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Relevant bibliographies by topics / FOXP4

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Academic literature on the topic 'FOXP4'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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Journal articles on the topic "FOXP4"

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Li, Shanru, Joel Weidenfeld, and Edward E. Morrisey. "Transcriptional and DNA Binding Activity of the Foxp1/2/4 Family Is Modulated by Heterotypic and Homotypic Protein Interactions." Molecular and Cellular Biology 24, no. 2 (January 15, 2004): 809–22. http://dx.doi.org/10.1128/mcb.24.2.809-822.2004.

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ABSTRACT Foxp1, Foxp2, and Foxp4 are large multidomain transcriptional regulators belonging to the family of winged-helix DNA binding proteins known as the Fox family. Foxp1 and Foxp2 have been shown to act as transcriptional repressors, while regulatory activity of the recently identified Foxp4 has not been determined. Given the importance of this Fox gene subfamily in neural and lung development, we sought to elucidate the mechanisms by which Foxp1, Foxp2, and Foxp4 repress gene transcription. We show that like Foxp1 and Foxp2, Foxp4 represses transcription. Analysis of the N-terminal repression domain in Foxp1, Foxp2, and Foxp4 shows that this region contains two separate and distinct repression subdomains that are highly homologous termed subdomain 1 and subdomain 2. However, subdomain 2 is not functional in Foxp4. Screening for proteins that interact with subdomains 1 and 2 of Foxp2 using yeast two-hybrid analysis revealed that subdomain 2 binds to C-terminal binding protein 1, which can synergistically repress transcription with Foxp1 and Foxp2, but not Foxp4. Subdomain 1 contains a highly conserved leucine zipper similar to that found in N-myc and confers homo- and heterodimerization to the Foxp1/2/4 family members. These interactions are dependent on the conserved leucine zipper motif. Finally, we show that the integrity of this subdomain is essential for DNA binding, making Foxp1, Foxp2, and Foxp4 the first Fox proteins that require dimerization for DNA binding. These data reveal a complex regulatory mechanism underlying Foxp1, Foxp2, and Foxp4 activity, demonstrating that Foxp1, Foxp2, and Foxp4 are the first Fox proteins reported whose activity is regulated by homo- and heterodimerization.

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Sin, Cora, Hongyan Li, and Dorota A. Crawford. "Transcriptional Regulation by FOXP1, FOXP2, and FOXP4 Dimerization." Journal of Molecular Neuroscience 55, no. 2 (July 16, 2014): 437–48. http://dx.doi.org/10.1007/s12031-014-0359-7.

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Mendoza, Ezequiel, Kirill Tokarev, Daniel N. Düring, Eva Camarillo Retamosa, Michael Weiss, Nshdejan Arpenik, and Constance Scharff. "Differential coexpression of FoxP1, FoxP2, and FoxP4 in the Zebra Finch (Taeniopygia guttata) song system." Journal of Comparative Neurology 523, no. 9 (April 2, 2015): 1318–40. http://dx.doi.org/10.1002/cne.23731.

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Liang, Jingchen, Duo Wang, Guanhua Qiu, Xiaoqi Zhu, Junjie Liu, Hang Li, and Pingping Guo. "Long Noncoding RNA FOXP4-AS1 Predicts Unfavourable Prognosis and Regulates Proliferation and Invasion in Hepatocellular Carcinoma." BioMed Research International 2021 (February 1, 2021): 1–12. http://dx.doi.org/10.1155/2021/8850656.

