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Summary Expression Phenotypes Gene Literature (8) GO Terms (4) Nucleotides (59) Proteins (29) Interactants (122) Wiki
XB-GENEPAGE-6460075

Papers associated with foxp3



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The Roles of Amphibian (Xenopus laevis) Macrophages during Chronic Frog Virus 3 Infections., Hossainey MRH, Yaparla A, Hauser KA, Moore TE, Grayfer L., Viruses. November 18, 2021; 13 (11):               


Targeting TMEM176B Enhances Antitumor Immunity and Augments the Efficacy of Immune Checkpoint Blockers by Unleashing Inflammasome Activation., Segovia M, Russo S, Jeldres M, Mahmoud YD, Perez V, Duhalde M, Charnet P, Rousset M, Victoria S, Veigas F, Louvet C, Vanhove B, Floto RA, Anegon I, Cuturi MC, Girotti MR, Rabinovich GA, Hill M., Cancer Cell. May 13, 2019; 35 (5): 767-781.e6.                                          


Genesis of the vertebrate FoxP subfamily member genes occurred during two ancestral whole genome duplication events., Song X, Tang Y, Wang Y., Gene. August 22, 2016; 588 (2): 156-62.


Xenopus as a model system for studying pancreatic development and diabetes., Kofent J, Spagnoli FM., Semin Cell Dev Biol. March 1, 2016; 51 106-16.  


Changes in the inflammatory response to injury and its resolution during the loss of regenerative capacity in developing Xenopus limbs., Mescher AL, Neff AW, King MW, King MW., PLoS One. January 1, 2013; 8 (11): e80477.          


The developing Xenopus limb as a model for studies on the balance between inflammation and regeneration., King MW, King MW, Neff AW, Mescher AL., Anat Rec (Hoboken). October 1, 2012; 295 (10): 1552-61.


Suppression of the immune response potentiates tadpole tail regeneration during the refractory period., Fukazawa T, Naora Y, Kunieda T, Kubo T, Kubo T., Development. July 1, 2009; 136 (14): 2323-7.                  


A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes., Proks P, Arnold AL, Bruining J, Girard C, Flanagan SE, Larkin B, Colclough K, Hattersley AT, Ashcroft FM, Ellard S., Hum Mol Genet. June 1, 2006; 15 (11): 1793-800.

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