas FOX1 is a homolog of the human ferroxidases but likely supports iron uptake in a ma

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La Fontaine, Sharon, Jeanette M. Quinn, Stacie S. Nakamoto, et al. "Copper-Dependent Iron Assimilation Pathway in the Model Photosynthetic Eukaryote Chlamydomonas reinhardtii." Eukaryotic Cell 1, no. 5 (2002): 736–57. http://dx.doi.org/10.1128/ec.1.5.736-757.2002.

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ABSTRACT The unicellular green alga Chlamydomonas reinhardtii is a valuable model for studying metal metabolism in a photosynthetic background. A search of the Chlamydomonas expressed sequence tag database led to the identification of several components that form a copper-dependent iron assimilation pathway related to the high-affinity iron uptake pathway defined originally for Saccharomyces cerevisiae. They include a multicopper ferroxidase (encoded by Fox1), an iron permease (encoded by Ftr1), a copper chaperone (encoded by Atx1), and a copper-transporting ATPase. A cDNA, Fer1, encoding ferr

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Zahiri, Alexander, Kai Heimel, Ramon Wahl, Magnus Rath, and Jörg Kämper. "The Ustilago maydis Forkhead Transcription Factor Fox1 Is Involved in the Regulation of Genes Required for the Attenuation of Plant Defenses During Pathogenic Development." Molecular Plant-Microbe Interactions® 23, no. 9 (2010): 1118–29. http://dx.doi.org/10.1094/mpmi-23-9-1118.

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Ustilago maydis is a plant-pathogenic fungus that establishes a biotrophic relationship with its host plant, Zea mays. The pathogenic stage of U. maydis is initiated by the fusion of two haploid cells, resulting in the formation of a dikaryotic hypha that invades the plant cell. The switch from saprophytic, yeast-like cells to the biotrophic hyphae requires the complex regulation of a multitude of biological processes to constitute the compatible host–fungus interaction. Transcriptional regulators involved in the establishment of the infectious dikaryon and penetration of the host tissue have

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Gallagher, Thomas L., Joshua Arribere, Shaunak Adkar, et al. "Fox1 and Fox4 regulate muscle-specific splicing in zebrafish and are required for cardiac and skeletal muscle functions." Developmental Biology 344, no. 1 (2010): 491–92. http://dx.doi.org/10.1016/j.ydbio.2010.05.432.

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Terzulli, Alaina J., and Daniel J. Kosman. "The Fox1 ferroxidase of Chlamydomonas reinhardtii: a new multicopper oxidase structural paradigm." JBIC Journal of Biological Inorganic Chemistry 14, no. 2 (2008): 315–25. http://dx.doi.org/10.1007/s00775-008-0450-z.

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9

Rong, Yuping, Jun Ren, Wei Song, et al. "Resveratrol Suppresses Severe Acute Pancreatitis-Induced Microcirculation Disturbance through Targeting SIRT1-FOXO1 Axis." Oxidative Medicine and Cellular Longevity 2021 (February 9, 2021): 1–8. http://dx.doi.org/10.1155/2021/8891544.

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Background. Resveratrol (RSV), one of the SIRT1 agonists, has the ability of alleviating severe acute pancreatitis (SAP); however, the concrete protective mechanism remains unknown. It is noteworthy that microcirculation disturbance plays a vital role in SAP, and the SIRT1/FOX1 axis can regulate microcirculation. Therefore, this study is aimed at ascertaining what is the underlying mechanism of the protective effect of RSV on SAP, and whether it is associated with alleviating microcirculation disturbance by regulating the SIRT1/FOX1 axis. Method. The model of SAP was induced by retrograde inje

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10

Fei, Xiaowen, Mats Eriksson, Yajun Li, and Xiaodong Deng. "A Novel Negative Fe-Deficiency-Responsive Element and a TGGCA-Type-Like FeRE Control the Expression ofFTR1inChlamydomonas reinhardtii." Journal of Biomedicine and Biotechnology 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/790247.