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Background. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer that has a high level of morbidity and mortality. Long noncoding RNA (lncRNA) is a novel regulatory factor of tumour proliferation, apoptosis, and metastasis. Our previous studies indicated that lncRNA FOXP4-AS1 is a functional oncogene in HCC; thus, this study is aimed at further evaluating the clinical and biological function of FOXP4-AS1 in HCC. Material and Methods. First, we detected the expression of FOXP4-AS1 in HCC tissues and paracarcinoma normal tissues by qRT-PCR. Second, the prognostic effects of FOXP4-AS1 in patients with HCC were analysed in a training group and a verification group. Subsequently, to investigate the biological effects of FOXP4-AS1 on HCC cells, downexpression tests were further conducted. Results. The expression of FOXP4-AS1 was higher in HCC tissues than adjacent nontumourous tissues, whereas the low expression of FOXP4-AS1 was correlated with optimistic treatment outcomes, which suggested that FOXP4-AS1 may be an independent prognostic biomarker for HCC. Moreover, the downregulation of FOXP4-AS1 significantly reduced the cell proliferation and clonal abilities and inhibited the invasion, migration, and angiogenesis of hepatoma cells ( P < 0.05 ). Conclusion. These results revealed the clinical significance and biological function of FOXP4-AS1 in HCC development, which may provide a new direction for finding therapeutic targets and potential prognostic biomarkers of HCC.

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Bowers, J. Michael, and Genevieve Konopka. "The Role of the FOXP Family of Transcription Factors in ASD." Disease Markers 33, no. 5 (2012): 251–60. http://dx.doi.org/10.1155/2012/456787.

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Autism spectrum disorders (ASD) is a neurodevelopmental disease with complex genetics; however, the genes that are responsible for this disease still remain mostly unknown. Here, we focus on the FOXP family of transcription factors as there is emerging evidence strongly linking these genes to ASD and other genes implicated in ASD. The FOXP family of genes includes three genes expressed in the central nervous system: FOXP1, FOPX2, and FOXP4. This unique group of transcription factors has known functions in brain development as well as the evolution of language. We will also discuss the other genes including transcriptional targets of FOXP genes that have been found to be associated with language and may be important in the pathophysiology of ASD. Finally, we will review the emerging animal models currently being used to study the function of the FOXP genes within the context of ASD symptomology. The combination of gene expression and animal behavior is critical for elucidating how genes such as the FOXP family members are key players within the framework of the developing brain.

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Lu, Min Min, Shanru Li, Honghua Yang, and Edward E. Morrisey. "Foxp4: a novel member of the Foxp subfamily of winged-helix genes co-expressed with Foxp1 and Foxp2 in pulmonary and gut tissues." Mechanisms of Development 119 (December 2002): S197—S202. http://dx.doi.org/10.1016/s0925-4773(03)00116-3.

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Lu, Min Min, Shanru Li, Honghua Yang, and Edward E. Morrisey. "RETRACTED: Foxp4: a novel member of the Foxp subfamily of winged-helix genes co-expressed with Foxp1 and Foxp2 in pulmonary and gut tissues." Gene Expression Patterns 2, no. 3-4 (December 2002): 223–28. http://dx.doi.org/10.1016/s1567-133x(02)00058-3.

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Spaeth, Jason M., Chad S. Hunter, Lauren Bonatakis, Min Guo, Catherine A. French, Ian Slack, Manami Hara, et al. "The FOXP1, FOXP2 and FOXP4 transcription factors are required for islet alpha cell proliferation and function in mice." Diabetologia 58, no. 8 (May 29, 2015): 1836–44. http://dx.doi.org/10.1007/s00125-015-3635-3.

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Norton, Philipp, Peggy Barschke, Constance Scharff, and Ezequiel Mendoza. "Differential Song Deficits after Lentivirus-Mediated Knockdown of FoxP1, FoxP2, or FoxP4 in Area X of Juvenile Zebra Finches." Journal of Neuroscience 39, no. 49 (October 22, 2019): 9782–96. http://dx.doi.org/10.1523/jneurosci.1250-19.2019.

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Teufel, Andreas, Eric A. Wong, Mahua Mukhopadhyay, Nasir Malik, and Heiner Westphal. "FoxP4, a novel forkhead transcription factor." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1627, no. 2-3 (June 2003): 147–52. http://dx.doi.org/10.1016/s0167-4781(03)00074-5.

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Dissertations / Theses on the topic "FOXP4"

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Campbell, Andrew J. "The role of FOXP4 and FOXP2 in haematological malignancy." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510935.

