Harmonizome 3.0

signal transducer and activator of transcription 5A

The protein encoded by this gene is a member of the STAT family of transcription factors. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. This protein is activated by, and mediates the responses of many cell ligands, such as IL2, IL3, IL7 GM-CSF, erythropoietin, thrombopoietin, and different growth hormones. Activation of this protein in myeloma and lymphoma associated with a TEL/JAK2 gene fusion is independent of cell stimulus and has been shown to be essential for tumorigenesis. The mouse counterpart of this gene is found to induce the expression of BCL2L1/BCL-X(L), which suggests the antiapoptotic function of this gene in cells. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Dec 2013]

From ChEA Transcription Factor Targets

target genes of the STAT5A transcription factor in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets dataset.

From ENCODE Transcription Factor Targets

target genes of the STAT5A transcription factor in ChIP-seq datasets from the ENCODE Transcription Factor Targets dataset.

From GeneRIF Biological Term Annotations

genes co-occuring with the biological term stat5a in literature-supported statements describing functions of genes from the GeneRIF Biological Term Annotations dataset.

From MotifMap Predicted Transcription Factor Targets

target genes of the STAT5A transcription factor predicted using known transcription factor binding site motifs from the MotifMap Predicted Transcription Factor Targets dataset.

From Pathway Commons Protein-Protein Interactions

interacting proteins for STAT5A from the Pathway Commons Protein-Protein Interactions dataset.

From LINCS L1000 CMAP CRISPR Knockout Consensus Signatures

genes differentially expressed following the STAT5A gene perturbation from the LINCS L1000 CMAP CRISPR Knockout Consensus Signatures dataset.

From JASPAR Predicted Mouse Transcription Factor Targets 2025

target genes of the Stat5a transcription factor predicted using known transcription factor binding site motifs from the JASPAR Predicted Mouse Transcription Factor Targets 2925 dataset.

From CM4AI KOLF21J CRISPRi Gene Perturbation Atlas

genes differentially expressed following the STAT5A gene perturbation from the CM4AI KOLF21J CRISPRi Gene Perturbation Atlas.

From CORUM Protein Complexes

proteins in the Stat5a-Jak2 complex protein complex from the CORUM Protein Complexes dataset.

From CORUM Protein Complexes

proteins in the STAT5A homodimer complex protein complex from the CORUM Protein Complexes dataset.

From MotifMap Predicted Transcription Factor Targets

target genes of the STAT5A (homodimer) transcription factor predicted using known transcription factor binding site motifs from the MotifMap Predicted Transcription Factor Targets dataset.

From MotifMap Predicted Transcription Factor Targets

target genes of the STAT5A (homotetramer) transcription factor predicted using known transcription factor binding site motifs from the MotifMap Predicted Transcription Factor Targets dataset.

From ChEA Transcription Factor Targets 2022

target genes of the STAT5A-28732065-J2E-MOUSE-BLOOD transcription factor in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets 2022 dataset.

From ChEA Transcription Factor Targets 2022

target genes of the STAT5A-24692510-EPITHELIUM-MOUSE-MAMMARY transcription factor in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets 2022 dataset.

From JASPAR Predicted Mouse Transcription Factor Targets 2025

target genes of the Stat5a::Stat5b transcription factor predicted using known transcription factor binding site motifs from the JASPAR Predicted Mouse Transcription Factor Targets 2925 dataset.