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We have reported three Fe-deficiency-responsive elements (FEREs),FOX1, ATX1,andFEA1, all of which are positive regulatory elements in response to iron deficiency inChlamydomonas reinhardtii. Here we describeFTR1, another iron regulated gene and mutational analysis of its promoter. Our results reveal that the FeREs ofFTR1distinguish itself from other iron response elements by containing bothnegativeandpositiveregulatory regions. InFTR1, the−291/−236 region from the transcriptional start site is necessary and sufficient for Fe-deficiency-inducible expression. This region contains two positive Fe

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11

Martin, Christa Lese, Jacqueline A. Duvall, Yesim Ilkin, et al. "Cytogenetic and molecular characterization of A2BP1 / FOX1 as a candidate gene for autism." American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 144B, no. 7 (2007): 869–76. http://dx.doi.org/10.1002/ajmg.b.30530.

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Deng, Xiaodong, Jinghao Yang, Xiaoxia Wu, YaJun Li, and Xiaowen Fei. "A C2H2 Zinc Finger Protein FEMU2 Is Required for fox1 Expression in Chlamydomonas reinhardtii." PLoS ONE 9, no. 12 (2014): e112977. http://dx.doi.org/10.1371/journal.pone.0112977.

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Hammock, Elizabeth A. D., and Pat Levitt. "Developmental Expression Mapping of a Gene Implicated in Multiple Neurodevelopmental Disorders, A2bp1 (Fox1)." Developmental Neuroscience 33, no. 1 (2011): 64–74. http://dx.doi.org/10.1159/000323732.

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Tang, Zhen Zhi, Sika Zheng, Julia Nikolic, and Douglas L. Black. "Developmental Control of CaV1.2 L-Type Calcium Channel Splicing by Fox Proteins." Molecular and Cellular Biology 29, no. 17 (2009): 4757–65. http://dx.doi.org/10.1128/mcb.00608-09.

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ABSTRACT CaV1.2 voltage-gated calcium channels play critical roles in the control of membrane excitability, gene expression, and muscle contraction. These channels show diverse functional properties generated by alternative splicing at multiple sites within the CaV1.2 pre-mRNA. The molecular mechanisms controlling this splicing are not understood. We find that two exons in the CaV1.2 channel are controlled in part by members of the Fox family of splicing regulators. Exons 9* and 33 confer distinct electrophysiological properties on the channel and show opposite patterns of regulation during co

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Sharma, Sanjeev K., Ulrike Leinemann, Regine Ratke, et al. "Characterization of a novel Foxa (hepatocyte nuclear factor-3) site in the glucagon promoter that is conserved between rodents and humans." Biochemical Journal 389, no. 3 (2005): 831–41. http://dx.doi.org/10.1042/bj20050334.

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The pancreatic islet hormone glucagon stimulates hepatic glucose production and thus maintains blood glucose levels in the fasting state. Transcription factors of the Foxa [Fox (forkhead box) subclass A; also known as HNF-3 (hepatocyte nuclear factor-3)] family are required for cell-specific activation of the glucagon gene in pancreatic islet α-cells. However, their action on the glucagon gene is poorly understood. In the present study, comparative sequence analysis and molecular characterization using protein–DNA binding and transient transfection assays revealed that the well-characterized F

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Chen, Yuping, Jinhuan Wu, Guang Liang, et al. "CHK2-FOXK axis promotes transcriptional control of autophagy programs." Science Advances 6, no. 1 (2020): eaax5819. http://dx.doi.org/10.1126/sciadv.aax5819.

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Autophagy is an evolutionarily conserved catabolic process, which plays a vital role in removing misfolded proteins and clearing damaged organelles to maintain internal environment homeostasis. Here, we uncovered the checkpoint kinase 2 (CHK2)–FOXK (FOXK1 and FOXK2) axis playing an important role in DNA damage–mediated autophagy at the transcriptional regulation layer. Mechanistically, following DNA damage, CHK2 phosphorylates FOXK and creates a 14-3-3γ binding site, which, in turn, traps FOXK proteins in the cytoplasm. Because FOXK functions as the transcription suppressor of ATGs, DNA damage

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Wang, Li-Li, Yin-Ling Xiu, Xi Chen, et al. "The transcription factor FOXA1 induces epithelial ovarian cancer tumorigenesis and progression." Tumor Biology 39, no. 5 (2017): 101042831770621. http://dx.doi.org/10.1177/1010428317706210.

