◀ Back to BCL2
BCL2 — BCL3
Text-mined interactions from Literome
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
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
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
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
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
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
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 )
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
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
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
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