HUGO ID Detailed Result 990

HUGO ID 990
Symbol BCL2
Name B-cell CLL/lymphoma 2
#Occurrence 74
#Paper 12

 

PMID Match String Actual String Score Flanking text Edited by Edit
11173059Bcl-2Bcl-21.0biochemical marker of apoptosis the altered expression of mRNA for Bcl-2 and Bax (an an anti-apoptotic and a proapoptotic gene respectively 
11173059Bcl-2Bcl-21.0and Bad (proapoptotic) proapoptotic genes is increased whereas that of Bcl-2 and Bcl-xL (anti-apoptotic) anti-apoptotic is decreased ( Vukosavic et al. 
11173059Bcl-2Bcl-21.0double transgenic mice expressing human mutant superoxide dismutase and human Bcl-2 the overexpression of Bcl-2 is associated with a significant delay 
11173059Bcl-2Bcl-21.0human mutant superoxide dismutase and human Bcl-2 the overexpression of Bcl-2 is associated with a significant delay in disease onset ( 
11173059Bcl-2Bcl-21.0The apoptosis-effector molecule caspase-3 and the anti-apoptotic molecule Bcl-2 are overexpressed in the basal ganglia of patients with Parkinson's 
11173059Bcl-2Bcl-21.0Gene polymorphisms of apoptosis-related factors (e.g., e.g. Bax and Bcl-2 or apoptosis-effector molecules (e.g., e.g. caspase enzymes have still to 
11173059Bcl-2Bcl-21.0pro-apoptotic molecules such as Bax down-regulates anti-apoptotic molecules such as Bcl-2 and induces caspase enzymes ( Paradis Harada and Troy 
12843244Bcl-2Bcl-21.0However the weak protection by Bcl-2 overexpression in a mouse model of ALS (Kostic Kostic et 
14739060Bcl2Bcl20.0the release of apoptogenic mitochondrial mediators _amp_#x2022 Pro-apoptotic members of Bcl2 family _amp_#x2022 elevated levels of intra-cellular calcium such as that 
15210305Bcl-2Bcl-21.0Towards the end stage of the disease Bcl-2 and Bcl-XL proteins acting as apoptosis inhibitors show reduced expression 
15571972Bcl-2Bcl-22.1been recently shown to up-regulate expression of the anti-apoptotic protein Bcl-2 ( Wang et al. 2004 
15571972Bcl-2Bcl-22.1thus the activation_amp_#x2014 of Bid a pro-apoptotic protein of the Bcl-2 family ( Wang et al. 2003a _amp_#x2014 10 mg/kg mg 
16624536Bcl-2Bcl-21.0survivin inhibitor of apoptosis protein-1 (IAP1), IAP1 IAP2 X-chromosome-linked IAP Bcl-2 Bcl-XL Bfl-1/A1, Bfl-1 A1 and FLIP 88 
17008387Bcl-2Bcl-21.0role of some NF-kappaB-regulated genes such as manganese SOD and Bcl-2 (Mattson Mattson and Camandola 2001 kappaB binding activity in the 
17015226Bcl-2Bcl-21.0Pasinelli et_amp_#xa0 al. 2000 and lowered levels of the antiapoptotic Bcl-2 have been reported in spinal cord motor neurons of ALS 
17015226Bcl-2Bcl-21.0alternate mechanism in which SOD1 is proposed to interact with Bcl-2 and possibly interferes with Bcl-2 antiapoptotic activity ( Pasinelli et_amp_#xa0 
17015226Bcl-2Bcl-21.0is proposed to interact with Bcl-2 and possibly interferes with Bcl-2 antiapoptotic activity ( Pasinelli et_amp_#xa0 al. 2004 is attractive but 
17015226Bcl-2Bcl-21.0However both constitutively increased expression of Bcl-2 ( Kostic et_amp_#xa0 al. 1997 and virally driven overexpression of 
17015226Bcl-2Bcl-21.0( Kostic et_amp_#xa0 al. 1997 and virally driven overexpression of Bcl-2 in motor neurons ( Azzouz et_amp_#xa0 al. 2000 protect motor 
17015226Bcl-2Bcl-21.0Bcl-2 is unable to similarly rescue motor neuron death in other 
17569578Bcl-2Bcl-21.0of the anti-apoptotic proteins FLIP and survivin 152 as well Bcl-2 2 and so could possibly counteract the capability of tumor 