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FOXA1 (forkhead box A1), a member of the FOXA transcription factor superfamily, plays an important role in tumor occurrence and development. However, the relationship between FOXA1 and ovarian cancer has not been reported. We examined normal ovarian tissue and ovarian cancer tissue and found increased FOXA1 expression in the cancer tissue. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry assays demonstrated that transfection with small interfering RNA to silence FOXA1 (si-FOXA1) in ovarian cancer cell lines decreased cell proliferation and induced apoptosis and S

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Nie, Hongyi, Haiyang Geng, Yan Lin, et al. "Genome-Wide Identification and Characterization of Fox Genes in the Honeybee, Apis cerana, and Comparative Analysis with Other Bee Fox Genes." International Journal of Genomics 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/5702061.

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The forkhead box (Fox) gene family, one of the most important families of transcription factors, participates in various biological processes. However, Fox genes in Hymenoptera are still poorly known. In this study, 14 Fox genes were identified in the genome of Apis cerana. In addition, 16 (Apis mellifera), 13 (Apis dorsata), 16 (Apis florea), 17 (Bombus terrestris), 16 (Bombus impatiens), and 18 (Megachile rotundata) Fox genes were identified in their genomes, respectively. Phylogenetic analyses suggest that FoxA is absent in the genome of A. dorsata genome. Similarly, FoxG is missing in the

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Xu, Guangzhong, Kai Li, Nengwei Zhang, Bin Zhu, and Guosheng Feng. "Screening Driving Transcription Factors in the Processing of Gastric Cancer." Gastroenterology Research and Practice 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/8431480.

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Background. Construction of the transcriptional regulatory network can provide additional clues on the regulatory mechanisms and therapeutic applications in gastric cancer.Methods. Gene expression profiles of gastric cancer were downloaded from GEO database for integrated analysis. All of DEGs were analyzed by GO enrichment and KEGG pathway enrichment. Transcription factors were further identified and then a global transcriptional regulatory network was constructed.Results. By integrated analysis of the six eligible datasets (340 cases and 43 controls), a bunch of 2327 DEGs were identified, in

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Lin, Jiefu, Tingting Wang, Yalan Li, et al. "N-Acetylcysteine Restores Sevoflurane Postconditioning Cardioprotection against Myocardial Ischemia-Reperfusion Injury in Diabetic Rats." Journal of Diabetes Research 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/9213034.

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The effect of sevoflurane postconditioning (sevo-postC) cardioprotection is compromised in diabetes which is associated with increased oxidative stress. We hypothesized that antioxidant N-Acetylcysteine may enhance or restore sevo-postC cardioprotection in diabetes. Control or streptozotocin-induced Type 1 diabetic rats were either untreated or treated with N-Acetylcysteine for four weeks starting at five weeks after streptozotocin injection and were subjected to myocardial ischemia-reperfusion injury (IRI), in the absence or presence of sevo-postC. Diabetes showed reduction of cardiac STAT3 a

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Besnard, V., S. E. Wert, K. H. Kaestner, and J. A. Whitsett. "Stage-specific regulation of respiratory epithelial cell differentiation by Foxa1." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 5 (2005): L750—L759. http://dx.doi.org/10.1152/ajplung.00151.2005.

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Foxa1 is a member of the winged helix family of transcription factors that is expressed in epithelial cells of the conducting airways and in alveolar type II cells of the lung. To determine the role of Foxa1 during lung morphogenesis, histology and gene expression were assessed in lungs from Foxa1−/− gene-targeted mice from embryonic day (E) 16.5 to postnatal day (PN) 13. Deletion of Foxa1 perturbed maturation of the respiratory epithelium at precise times during lung morphogenesis. While dilatation of peripheral lung saccules was delayed in Foxa1−/− mice at E16.5, sacculation was unperturbed

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Minoo, Parviz, Lingyan Hu, Yiming Xing, et al. "Physical and Functional Interactions between Homeodomain NKX2.1 and Winged Helix/Forkhead FOXA1 in Lung Epithelial Cells." Molecular and Cellular Biology 27, no. 6 (2007): 2155–65. http://dx.doi.org/10.1128/mcb.01133-06.

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ABSTRACT NKX2.1 is a homeodomain transcription factor that controls development of the brain, lung, and thyroid. In the lung, Nkx2.1 is expressed in a proximo-distal gradient and activates specific genes in phenotypically distinct epithelial cells located along this axis. The mechanisms by which NKX2.1 controls its target genes may involve interactions with other transcription factors. We examined whether NKX2.1 interacts with members of the winged-helix/forkhead family of FOXA transcription factors to regulate two spatially and cell type-specific genes, SpC and Ccsp. The results show that NKX

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LIU, Yuanfang, Wei SHEN, Patricia L. BRUBAKER, Klaus H. KAESTNER та Daniel J. DRUCKER. "Foxa3 (HNF-3γ) binds to and activates the rat proglucagon gene promoter but is not essential for proglucagon gene expression". Biochemical Journal 366, № 2 (2002): 633–41. http://dx.doi.org/10.1042/bj20020095.