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Mendoza, Ezequiel [Verfasser]. "FoxP1, FoxP2 and FoxP4 in the song control system of zebra finches: molecular interactions and relevance for vocal learning / Ezequiel Mendoza." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1026695775/34.

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Kozma, Radoslav. "Inferring demographic history and speciation of grouse using whole genome sequences." Doctoral thesis, Uppsala universitet, Zooekologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-299926.

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From an ecological perspective, knowledge of demographic history is highly valuable because population size fluctuations can be matched to known climatic events, thereby revealing great insight into a species’ reaction to past climate change. This in turn enables us to predict how they might respond to future climate scenarios. Prominently, with the advent of high-throughput sequencing it is now becoming possible to assemble genomes of non-model organisms thereby providing unprecedented resolution to the study of demographic history and speciation. This thesis utilises four species of grouse (Aves, subfamily Tetraoninae) in order to explore the demographic history and speciation within this lineage; the willow grouse, red grouse, rock ptarmigan and the black grouse. I, and my co-authors, begin by reviewing the plethora of methods used to estimate contemporary effective population size (Ne) and demographic history that are available to animal conservation practitioners. We find that their underlying assumptions and necessary input data can bias in their application, and thus we provide a summary of their applicability. I then use the whole genomes of the black grouse, willow grouse and rock ptarmigan to infer their population dynamics within the last million years. I find three dominant periods that shape their demographic history: early Pleistocene cooling (3-0.9 Mya), the mid-Brunhes event (430 kya) and the last glacial period (110-10 kya). I also find strong signals of local population history – recolonization and subdivision events – affecting their demography. In the subsequent study, I explore the grouse dynamics within the last glacial period in more detail by including more distant samples and using ecological modelling to track habitat distribution changes. I further uncover strong signals of local population history, with multiple fringe populations undergoing severe bottlenecks. I also determine that future climate change is expected to drastically constrict the distribution of the studied grouse. Lastly, I use whole genome sequencing to uncover 6 highly differentiated regions, containing 7 genes, hinting at their role in adaptation and speciation in three grouse taxa. I also locate a region of low differentiation, containing the Agouti pigmentation gene, indicating its role in the grouse plumage coloration.

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Goatly, Alison. "FOXP1 abnormalities in lymphoma." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611626.

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Baumann, Katrin [Verfasser]. "DNA-Methylierungsmuster im foxp3 Gen in humanen CD4+ FOXP3-exprimierenden T-Zellen / Katrin Baumann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023494183/34.

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Nishioka, Tomohisa. "CD4[+]CD25[+]Foxp3[+] T cells and CD4[+]CD25[-]Foxp3[+] T cells in aged mice." Kyoto University, 2007. http://hdl.handle.net/2433/135647.

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Tse, Yuen-yu Belinda, and 謝宛余. "Expression of FOXP1 in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193527.

