◀ Back to STAT3

BCL2L1 — STAT3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: BCL2L1 → STAT3 (increases, BCL2L1 Activity)
  Evidence: To explore this further, we have blocked endogenous ErbB3 transcription, thereby engineering tumor cells with overexpressed, fully active ErbB2 but lacking ErbB3 (T. Holbro and N.E. Hynes, unpublished data). As a consequence, these cells have decreased PI-3K/PKB signaling, a reduction in D-type cyclin levels, and show an increase in the G1 phase of the cell cycle. A main effector of ErbB signaling, the PI-3K/PKB pathway, is particularly important in mediating cell survival 103 T. Holbro et al. /...
• NCI Pathway Database IL6-mediated signaling events: STAT3 (dimer ) complex (STAT3) → BCL-X(L) (BCL2L1) (transcription, activates) Catlett-Falcone et al., Immunity 1999*
  Evidence: mutant phenotype, reporter gene

Text-mined interactions from Literome

Beales et al., J Mol Endocrinol 2009 (Adenocarcinoma...) : Novel small molecule inhibitors of JAK2 and STAT3 as well as STAT3 siRNA blocked the anti-apoptotic effects of G-Gly and inhibited the induction of survivin and BCL2L1 in OE33 cells
Adach-Kilon et al., J Cell Biochem 2011 (Brain Neoplasms...) : In this study, we employed DNA decoys, siRNAs, and protein overexpression, to elucidate the role of Stat1 and Stat3 in regulation of expression of endogenous Stat3-target genes ( Bcl2l1 , Myc, Ccnd1 ) and a Stat-driven reporter plasmid, in rat C6 glioma cells