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Members of the Forkhead box a (Foxa) transcription factor family are expressed in the liver, pancreatic islets and intestine and both Foxa1 and Foxa2 regulate proglucagon gene transcription. As Foxa proteins exhibit overlapping DNA-binding specificities, we examined the role of Foxa3 [hepatocyte nuclear factor (HNF)-3γ] in control of proglucagon gene expression. Foxa3 was detected by reverse transcriptase PCR in glucagon-producing cell lines and binds to the rat proglucagon gene G2 promoter element in GLUTag enteroendocrine cells. Although Foxa3 increased rat proglucagon promoter activity in B

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Stanway, Clive A., Jennie M. Gibbs, and Enrico Berardi. "Expression of the FOX1 gene of Saccharomyces cerevisiae is regulated by carbon source, but not by the known glucose repression genes." Current Genetics 27, no. 5 (1995): 404–8. http://dx.doi.org/10.1007/bf00311208.

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Ammous-Boukhris, Nihel, Wajdi Ayadi, Mariem Derbel, et al. "FOXA1 Expression in Nasopharyngeal Carcinoma: Association with Clinicopathological Characteristics and EMT Markers." BioMed Research International 2020 (June 23, 2020): 1–9. http://dx.doi.org/10.1155/2020/4234632.

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The forkhead box (FOXA) family of transcription factors regulates gene expression and chromatin structure during tumorigenesis and embryonic development. Until now, the relationship between FOXA1 and the nasopharyngeal carcinoma (NPC) has not yet been reported. Therefore, our purpose is to analyze the expression of FOXA1 in 56 NPC patients compared to 10 normal nasopharyngeal mucosae and to correlate the expression with the clinicopathological features. Besides, we investigated the association between FOXA1 and LMP1 gene expression, as well as the EMT markers namely the E-cadherin and Twist1.

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Kanamoto, Naotetsu, Tetsuya Tagami, Yoriko Ueda-Sakane, et al. "Forkhead Box A1 (FOXA1) and A2 (FOXA2) Oppositely Regulate Human Type 1 Iodothyronine Deiodinase Gene in Liver." Endocrinology 153, no. 1 (2012): 492–500. http://dx.doi.org/10.1210/en.2011-1310.

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Type 1 iodothyronine deiodinase (D1), a selenoenzyme that catalyzes the bioactivation of thyroid hormone, is expressed mainly in the liver. Its expression and activity are modulated by several factors, but the precise mechanism of its transcriptional regulation remains unclear. In the present study, we have analyzed the promoter of human D1 gene (hDIO1) to identify factors that prevalently increase D1 activity in the human liver. Deletion and mutation analyses demonstrated that a forkhead box (FOX)A binding site and an E-box site within the region between nucleotides −187 and −132 are importan

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Gosalia, Nehal, Rui Yang, Jenny L. Kerschner, and Ann Harris. "FOXA2 regulates a network of genes involved in critical functions of human intestinal epithelial cells." Physiological Genomics 47, no. 7 (2015): 290–97. http://dx.doi.org/10.1152/physiolgenomics.00024.2015.

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The forkhead box A (FOXA) family of pioneer transcription factors is critical for the development of many endoderm-derived tissues. Their importance in regulating biological processes in the lung and liver is extensively characterized, though much less is known about their role in intestine. Here we investigate the contribution of FOXA2 to coordinating intestinal epithelial cell function using postconfluent Caco2 cells, differentiated into an enterocyte-like model. FOXA2 binding sites genome-wide were determined by ChIP-seq and direct targets of the factor were validated by ChIP-qPCR and siRNA

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Pohl, Barbara S., and Walter Kn�chel. "Isolation and developmental expression of Xenopus FoxJ1 and FoxK1." Development Genes and Evolution 214, no. 4 (2004): 200–205. http://dx.doi.org/10.1007/s00427-004-0391-7.

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Katoh, Masaru. "Genomic testing, tumor microenvironment and targeted therapy of Hedgehog-related human cancers." Clinical Science 133, no. 8 (2019): 953–70. http://dx.doi.org/10.1042/cs20180845.