18436268Bcl-2Bcl-23.2polymerase (PARP) PARP but up-regulated the level of anti-apoptotic protein Bcl-2 
18436268Bcl-2Bcl-23.2CA USA TNF-_amp_#x3b1 (1:1000, 1 1000 Cell signaling MA USA Bcl-2 (1:1000, 1 1000 Santa Cruz Biotechnology Inc. Santa Cruz cleaved 
18436268Bcl-2Bcl-23.2SOD1 G93A transgenic mice we determined the protein level of Bcl-2 cleaved caspase-3 and PARP in the spinal cord after FA 
18436268Bcl-2Bcl-23.2FA or FA B12 treatment can increase the level of Bcl-2 and reduce the level of cleaved caspase-3 and cleaved PARP 
18436268Bcl-2Bcl-23.2we found FA B12 treatment can elevate the level of Bcl-2 in SOD1 G93A mice up to the level of wild-type 
18436268Bcl-2Bcl-23.2or FA B12 treatment has significant anti-apoptotic effects by increasing Bcl-2 expression and inhibiting cleaved caspase-3 and cleaved PARP 
18436268Bcl-2Bcl-23.2by regulating the expression of several important proteins such as Bcl-2 cleaved caspase-3 and cleaved PARP ( Baydas et_amp_#xa0 al. 2005 
18436268Bcl-2Bcl-23.2Bcl-2 plays a prominent role in ALS pathogenesis which is involved 
18436268Bcl-2Bcl-23.2Bcl-2 family is implicated in the regulation of motor neuron death 
18436268Bcl-2Bcl-23.2death in SOD1 G93A transgenic mice model and over-expression of Bcl-2 can significantly protect motor neurons in SOD1 G93A mice ( 
18436268Bcl-2Bcl-23.2FA or FA B12 treatment can increase the expression of Bcl-2 which provided an evidence for the neuroprotective effect of FA 
18436268Bcl-2Bcl-23.2FA B12 treatment could up-regulate the expression of anti-apoptotic protein Bcl-2 as well as down-regulated the expression of apoptosis-related proteins such 
18436268Bcl-2Bcl-23.2and cleaved PARP as well as up-regulate the levels of Bcl-2 
18436268Bcl-2Bcl-23.2(B) B Western blot of Bcl-2 cleaved caspase-3 and cleaved PARP from spinal cord samples 
18436268Bcl-2Bcl-23.2C_amp_#x2013 G Quantitative data of the expression of iNOS TNF-_amp_#x3b1 Bcl-2 cleaved caspase-3 and cleaved PARP in five groups 
18464922Bcl-2Bcl-21.8Both mutant and wild type SOD1 bind to antiapoptotic protein Bcl-2 on the outer mitochondrial membrane blocking its antiapoptotic activity 42 
18464922Bcl-2Bcl-21.8in the mitochondria leads to formation of SOD1 aggregates entrapping Bcl-2 blocking protein importation to mitochondria which may trigger neuronal cell 
11173059bcl 2bcl 21.0these findings include evidence of dna fragmentation a biochemical marker of apoptosis the altered expression of mrna for bcl 2 and bax an anti apoptotic and a proapoptotic gene respectively and the demonstration of caspase 1 and caspase 3 activation which are specific intracellular proteases responsible for the execution of  
11173059bcl 2bcl 21.0in spinal cord of human mutant superoxide dismutase transgenic mice the expression of bax and bad proapoptotic genes is increased whereas that of bcl 2 and bcl xl anti apoptotic is decreased vukosavic et al. 1999 .  
11173059bcl 2bcl 21.0in double transgenic mice expressing human mutant superoxide dismutase and human bcl 2 the overexpression of bcl 2 is associated with a significant delay in disease onset kostic et al. 1997 .  
11173059bcl 2bcl 21.0the apoptosis effector molecule caspase 3 and the anti apoptotic molecule bcl 2 are overexpressed in the basal ganglia of patients with parkinson's disease confirming that apoptosis is a relevant mechanism of neural death in this paradigm marshall and hartmann .  
