Gene interactions and pathways from curated databases and text-mining

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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

Tagami et al., Oncogene 2000 (Translocation, Genetic) : RTN-XS interacted with both Bcl-XL and Bcl-2 , increased the localization of Bcl-XL and Bcl-2 on the ER, and reduced the anti-apoptotic activity of Bcl-XL and Bcl-2
Tripathi et al., Cell Death Differ 2013 : Although Bcl-2 is an important Bim antagonist in effector T cells, and Bcl-xL is not required for effector T-cell survival, the roles of other anti-apoptotic Bcl-2 family members remain unclear
Elliott et al., Cancer Chemother Pharmacol 1999 (Cell Transformation, Neoplastic) : In addition, Bcl-2 also prevented the increase in cellular levels of Bak, Bax and Bcl-xL , along with degradation of actin and Bax
Tao et al., J Biol Chem 1998 : Bcl-xS and Bad potentiate the death suppressing activities of Bcl-xL, Bcl-2 , and A1 in yeast
Erdman et al., Adv Gerontol 2012 : In female of longevity age, the number of CASP8*I/*D, BCL2*T/*T and BAX*A/*A genotype carriers was higher and number of CASP8*DI/*D, BCL2*C/*C , BAX*A/*G and BAX *G/*G genotype carriers was reduced
Whitehead et al., J Perinatol 2013 (Fetal Growth Retardation...) : In preterm PE, but not FGR, there was increased placental expression of BCL-XL and BCL2 ( 1.6 to 2.5-fold, P < 0.05 ), but only BCL2 was significantly increased in the maternal blood ( 1.8-fold, P < 0.05 )
Greenlund et al., Neuron 1995 : Therefore, BCL-2 is an important regulator of the survival of sympathetic neurons after NGF deprivation during the period of naturally occurring programmed neuronal death, but BCL-2 is not involved in the development of trophic factor independence in mature sympathetic neurons
Sumantran et al., Cancer Res 1995 (Breast Neoplasms) : We used Bcl-XS , a dominant negative inhibitor of Bcl-2 and Bcl-XL, to demonstrate the role of these genes in modulating chemotherapy induced apoptosis
Hu et al., Gut 2011 (Disease Models, Animal...) : It was shown that arginine induced expression of Bcl-2 and Bcl-xL , while rReg4 upregulated Bcl-2 and Bcl-xL expression by activating the EGFR/Akt pathway
Mihara et al., Int J Oncol 2002 (Carcinoma, Squamous Cell...) : We also found up-regulation of Bcl-xS in the former cell lines, and in the latter cell lines, the expressions of Bcl-2 and Bcl-xL were induced simultaneously
Tung et al., Am J Physiol Heart Circ Physiol 2003 : These changes in the Fas-Fas ligand pathway and Bcl-2 mitochondrial apoptosis regulation are enhanced by complete suppression of antiapoptotic FADD-like IL-1beta converting enzyme inhibitory protein ( FLIP ) ( from 30.5 to 0.0 %, P < 0.01 ) and Bcl-xL ( from 22.5 to 0.1 %, P = 0.03 ) expression among these cells from the earliest days after gene transfer
Roberts et al., J Immunol 1999 : We show that B cell Ag receptor signaling in the absence of coreceptor recruitment induces cellular accumulation of the anti-apoptotic protein Bcl-xL , whereas CD19 mediated signals are required for Bcl-2 accumulation
Zeng et al., J Ethnopharmacol 2010 : Moreover, MWG extract decreased the level of intracellular reactive oxygen species ( ROS ), increased MMP, regulated Bcl-2 family protein expression ( Bcl-2 and Bcl-XL ) and inhibited the release of cytochrome c from the mitochondria
Woolveridge et al., Mol Hum Reprod 1998 (Prostatic Neoplasms) : However, in the long-term treated testes, Bcl-xl and PARP expression declined, Bax and p53 protein concentrations were unchanged, and Bcl-2 was up-regulated