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AbstractHedgehog signals are transduced through Patched receptors to the Smoothened (SMO)-SUFU-GLI and SMO-Gi-RhoA signaling cascades. MTOR-S6K1 and MEK-ERK signals are also transduced to GLI activators through post-translational modifications. The GLI transcription network up-regulates target genes, such as BCL2, FOXA2, FOXE1, FOXF1, FOXL1, FOXM1, GLI1, HHIP, PTCH1 and WNT2B, in a cellular context-dependent manner. Aberrant Hedgehog signaling in tumor cells leads to self-renewal, survival, proliferation and invasion. Paracrine Hedgehog signaling in the tumor microenvironment (TME), which harb

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Wotton, Karl R., Françoise Mazet, and Sebastian M. Shimeld. "Expression of FoxC, FoxF, FoxL1, and FoxQ1 genes in the dogfishScyliorhinus canicula defines ancient and derived roles for fox genes in vertebrate development." Developmental Dynamics 237, no. 6 (2008): 1590–603. http://dx.doi.org/10.1002/dvdy.21553.

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Bach, Duc-Hiep, Nguyen Long, Thi-Thu-Trang Luu, Nguyen Anh, Sung Kwon, and Sang Lee. "The Dominant Role of Forkhead Box Proteins in Cancer." International Journal of Molecular Sciences 19, no. 10 (2018): 3279. http://dx.doi.org/10.3390/ijms19103279.

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Forkhead box (FOX) proteins are multifaceted transcription factors that are significantly implicated in cancer, with various critical roles in biological processes. Herein, we provide an overview of several key members of the FOXA, FOXC, FOXM1, FOXO and FOXP subfamilies. Important pathophysiological processes of FOX transcription factors at multiple levels in a context-dependent manner are discussed. We also specifically summarize some major aspects of FOX transcription factors in association with cancer research such as drug resistance, tumor growth, genomic alterations or drivers of initiati

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Li, Ting, Hanqing Guo, Hong Li, et al. "MicroRNA-92a-1–5p increases CDX2 by targeting FOXD1 in bile acids-induced gastric intestinal metaplasia." Gut 68, no. 10 (2019): 1751–63. http://dx.doi.org/10.1136/gutjnl-2017-315318.

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Background and aimsGastric intestinal metaplasia (IM) is common in the gastric epithelium of patients with chronic atrophic gastritis. CDX2 activation in IM is driven by reflux of bile acids and following chronic inflammation. But the mechanism underlying how bile acids activate CDX2 in gastric epithelium has not been fully explored.MethodsWe performed microRNA (miRNA) and messenger RNA (mRNA) profiling using microarray in cells treated with bile acids. Data integration of the miRNA/mRNA profiles with gene ontology (GO) analysis and bioinformatics was performed to detect potential miRNA-mRNA r

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Le lay, John, and Klaus H. Kaestner. "The Fox Genes in the Liver: From Organogenesis to Functional Integration." Physiological Reviews 90, no. 1 (2010): 1–22. http://dx.doi.org/10.1152/physrev.00018.2009.

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Formation and function of the liver are highly controlled, essential processes. Multiple signaling pathways and transcriptional regulatory networks cooperate in this complex system. The evolutionarily conserved FOX, for Forkhead bOX, class of transcriptional regulators is critical to many aspects of liver development and function. The FOX proteins are small, mostly monomeric DNA binding factors containing the so-called winged helix DNA binding motif that distinguishes them from other classes of transcription factors. We discuss the biochemical and genetic roles of Foxa, Foxl1, Foxm1, and Foxo,

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Pringsheim, Milka, Diana Mitter, Simone Schröder, et al. "Structural brain anomalies in patients with FOXG 1 syndrome and in Foxg1+/− mice." Annals of Clinical and Translational Neurology 6, no. 4 (2019): 655–68. http://dx.doi.org/10.1002/acn3.735.

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Yu, Xiuping, Kichiya Suzuki, Yongqing Wang, et al. "The Role of Forkhead Box A2 to Restrict Androgen-Regulated Gene Expression of Lipocalin 5 in the Mouse Epididymis." Molecular Endocrinology 20, no. 10 (2006): 2418–31. http://dx.doi.org/10.1210/me.2006-0008.