11173059bcl 2bcl 21.0gene polymorphisms of apoptosis related factors e.g. bax and bcl 2 or apoptosis effector molecules e.g. caspase enzymes have still to be investigated in parkinson's disease although they may play a role in modulating the susceptibility of nigral neurons to set off a 
11173059bcl 2bcl 21.0est that chronic deposition of _amp_#x3b2; amyloid protein may be crucial. _amp_#x3b2; amyloid protein up regulates pro apoptotic molecules such as bax down regulates anti apoptotic molecules such as bcl 2 and induces caspase enzymes paradis ; harada and troy .  
12843244bcl 2bcl 21.0however the weak protection by bcl 2 overexpression in a mouse model of als kostic et al. 1997 suggests an involvement of alternative cell death mechanisms as well.  
14739060bcl 2bcl21.0three main signals cause the release of apoptogenic mitochondrial mediators: _amp_#x2022; pro apoptotic members of bcl2 family _amp_#x2022; elevated levels of intra cellular calcium such as that triggered by excitotoxicity _amp_#x2022; elevated levels of ros_amp_#x2013;rns  
15210305bcl 2bcl 21.0towards the end stage of the disease bcl 2 and bcl xl proteins acting as apoptosis inhibitors show reduced expression whereas bad and bax which promote apoptosis appear to be up regulated in spinal cord of the animal model of als [ 109 ].  
15512862bcl 2bcl 21.0neuroprotective agents|proto oncogene proteins c bcl 2|superoxide dismutase 1|superoxide dismutase|peptide hydrolases|caspases|  
15571972bcl 2bcl 21.0additionally minocycline has been recently shown to up regulate expression of the anti apoptotic protein bcl 2 wang et al. 2004 .  
15571972bcl 2bcl 21.0minocycline can also reduce the cleavage_amp_#x2014;and thus the activation_amp_#x2014;of bid a pro apoptotic protein of the bcl 2 family wang et al. 2003a _amp_#x2014;10 mg/kg i.p. .  
16624536bcl 2bcl 21.0 nf_amp_#x3ba;b dependent reporter gene expression that in turn drives expression of anti apoptotic gene products including survivin inhibitor of apoptosis protein 1 iap1 iap2 x chromosome linked iap bcl 2 bcl xl bfl 1/a1 and flip [88] .  
17008387bcl 2bcl 21.0ed with tissue and cellular protection inhibition of nf kappab may also accelerate neurodegeneration because of the survivalsupporting role of some nf kappab regulated genes such as manganese sod and bcl 2 mattson and camandola 2001 kappab binding activity in the spinal cords of g93a sod1 tg rats no statistically significant differences between any of the untreated/pdtc treated tg and wt rat groups wer 
17015226bcl 2bcl 21.0activation of the executioner caspase 3 is found in mouse models contemporaneous with neuronal death li et_amp_#xa0;al. 2000 and pasinelli et_amp_#xa0;al. 2000 and lowered levels of the antiapoptotic bcl 2 have been reported in spinal cord motor neurons of als patients ekegren et_amp_#xa0;al. 1999 and mu et_amp_#xa0;al. 1996 and mutant sod1 mice gonzalez de aguilar et_amp_#xa0;al. 2000 and vukosavic et 
17015226bcl 2bcl 21.0an alternate mechanism in which sod1 is proposed to interact with bcl 2 and possibly interferes with bcl 2 antiapoptotic activity pasinelli et_amp_#xa0;al. 2004 is attractive but has recently been disputed gould et_amp_#xa0;al. 2006 .  
17015226bcl 2bcl 21.0however both constitutively increased expression of bcl 2 kostic et_amp_#xa0;al. 1997 and virally driven overexpression of bcl 2 in motor neurons azzouz et_amp_#xa0;al. 2000 protect motor neurons delaying disease onset but not progression.  
17015226bcl 2bcl 21.0bcl 2 is unable to similarly rescue motor neuron death in other models such as wobbler and transgenic mice expressing a point mutation in the nf l gene coulpier et_amp_#xa0;al. 1996 and houseweart and clev 
17569578bcl 2bcl 21.0electron microscopy and western blot analysis revealed dna condensation and down regulation of bcl 2 suggesting the induction of apoptosis in activated t lymphocytes [151] .  