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Objectives: Forkhead box protein P1 (FOXP1) is a transcription factor, and a member of the P-subfamily of forkhead box transcription factor and regulate transcription of a subset of genes that involved in various cellular events. It plays a critical role in regulating cell growth and proliferation, differentiation, embryogenesis, adult tissue homeostasis, and possibly tumorigenesis. Predominant nuclear localisation of FOXP1 protein is commonly expressed at low level in normal tissues and upregulated in proliferative cells. Studies have demonstrated that the loss of FOXP1 expression and cytoplasmic mis-localisation is significantly associated with various malignant cancers, including breast cancer. FOXP1 can act either as a tumor suppressor or as an oncogenic protein in cell-type specific functions. It has been shown to be a co-regulator of estrogen receptor alpha and can modify a specific subset of forkhead box transcription factor class O (FOXO)-target genes. We hypothesise that there is association between FOXP1 expression and patient survival, and explore the potential role of FOXP1 expression as a prognostic marker in breast cancer. Methods: One hundred and twenty breast cancer samples in tissue microarray blocks were examined for FOXP1 expression by immuno-histochemistry. Nuclear and cytoplasmic FOXP1 expression patterns were analysed with clinico-pathological parameters. Statistical analysis was performed using SPSS software to determine the correlation between FOXP1 expression and clinico-pathological parameters. The correlation between subcellular FOXP1 expression and survival was evaluated by COX regression analysis. Results: Nuclear or cytoplasmic FOXP1 expression showed no association with clinico-pathological parameters. However, our results showed that there was significant association with estrogen receptor and progesterone receptor when nuclear and cytoplasmic scores were combined as total FOXP1 score (p=0.022 and p=0.028 respectively). In univariate analysis, high nuclear and cytoplasmic FOXP1 expression had no significant correlation with poor survival, while high total FOXP1 expression was associated with poor overall and disease-specific survival (p=0.045). Tumor stage and lymph-node involvement were significantly related to poorer overall and disease-specific survival, while other clinico-pathological parameters did not. In breast cancer with advanced tumor grade and lymph-node involvement, overall and disease-specific survival are significantly associated with high FOXP1 expression (p=0.041 and p=0.015 respectively). Conclusion: Unlike previous reports, our findings show that increased nuclear and cytoplasmic FOXP1 expression were both observed and high total FOXP1 expression was associated with poorer survival, particularly in cases of advance tumor grade and with lymph node metastases. These finding are supported by a recent report that showed that FOXP1 can up-regulate its own expression by binding to the promoter of FOXP1 and promote cell survival of breast cancer cells by suppressing FOXO-induced apoptosis. It may be possible that FOXP1 expression is up-regulated in a positive feedback loop in breast cancer cells such that there is both increased nuclear transcriptional activity and cytoplasm localisation of FOXP1. Further investigation is necessary to understand the role of FOXP1 in the progression of breast cancer and determine its potential use as a prognostic marker.
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Tolosa, Montero Mª Amparo. "Gen FOXP2: Esquizofrenia, alucinaciones auditivas y lenguaje." Doctoral thesis, Universitat de València, 2009. http://hdl.handle.net/10803/9945.