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Abstract Murine epididymal retinoic acid-binding protein [or lipocalin 5 (Lcn5)] is synthesized and secreted by the principal cells of the mouse middle/distal caput epididymidis. A 5-kb promoter fragment of the Lcn5 gene can dictate androgen-dependent and epididymis region-specific gene expression in transgenic mice. Here, we reported that the 1.8-kb Lcn5 promoter confers epididymis region-specific gene expression in transgenic mice. To decipher the mechanism that directs transcription, 14 chimeric constructs that sequentially removed 100 bp of 1.8-kb Lcn5 promoter were generated and transfect

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Picarsic, J., A. Brufsky, A. Onisko, and M. Chivukula. "Predictors of invasive breast cancer or DCIS recurrence in estrogen receptor positive (ER+) and estrogen receptor negative (ER-) ductal carcinoma in situ (DCIS) patients with and without associated invasive carcinoma (IC)." Journal of Clinical Oncology 27, no. 15_suppl (2009): e11523-e11523. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e11523.

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e11523 Background: DCIS is a heterogeneous pre-invasive carcinoma with a spectrum of clinical behavior. Patients with ER+ IC have better outcomes compared to ER- patients. FOXA1 and GATA 3 family of transcription factors have been shown to be associated with hormone receptors (ER and PR) and other variables of good prognosis with better overall and relapse-free survival rate. The specific aim of this study is to analyze the expression of these novel biological markers: FOXA1, GATA-3, with recognized markers: MIB-1(Ki-67) and HER2 /neu in DCIS patients with/without associated IC. Methods: Sixty

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Forma, Ewa, Paweł Jóźwiak, Piotr Ciesielski, et al. "Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells." PLOS ONE 13, no. 6 (2018): e0198351. http://dx.doi.org/10.1371/journal.pone.0198351.

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Malin, Dmitriy, Il-Man Kim, Evan Boetticher, et al. "Forkhead Box F1 Is Essential for Migration of Mesenchymal Cells and Directly Induces Integrin-Beta3 Expression." Molecular and Cellular Biology 27, no. 7 (2007): 2486–98. http://dx.doi.org/10.1128/mcb.01736-06.

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ABSTRACT The Forkhead box f1 (Foxf1) transcription factor is expressed in mesenchymal cells of the lung, liver, and gallbladder. Although Foxf1 deficiency causes severe abnormalities in the development of these organs, the molecular mechanisms underlying Foxf1 function remain uncharacterized. In this study we inactivated Foxf1 function in lung mesenchymal cells and mouse embryonic fibroblasts (MEFs) by use of either short interfering RNA duplexes or a membrane-transducing Foxf1 dominant negative (DN) mutant protein (Foxf1 DN), the latter of which is fused to the human immunodeficiency virus TA

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Kalinichenko, Vladimir V., Galina A. Gusarova, Il-Man Kim, et al. "Foxf1 haploinsufficiency reduces Notch-2 signaling during mouse lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 3 (2004): L521—L530. http://dx.doi.org/10.1152/ajplung.00212.2003.

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The forkhead box (Fox) f1 transcription factor is expressed in the mouse splanchnic (visceral) mesoderm, which contributes to development of the liver, gallbladder, lung, and intestinal tract. Pulmonary hemorrhage and peripheral microvascular defects were found in approximately half of the newborn Foxf1(+/-) mice, which expressed low levels of lung Foxf1 mRNA [low- Foxf1(+/-) mice]. Microvascular development was normal in the surviving newborn high- Foxf1(+/-) mice, which compensated for pulmonary Foxf1 haploinsufficiency and expressed wild-type Foxf1 levels. To identify expression of genes re

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Li, Chien-Hsiu, Yu-Chan Chang, Michael Hsiao, and Shu-Mei Liang. "FOXD1 and Gal-3 Form a Positive Regulatory Loop to Regulate Lung Cancer Aggressiveness." Cancers 11, no. 12 (2019): 1897. http://dx.doi.org/10.3390/cancers11121897.

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Dysregulation of forkhead box D1 (FOXD1) is known to promote tumor progression; however, its molecular mechanism of action is unclear. Based on microarray analysis, we identified galectin-3/LGALS3 (Gal-3) as a potential downstream target of FOXD1, as FOXD1 transactivated Gal-3 by interacting with the Gal-3 promoter to upregulate Gal-3 in FOXD1-overexpressing CL1-0 lung cancer cells. Ectopic expression of FOXD1 increased the expression of Gal-3 and the growth and motility of lung cancer cells, whereas depletion of Gal-3 attenuated FOXD1-mediated tumorigenesis. ERK1/2 interacted with FOXD1 in th

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Credendino, Sara C., Carmen Moccia, Elena Amendola, et al. "FOXE1 Gene Dosage Affects Thyroid Cancer Histology and Differentiation In Vivo." International Journal of Molecular Sciences 22, no. 1 (2020): 25. http://dx.doi.org/10.3390/ijms22010025.

