Gene interactions and pathways from curated databases and text-mining

◀ Back to AKT1

AKT1 — TCL1A

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: AKT1 → TCL1A (increases, TCL1A Activity) Laine et al., J Biol Chem 2002*
    Evidence: The members of the TCL1 proto-oncogene family (TCL1, MTCP1, and TCL1b) bind to Akt1, increasing its phosphorylation status and kinase activity in contrast to Akt1 and Akt2, which bind to all members of the TCL1 family,
  • OpenBEL Selventa BEL large corpus: AKT1 → Complex of AKT1-TCL1A (directlyIncreases, AKT1/TCL1A Activity) Laine et al., J Biol Chem 2002*
    Evidence: The members of the TCL1 proto-oncogene family (TCL1, MTCP1, and TCL1b) bind to Akt1, increasing its phosphorylation status and kinase activity in contrast to Akt1 and Akt2, which bind to all members of the TCL1 family,
  • WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: TCL1A/TCL1B/TCL1B → AKT1/AKT3/AKT2 (activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Pekarsky et al., Proc Natl Acad Sci U S A 2000 : Tcl1 enhances Akt kinase activity and mediates its nuclear translocation
Künstle et al., Mol Cell Biol 2002 : In vitro kinase assays and overexpression experiments in mammalian cells demonstrated that both TCL1-Akt interaction and oligomerization of TCL1 were required for TCL1 induced Akt activation and substrate phosphorylation ... The results demonstrate the structural basis of TCL1 induced activation of Akt , which causes human T-PLL
Feng et al., Am J Physiol Gastrointest Liver Physiol 2010 (Atrophy) : We used a novel Akt activating peptide, TCL1 ( a head-to-tail dimer of the Akt binding domain of T-cell lymphoma-1 ), or an inactive mutant sequence TCL1G conjugated to a transactivator of transcription peptide sequence to promote intracellular uptake
Popal et al., Leukemia & lymphoma 2010 (Leukemia, Lymphocytic, Chronic, B-Cell...) : We discuss inhibitory strategies that are based on TCL1A 's activation of the growth modulating kinase AKT and on influences that regulate TCL1A expression
Miyazaki et al., PloS one 2013 : We found that Tcl1 expression levels correlated positively with the proliferation rate and negatively with the apoptosis of ES cells, but did not affect Akt phosphorylation