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La presente tesis se ha centrado en la evaluación a través de diferentes aproximaciones de la implicación del gen FOXP2, gen sometido a selección positiva en el linaje humano y relacionado directamente con una alteración de uno de los rasgos más característicos de la especie humana, el lenguaje, en la vulnerabilidad a la esquizofrenia. El estudio de asociación caso-control no ha permitido establecer una implicación consistente entre las variantes estructurales analizadas (SNPs y posibles expansiones de trinucleótidos) con las alucinaciones auditivas como fenotipo alternativo a la esquizofrenia. No obstante, la participación del gen FOXP2 en la vulnerabilidad a las alucinaciones auditivas, como componente referido al lenguaje no puede descartarse por completo, ya que el SNP rs2396753 mostró una tendencia hacia la significación y el SNP rs2253478 mostró diferencias significativas para el ítem de Pobreza del Lenguaje de la Escala Manchester.El análisis de la región promotora nos ha permitido valorar que la regulación de la expresión del gen debe ser más compleja de lo que inicialmente se esperaba. El análisis evolutivo muestra que diferentes tramos de la región promotora analizada han evolucionado diferencialmente, encontrándose una región altamente conservada, que curiosamente no parece contener una elevada concentración de sitios de unión a factores de transcripción, como sería lo esperado dada su posible importancia funcional. Esta secuencia se localiza inmediatamente aguas arriba del potencial promotor extraído de las bases de datos mediante herramientas bioinformáticas. Bajo la hipótesis de su pertenencia al núcleo central del promotor, la evaluación funcional de esta región conservada indica que posiblemente contenga elementos represores de la transcripción, al menos en el tipo celular testado, esto es, células procedentes del pulmón, ya que se obtienen mayores niveles de expresión en su ausencia.Dentro de la hipótesis epigenética de la esquizofrenia se llevó a cabo un análisis de los patrones de metilación en dos fragmentos incluidos en una isla CG adyacente al primer exón, no traducido, del gen en tejidos postmorten de pacientes esquizofrénicos y controles. En primer lugar se obtuvo una clara diferencia en el grado de metilación entre el fragmento analizado localizado aguas arriba del primer exón, con ausencia de metilación respecto al localizado aguas abajo, para el que se obtuvieron patrones específicos de metilación. Comparando el grado de metilación en diferentes áreas cerebrales en pacientes con esquizofrenia y controles, se observó que en la circunvolución del parahipocampo el grado de metilación es mayor que en las otras áreas analizadas y además hay indicios de diferencias entre ambos grupos analizados en ambos hemisferios. Los análisis de expresión encaminados a determinar si el grado de de metilación estaba correlacionado con los niveles de expresión no permitieron llegar a resultados concluyentes al respecto.Otro gen de gran interés en la evolución de la especie humana es el gen HAR1A el cual se caracteriza por incluir una región con evolución acelerada en el linaje humano. Se consideró que un gen de las características del gen HAR1A podría constituir también un buen gen candidato para la esquizofrenia, por lo que se llevó un estudio caso control de las mismas características que el realizado con el gen FOXP2. El hecho de no encontrar diferencias significativas en las frecuencias genotípicas, alélicas o haplotípicas en el estudio de asociación caso-control llevado a cabo con el gen HAR1A indica que no parece estar relacionado con la vulnerabilidad a la esquizofrenia, aunque podría estar relacionado con la susceptibilidad a padecer alucinaciones auditivas dentro del contexto psicótico, al obtenerse diferencias globales en la comparación de haplotipos entre pacientes alucinadores y pacientes sin alucinaciones.
This thesis has focused in the study of FOXP2 gene, which is the first gene related to a language disorder and which has been subject to positive selection in human lineage, as candidate gene for schizophrenia through different approaches Case-control study didn't allow establishing a consistent relationship between the analyzed structural variants (SNPs and trinucleotide repetitions) and auditory hallucination as alternative phenotype for schizophrenia. Nevertheless, a role of FOXP2 in vulnerability to schizophrenia through its relationship with language cannot be ruled out since SNP rs2396753 showed a trend to significance and SNP rs2253478 showed significative differences for Poverty of Speech. Analysis of promoter region suggests regulation of the expression of the gene is more complex than it was initially expected.Evolutionary analysis of a 6Kb fragment surrounding first exon of the gene revealed different evolutionary rates in different fragments as well as some potential promoter regions. A highly conserved region was detected upstream of the annotated promoter. In order to determine if this highly conserved region should be included in the promoter core functional analyses were performed. These experiments indicated that this region probably contains repressor elements. Under the epigenetic hypothesis of the origin of schizophrenia an analysis of the methylation patterns of a CpG island adjacent to first untranslated was performed. Differences between upstream and downstream region were detected as well as differences for methylation of parahippocampal gyrus in patients and controls and between hemispheres. Quantification of mRNA levels was conducted in order to correlate methylation and expression levels of the gene, with inconclusive results.As a summary, with our results we cannot rule out a role of FOXP2 in the susceptibility to schizophrenia, although no direct evidence has been obtained.

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Lindmayer, Christian [Verfasser], and Sebastian [Akademischer Betreuer] Grundmann. "Die Rolle des Transkriptionsfaktors FoxP1 beim Blutgefäßwachstum." Freiburg : Universität, 2021. http://d-nb.info/1236846036/34.

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Ramcke, Torben [Verfasser]. "The function of RORγt+Foxp3+ biTregs in glomerulonephritis : Die Rolle von RORγt+Foxp3+ biTregs im Rahmen der Glomerulonephritis / Torben Ramcke." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2019. http://d-nb.info/1221721011/34.

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Books on the topic "FOXP4"

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Kaufman, Wallace, and David Deamer. The Hunt for FOXP5. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28961-8.

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Konopka, Genevieve. FOXP2: Linking Language and Autism. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0019.