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The transcription factor Forkhead box E1 (FOXE1) is a key player in thyroid development and function and has been identified by genome-wide association studies as a susceptibility gene for papillary thyroid cancer. Several cancer-associated polymorphisms fall into gene regulatory regions and are likely to affect FOXE1 expression levels. However, the possibility that changes in FOXE1 expression modulate thyroid cancer development has not been investigated. Here, we describe the effects of FOXE1 gene dosage reduction on cancer phenotype in vivo. Mice heterozygous for FOXE1 null allele (FOXE1+/−)

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Wang, Ya, and Jiang Zhu. "FOXM1 and UBE2C Are Distinct Biomarkers for Non-Small Cell Lung Cancer Survival Prediction: Data-Mining Based on ONCOMINE." Journal of Advances in Medicine Science 2, no. 2 (2019): 18. http://dx.doi.org/10.30564/jams.v2i2.611.

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Non-small cell lung cancer (NSCLC) remains to be primary reason of tumor deaths in the past few decades. The mortality of this malignancy could be reduced by developing new prognostic biomarkers and discovering novel therapeutic biological target. Here, we studied the mRNA expression of FOX gene family and UBE2C in different types of cancer compared with normal tissue through ONCOMINE differential analysis. CCLE analysis was mined to explore the expression profiles of target genes in different tumor cells. GEPIA was used to discover the expression of target genes in different subtypes and the

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Ray, P. S., J. Wang, Y. Qu, et al. "Role of FOXC1 in regulation of basal-like/triple-negative breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (2009): 11016. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.11016.

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11016 Background: Class identification studies have proposed 3 prognostically relevant molecular subtypes of breast cancer: luminal, HER2 and basal-like. The latter is associated with poor prognosis but its molecular basis is not clear. We hypothesized a direct correlation between FOXC1 expression and basal-like breast cancer. Methods: Expression of FOXC1, CK5, CK14, EGFR, c-Kit, αB-crystallin, ITGB4 and FOXC2 in basal-like breast cancer was examined using publicly available microarray datasets. A molecular signature of 40 genes sharing co-ordinate up or down regulation with FOXC1 was identifi

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Lomenick, Jefferson P., Michael A. Hubert, and Stuart Handwerger. "Transcription factor FOXF1 regulates growth hormone variant gene expression." American Journal of Physiology-Endocrinology and Metabolism 291, no. 5 (2006): E947—E951. http://dx.doi.org/10.1152/ajpendo.00128.2006.

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Deletion analysis of the human growth hormone variant (GHV) promoter in transient transfection studies in BeWo choriocarcinoma and HepG2 cells indicated that the region extending from nt −158/+57 retained full transcriptional activity. DNase I footprint analysis of the fragment revealed a protected region at nt −82/−77, which is in a putative FOXF1/FOXF2 binding site. Supershift assays using an antiserum to human FOXF1 demonstrated that the protected region binds FOXF1. Overexpression of FOXF1 in BeWo and HepG2 cells induced the GHV promoter, whereas overexpression of FOXF2 was without effect.

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Xue, Hongni, Fayang Liu, Zhiying Ai, et al. "FOXC1 Downregulates Nanog Expression by Recruiting HDAC2 to Its Promoter in F9 Cells Treated by Retinoic Acid." International Journal of Molecular Sciences 22, no. 5 (2021): 2255. http://dx.doi.org/10.3390/ijms22052255.

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FOXC1, a transcription factor involved in cell differentiation and embryogenesis, is demonstrated to be a negative regulator of Nanog in this study. FOXC1 is up-regulated in retinoic acid-induced differentiation of F9 Embryonal Carcinoma (EC) cells; furthermore, FOXC1 specifically inhibits the core pluripotency factor Nanog by binding to the proximal promoter. Overexpression of FOXC1 in F9 or knockdown in 3T3 results in the down-regulation or up-regulation of Nanog mRNA and proteins, respectively. In order to explain the mechanism by which FOXC1 inhibits Nanog expression, we identified the co-

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Yang, Zhi, Shuai Jiang, Yicheng Cheng, et al. "FOXC1 in cancer development and therapy: deciphering its emerging and divergent roles." Therapeutic Advances in Medical Oncology 9, no. 12 (2017): 797–816. http://dx.doi.org/10.1177/1758834017742576.