17569578bcl 2bcl 21.0troglitazone treatment led to a marked down regulation of the anti apoptotic proteins flip and survivin [152] as well bcl 2 [2] and so could possibly counteract the capability of tumor cells to become resistant to apoptosis.  
18436268bcl 2bcl 21.0moreover fa or fa + b12 treatment decreased the levels of cleaved caspase 3 and poly adp ribose polymerase parp but up regulated the level of anti apoptotic protein bcl 2.  
18436268bcl 2bcl 21.0 each sample was separated in 8% sds gel transferred onto 0.45 _amp_#x3bc;m pvdf membrane incubated with primary antibodies of inos 1:5000 chemicon ca usa tnf _amp_#x3b1; 1:1000 cell signaling ma usa bcl 2 1:1000 santa cruz biotechnology inc. santa cruz cleaved caspase 3 1:1000 cell signaling ma usa parp and cleavage 1:1000 cell signaling ma usa respectively.  
18436268bcl 2bcl 21.0to investigate whether hcy lowering drugs fa and b12 had the anti apoptotic effects in the sod1 g93a transgenic mice we determined the protein level of bcl 2 cleaved caspase 3 and parp in the spinal cord after fa b12 or fa + b12 treatment.  
18436268bcl 2bcl 21.0we found that fa or fa + b12 treatment can increase the level of bcl 2 and reduce the level of cleaved caspase 3 and cleaved parp fig._amp_#xa0;5 b .  
18436268bcl 2bcl 21.0especially we found fa + b12 treatment can elevate the level of bcl 2 in sod1 g93a mice up to the level of wild type which could suggest that fa + b12 is effective in suppressing apoptosis in the sod1 mice model.  
18436268bcl 2bcl 21.0moreover we demonstrated that fa or fa + b12 treatment has significant anti apoptotic effects by increasing bcl 2 expression and inhibiting cleaved caspase 3 and cleaved parp.  
18436268bcl 2bcl 21.0hcy could induce apoptosis by regulating the expression of several important proteins such as bcl 2 cleaved caspase 3 and cleaved parp [baydas et_amp_#xa0;al. 2005] and [kruman et_amp_#xa0;al. 2000] .  
18436268bcl 2bcl 21.0bcl 2 plays a prominent role in als pathogenesis which is involved in the oxidative stress and in the mitochondria mediated apoptosis pasinelli et_amp_#xa0;al. 2004 .  
18436268bcl 2bcl 21.0bcl 2 family is implicated in the regulation of motor neuron death in sod1 g93a transgenic mice model and over expression of bcl 2 can significantly protect motor neurons in sod1 g93a mice kostic et_amp_#xa0;al. 1997 .  
18436268bcl 2bcl 21.0in our study we found that fa or fa + b12 treatment can increase the expression of bcl 2 which provided an evidence for the neuroprotective effect of fa or fa + b12 treatment in sod1 g93a mice.  
18436268bcl 2bcl 21.0our study suggested that fa or fa + b12 treatment could up regulate the expression of anti apoptotic protein bcl 2 as well as down regulated the expression of apoptosis related proteins such as cleaved caspase 3 and cleaved parp.  
18436268bcl 2bcl 21.0moreover we found that fa or fa + b12 treatment can significantly inhibit the levels of cleaved caspase 3 and cleaved parp as well as up regulate the levels of bcl 2.  
18436268bcl 2bcl 21.0 b western blot of bcl 2 cleaved caspase 3 and cleaved parp from spinal cord samples.  
18436268bcl 2bcl 21.0 c_amp_#x2013;g quantitative data of the expression of inos tnf _amp_#x3b1; bcl 2 cleaved caspase 3 and cleaved parp in five groups.  
18464922bcl 2bcl 21.0both mutant and wild type sod1 bind to antiapoptotic protein bcl 2 on the outer mitochondrial membrane blocking its antiapoptotic activity [ 42 ].  
18464922bcl 2bcl 21.0 ii the presence of mutant sod1 in the mitochondria leads to formation of sod1 aggregates entrapping bcl 2 blocking protein importation to mitochondria which may trigger neuronal cell death due to mitochondrial dysfunction [ 42 ].