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Identifying the genes involved in language not only is important for the understanding of disorders such as ASDs but also provides a window into understanding the evolution of the human brain. Spoken language is only present in humans. For example, while other animals have developed methods of vocal communication, none have the ability to convey recursive ideas (i.e., ideas embedded within other ideas), although the idea of human-specific recursion is still being debated (Hauser, Chomsky, & Fitch, 2002; Penn, Holyoak, & Povinelli, 2008; Pinker & Jackendoff, 2005; Premack, 2007). Other potentially human-specific features of language include teaching language, the use of language to teach an extrinsic skill, and the use of language to develop the theory of mind (Penn et al., 2008; Premack, 2007). It is therefore not surprising that inherently human-specific diseases such as ASDs are defined by disruption of spoken language (Abrahams & Geschwind, 2008).

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The Hunt for FOXP5: A Genomic Mystery Novel. Springer, 2016.

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Book chapters on the topic "FOXP4"

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Peng, Stanford. "Foxp3." In Encyclopedia of Inflammatory Diseases, 1–5. Basel: Springer Basel, 2013. http://dx.doi.org/10.1007/978-3-0348-0620-6_206-1.

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Peng, Stanford. "FOXP3." In Compendium of Inflammatory Diseases, 497–500. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_206.

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Kaufman, Wallace, and David Deamer. "Scientific Appendices." In The Hunt for FOXP5, 239–51. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28961-8_2.

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Kaufman, Wallace, and David Deamer. "The Hunt for FOXP5." In The Hunt for FOXP5, 3–235. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28961-8_1.

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White, Stephanie. "FoxP2 and vocalization." In Studies in Language Companion Series, 211–36. Amsterdam: John Benjamins Publishing Company, 2013. http://dx.doi.org/10.1075/slcs.144.09whi.

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Kretschmer, Karsten, Irina Apostolou, Panos Verginis, and Harald von Boehmer. "FoxP3 and Regulatory T Cells." In Regulatory T Cells and Clinical Application, 17–28. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-77909-6_2.

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Zheng, Ye. "ChIP-on-Chip for FoxP3." In Regulatory T Cells, 71–82. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-979-6_6.

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McMurchy, Alicia N., Sara Di Nunzio, Maria Grazia Roncarolo, Rosa Bacchetta, and Megan K. Levings. "Molecular Regulation ofCellular Immunity by FOXP3." In Advances in Experimental Medicine and Biology, 30–45. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1599-3_3.

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Entin-Meer, Michal, Arnon Afek, and Jacob George. "Regulatory T-Cells, FoxP3 and Atherosclerosis." In Advances in Experimental Medicine and Biology, 106–14. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1599-3_8.

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Larson, Ryan P., Shahin Shafiani, and Kevin B. Urdahl. "Foxp3+ Regulatory T Cells in Tuberculosis." In Advances in Experimental Medicine and Biology, 165–80. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6111-1_9.

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Conference papers on the topic "FOXP4"

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Zheng, Ying, and Wilson S. Meng. "Polycation Coated Polymeric Particles as Vehicles of RNA Delivery Into Immune Cells." In ASME 2010 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2010. http://dx.doi.org/10.1115/smasis2010-3714.

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The purpose of this work is to develop a carrier system for delivering RNA molecules aimed to downregulate specific functions in T cells. In many forms of cancer, T cells that express the protein Forkhead Box P3 (Foxp3) are associated with cancer progression. These cells can be identified by CD4 and CD25, molecules express on the cell surface. Studies have shown that downregulation of Foxp3 can increase the ability of other immune cells to destroy tumors. A class of RNA molecules, commonly referred to as “siRNA”, bind to and degrade specific messenger RNA (mRNA) in a sequence-dependent manner such that expression of the encoded protein is terminated. Because mRNA molecules are located inside cells, a carrier system is required to facilitate the uptake of siRNA, which does not passively diffuse through the plasma membrane. To this end, nanosized polymeric particles coated with the polycation, ornithinex10-histidinex6 (or O10H6) were used to adsorb siRNA that bind to the mRNA encoding Foxp3. The RNA-loaded particles are spherical and uniform in size (normally distributed, polydispersity index = 0.072). Loading of RNA to the particles was confirmed using gel electrophoresis. RNA complexed with the particles are protected from serum destabilization: 83.1% of RNA were recovered compared to 36.1% in RNA that were not associated with the particles. Association with the particles increased the uptake of the RNA in mouse T cells from 3.2±0.2% (free RNA) to 20.1±3.9%. Specifically, uptake of the RNA in T cells that express CD4 increased from 2.7±0.2% to 27.1±1.3% when particles were employed. These differences are statistically significant in three experiments conducted (p < 0.01). Internalization of the RNA into T cells was confirmed using confocal imaging. Flow cytometric analysis showed that the particle-complexed RNA reduced the percentage of T cells that express both CD4 and CD25 in mice carrying tumors from 24.0% when free RNA molecules were used to 13.5%. In these cells, the level of Foxp3 mRNA was reduced by 30%. In conclusion, the particles facilitate the uptake of siRNA molecules into a population of T cells that is known to promote cancer growth.

