Gene Ontology annotation through association of InterPro records with GO terms

Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity

Annotation inferences using phylogenetic trees

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

Gene Ontology annotation of human sequence-specific DNA binding transcription factors (DbTFs) based on the TFClass database

Electronic Gene Ontology annotations created by ARBA machine learning models

Combined Automated Annotation using Multiple IEA Methods

Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2.

ZFP36L1 negatively regulates erythroid differentiation of CD34+ hematopoietic stem cells by interfering with the Stat5b pathway.

The tumor suppressor hTid1 inhibits STAT5b activity via functional interaction.

STAT heterodimers in immunity: A mixed message or a unique signal?

Dominant-negative STAT5B mutations cause growth hormone insensitivity with short stature and mild immune dysregulation.

Structural and functional consequences of the STAT5B(N642H) driver mutation.

A reference map of the human binary protein interactome.

Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.

Cloning of human Stat5B. Reconstitution of interleukin-2-induced Stat5A and Stat5B DNA binding activity in COS-7 cells.

Erythropoietin induces tyrosine phosphorylation of Jak2, STAT5A, and STAT5B in primary cultured human erythroid precursors.

Functional association of Nmi with Stat5 and Stat1 in IL-2- and IFNgamma-mediated signaling.

p-STAT5A/B dissociates from the Growth Hormone receptor

IL7:p-Y449-IL7R:JAK1:IL2RG:p-JAK3:STAT5A,STAT5B phosphorylates STAT5

Recruitment of STATs

Phosphorylation of STATs

Dimerization of STATs

Disassociation and translocation of STATs to the nucleus

Phosphorylation of STAT5 by cytosolic FGFR1 fusions

STAT binds to the active receptor

Recruited STAT5 is phosphorylated

Phosphorylation of IL2RB Y338, Y392 or Y510 enables STAT recruitment

p-STAT5A, p-STAT5B dissociate from IL7:p-Y449-IL7R:JAK1:IL2RG:p-JAK3:p-STAT5A,p-STAT5B

Activation of STAT5a/b by JAK2

STAT5 is recruited by JAK2

p-Y-STAT3:p-STAT5 translocates to the nucleus

IL9:p-Y407-IL9R:JAK1:IL2RG:p-904,939-JAK3 binds STAT1, STAT3, STAT5A or STAT5B

IL9:p-Y116-IL9R:JAK1:IL2RG:p-904,939-JAK3:STAT3 phosphorylates STAT1, STAT3 or STAT5

p-STAT5 binds CISH, SOCS1 and SOCS2 gene

IL7:p-Y449-IL7R:JAK1:IL2RG:p-JAK3 binds STAT5

Phosphorylated STAT5 is released

p-STAT5 dissociates from the receptor complex

Phosphorylation of STATs downstream of KIT mutants

Recruitment of STATs by KIT mutants

Dimerization of STATs downstream of KIT mutants

Disassociation and translocation of STATs to the nucleus downstream of KIT mutants

FLT3 ITD mutants phosphorylate STAT5

PTPN11:p-STAT5 dissociates from mutant FLT3

PTPN11:p-STAT5 translocates to nucleus downstream of mutant FLT3

PTPN11:p-STAT5 binds BCL2L1 promoter

p-STAT5 dissociates from mutant FLT3

p-STAT5 translocates to nucleus downstream of mutant FLT3

p-STAT5 binds the CDKN1A gene

p-STAT5 binds the NOX4 promoter

p-STAT5 dissociates from FLT3 fusion proteinsp-

FLT3 fusions activate STAT5

Phosphorylated STAT5 dimer binds the IL4R gene