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Forkhead box C1 (FOXC1) is an essential member of the forkhead box transcription factors and has been highlighted as an important transcriptional regulator of crucial proteins associated with a wide variety of carcinomas. FOXC1 regulates tumor-associated genes and is regulated by multiple pathways that control its mRNA expression and protein activity. Aberrant FOXC1 expression is involved in diverse tumorigenic processes, such as abnormal cell proliferation, cancer stem cell maintenance, cancer migration, and angiogenesis. Herein, we review the correlation between the expression of FOXC1 and t

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Credendino, Sara, Marta De Menna, Irene Cantone, et al. "FOXE1-Dependent Regulation of Macrophage Chemotaxis by Thyroid Cells In Vitro and In Vivo." International Journal of Molecular Sciences 22, no. 14 (2021): 7666. http://dx.doi.org/10.3390/ijms22147666.

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Forkhead box E1 (FOXE1) is a lineage-restricted transcription factor involved in thyroid cancer susceptibility. Cancer-associated polymorphisms map in regulatory regions, thus affecting the extent of gene expression. We have recently shown that genetic reduction of FOXE1 dosage modifies multiple thyroid cancer phenotypes. To identify relevant effectors playing roles in thyroid cancer development, here we analyse FOXE1-induced transcriptional alterations in thyroid cells that do not express endogenous FOXE1. Expression of FOXE1 elicits cell migration, while transcriptome analysis reveals that s

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Morillo-Bernal, Jesús, Lara P. Fernández, and Pilar Santisteban. "FOXE1 regulates migration and invasion in thyroid cancer cells and targets ZEB1." Endocrine-Related Cancer 27, no. 3 (2020): 137–51. http://dx.doi.org/10.1530/erc-19-0156.

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FOXE1 is a thyroid-specific transcription factor essential for thyroid gland development and maintenance of the differentiated state. Interestingly, a strong association has been recently described between FOXE1 expression and susceptibility to thyroid cancer, but little is known about the mechanisms underlying FOXE1-induced thyroid tumorigenesis. Here, we used a panel of human thyroid cancer-derived cell lines covering the spectrum of thyroid cancer phenotypes to examine FOXE1 expression and to test for correlations between FOXE1 expression, the allele frequency of two SNPs and a length polym

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Melboucy-Belkhir, Sara, Pauline Pradère, Sara Tadbiri, et al. "Forkhead Box F1 represses cell growth and inhibits COL1 and ARPC2 expression in lung fibroblasts in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 11 (2014): L838—L847. http://dx.doi.org/10.1152/ajplung.00012.2014.

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Aberrant expression of master phenotype regulators or alterations in their downstream pathways in lung fibroblasts may play a central role in idiopathic pulmonary fibrosis (IPF). Interrogating IPF fibroblast transcriptome datasets, we identified Forkhead Box F1 (FOXF1), a DNA-binding protein required for lung development, as a candidate actor in IPF. Thus we determined FOXF1 expression levels in fibroblasts cultured from normal or IPF lungs in vitro, and explored FOXF1 functions in these cells using transient and stable loss-of-function and gain-of-function models. FOXF1 mRNA and protein were

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Li, Dawei, Qingguo Li, Sanjun Cai, and Keping Xie. "The FOXC1/FBP1 signaling axispromotes tumorigenicity by enhancing the Warburg effect in colorectal cancer." Journal of Clinical Oncology 35, no. 15_suppl (2017): e15123-e15123. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e15123.

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e15123 Background: Aberrant expression of Forkhead Box transcription factors plays vital roles in the oncogenesis and metastasis of many types of cancer. The purpose of this study is to elucidate the function of Forkhead Box C1(FOXC1) in colorectal cancer (CRC)malignancy maintenance. Methods: FOXC1 expression in CRC specimens was analyzed in the TCGA database and validated by immunohistochemistry using a tissue microarray (TMA). The effect of FOXC1 expression on cancer proliferation and glycolysis was assessed in cells by altering the expression of FOXC1 in vitro and in vivo. Mechanistic inves

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