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Zhang, Chong, Zhiyi Qu, and Zhendong Yu. "Improbable Differential Attacks on Reduced FOX64." In 2015 4th International Conference on Mechatronics, Materials, Chemistry and Computer Engineering. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/icmmcce-15.2015.471.

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Yang, Wei-Hsiung, Chiung-Min Wang, and William H. Yang. "Abstract 181A: PIN1 and FOXP3 regulate SKP2 expression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-181a.

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4

Yang, Wei-Hsiung, Chiung-Min Wang, and William H. Yang. "Abstract 181A: PIN1 and FOXP3 regulate SKP2 expression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-181a.

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Yang, Wei-Hsiung, Chiung-Min Wang, and William Yang. "Abstract 310A: Transcription factors FOXP3 regulate ATF3 expression." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-310a.

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6

Deshane, Jessy, Tong H. Jin, Zhihuan Sun, Marion Spell, Kim Estell, Casey T. Weaver, Victor J. Thannickal, Lisa M. Schwiebert, and David D. Chaplin. "Immunoregulatory Foxp3+ Myeloid Lineage Cells In Allergic Airway Inflammation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4286.

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Jones, KP, A. Phillips, L. Butcher, K. Morris, and BH Davies. "FOXP3 Gene Expression in Sarcoidosis Is Related to sACE Levels." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3183.

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Silva, Pushpamali De, Soizic Garaud, Roland de Wind, Gert Van den Eynden, Anaïs Boisson, Cinzia Solinas, Edoardo Migliori, et al. "Abstract 3694: FOXP1 suppresses immune cell migration in breast tumors." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3694.

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BENÍTEZ-BURRACO, ANTONIO, and VÍCTOR M. LONGA. "ON THE INFERENCE 'NEANDERTHALS HAD FOXP2 = THEY HAD COMPLEX LANGUAGE'." In Proceedings of the 9th International Conference (EVOLANG9). WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814401500_0007.

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Lo Re, Sandra, Marylène Lecocq, Francine Uwambayinema, Yousof Yakoub, Monique Delos, Jean-Baptiste Demoulin, Sophie Lucas, et al. "PDGF-Producing CD4+ Foxp3+ Regulatory T Lymphocytes Promote Lung Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5552.

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Reports on the topic "FOXP4"

1

Liu, Yang. FoxP3 as a Missing Link between Breast Cancer and Inflammation. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada525911.

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Liu, Yang. FoxP3 as a Missing Link Between Inflammation and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada568162.

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3

Wang, Lizhong. Synergistic Action of FOXP3 and TSC1 Pathways During Tumor Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2015. http://dx.doi.org/10.21236/ada625959.

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4

Brembs, Björn. What is the function of FoxP in operant self-learning? [proposal]. ThinkLab, November 2015. http://dx.doi.org/10.15363/thinklab.a8.

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Brembs, Björn. What is the function of FoxP in operant self-learning? [project]. ThinkLab, November 2015. http://dx.doi.org/10.15363/thinklab.11.

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6

Li, Weiquan. FoxP3 Functions as a Novel Breast Cancer Suppressor Gene Through Cooperation with NFAT. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada524945.

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7

Shen, Li. A Novel Tumor Antigen and Foxp3 Dual-Targeting Tumor Cell Vaccine Enhances the Immunotherapy in a Murine Model of Renal Cell Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada615157.

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