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PIM1 — STAT3
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Shirogane et al., Immunity 1999
:
We found that
Pim-1 and Pim-2 are
targets for the gp130 mediated
STAT3 signal
Zemskova et al., J Biol Chem 2008
(Prostatic Neoplasms) :
Docetaxel activates
STAT3 phosphorylation and transcriptional activity, which in turns
induces expression of the
PIM1 gene, encoding a serine-threonine kinase activated by many cellular stresses
Meloche et al., Arterioscler Thromb Vasc Biol 2011
:
Therefore, we hypothesized that
RAGE/STAT3 activation in VSMC
activates Pim1 , promoting NFAT and thus VSMC proliferation and resistance to apoptosis ... Methods/Results- In vitro, freshly isolated human carotid VSMCs exposed to RAGE activator Ne- ( carboxymethyl ) lysine ( CML ) for 48 hours had ( 1 ) activated STAT3 ( increased P-STAT3/STAT3 ratio and P-STAT3 nuclear translocation ) ; ( 2 ) increased
STAT3 dependent
Pim1 expression resulting in NFATc1 activation ; and ( 3 ) increased Pim1/NFAT dependent VSMC proliferation ( PCNA, Ki67 ) and resistance to mitochondrial dependent apoptosis ( TMRM, Annexin V, TUNEL )
Block et al., Pancreas 2012
(Pancreatic Neoplasms) :
Cucurbitacin I was used as a pharmacological tool to investigate the
role of
STAT3 in
Pim-1 activation