Warning: The NCBI web site requires JavaScript to function. more...
An official website of the United States government
The .gov means it's official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you're on a federal government site.
The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.
Opposing regulation of the Il17 locus through direct, reciprocal actions of STAT3 and STAT5
PubMed Full text in PMC Similar studies Analyze with GEO2R
Genome-wide binding of STAT3 and STAT5 under Th17 conditions (ChIP-Seq)
PubMed Full text in PMC Similar studies SRA Run Selector
Roles of STAT3 and STAT5 in regulation of gene expression under Th17 differentiation
Cytokine receptor modulation by interleukin-2 broadly regulates T helper cell lineage differentiation
STAT5-mediated chromatin interactions in superenhancers activate IL-2 highly inducible genes: Functional dissection of the Il2ra gene locus
Opposing actions of IL-2 and IL-21 on Th9 differentiation correlate with their differential regulation of BCL6 expression
The Cytokines IL-21 and GM-CSF have Opposing Regulatory Roles in the Apoptosis of Conventional Dendritic Cells
Mouse gene expression in wild-type Th17 cells and Pten deficient Th17 cells
Epigenetic activation during Th17 cell differentiation is impaired after TRIM28 deletion
IGH analysis in pro-B cells with H3K4me3, H3K4me2 and H3K9ac
Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis
Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis [Affymetrix Expression]
Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis [ChIP-seq]
Progesterone-regulated genes in immune cells: Regulation of T cell genes by progesterone
Cell type-specific induction of mRNA in human B cells and monocytes by IFN-beta
Loss-of-function of PTPN2 promotes pathogenic loss of FoxP3+ in RORgt+ Tregs
PubMed Full text in PMC Similar studies
Loss-of-function of PTPN2 promotes pathogenic loss of FoxP3+ in RORgt+ Tregs [ATAC-seq]
Loss-of-function of PTPN2 promotes pathogenic loss of FoxP3+ in RORgt+ Tregs [RNA-seq]
Priming for Th2 differentiation requires IL-2-mediated induction of IL-4 receptor alpha chain expression
Filters: Manage Filters
Your browsing activity is empty.
Activity recording is turned off.
Turn recording back on