protein
| recruiting a minichromosome maintenance complex MCM5/MCM3 through direct interaction with MCM5 in the process of IFNG-induced gene activation |
|
KPNA2 for translocation into the nucleus |
|
IFNA1 (protection against IFNA1-mediated injury in the CNS ) |
|
associating with SPI1 and coactivating Fcgamma receptor 1 promoter |
|
dimerizing with phosphorylated STAT2 and associating with ISGF3G in ISGF3 transcription factor complex |
|
STAT1-DOT1L interaction is required for the regulation JAK-STAT-inducible gene expression |
|
interacting with NMI |
|
SMURF1 interacted with STAT1 through the WW domains of SMURF1 and the PY motif in STAT1 and catalyzed K48-linked polyubiquitination of STAT1 |
|
STAT1 inhibited VEGFA expression, while STAT3 promoted the expression of VEGFA |
|
STAT1 and STAT3 have opposing roles in modulating HIF1A activity and subsequently, VEGFA expression |
|
TYK2 controls STAT1 and STAT6 activation in response to IL13 stimulation |
|
physically interacts with both STAT1A and STAT1B through its macrodomains in an ADP-ribosylation-dependent manner, and directly inhibits, together with STAT1B, the expression of tumor suppressor and interferon response factor IRF1 |
|
RELA and STAT1 cooperate to control NOS2 gene transcription in response to proinflammatory cytokines by a coactivator exchange mechanism |
|
IFNG directly controls IL33 protein level through a STAT1- and PSMB9-dependent mechanism |
|
NDN bound to PIAS1 central domains that are highly conserved among PIAS family proteins and suppressed PIAS1-dependent sumoylation of the substrates STAT1 and PML |
|
endogenous STAT1 and IFNGR1 in target cells are indispensable to sustain the activation of STAT1 signaling by extracellular vesicles (EVs)-associated IFNG/IFNGR1 complexes |
|
IFIT3 showed binding to MAPK8 and STAT1, the latter being an important inducer of IFIT3 expression |
|
STAT1 and STAT3 have at least partially opposing roles in IL21 signaling in CD4(+) T cells |
|
positive feedback loop between phosphorylated STAT1 and IFIT1, IFIT2, IFIT3 |
|
IRF1 could induce STAT1 phosphorylation and in turn STAT1 activation |
|
HDAC3 interacts with FOXK1, co-localizes with FOXK1 at the promoter of STAT1 and STAT2, and is required for protecting FOXK1 from lysosomal system-mediated degradation |