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BCL2 — PARP2

Text-mined interactions from Literome

Stoetzer et al., Leukemia 1999 (Leukemia, Lymphocytic, Chronic, B-Cell) : We determined the role of Bcl-2-family proteins Bcl-2 ( anti-apoptotic ) and Bax ( pro-apoptotic ), activation of caspase-3 ( CPP32/Yama ) and activation of PARP in CLL apoptosis
Song et al., Biochemistry 2002 : Furthermore, we demonstrated that Bcl-2 interacts with PARP in association with S3a and that the interaction of S3a and Bcl-2 with PARP causes a significant decrease in PARP activity
Guseva et al., Prostate 2002 (Prostatic Neoplasms) : Overexpression of FADD-DN and Bcl-2 affected the activation of caspase-3 and PARP cleavage differently : FADD-DN attenuated the activation of caspase-3 and PARP cleavage whereas Bcl-2 overexpression prevented caspase-3 activation and completely blocked cleavage of PARP
Jang et al., Biochem Biophys Res Commun 2002 : The L-canavanine induced caspase-3 activation, degradation of PARP , and apoptotic DNA fragmentation were suppressed by ectopic expression of Bcl-2 or Bcl-xL , both of which are known to play roles as anti-apoptotic regulators
Subhashini et al., Biochem Pharmacol 2004 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : The present study thus demonstrates that C-PC induces apoptosis in K562 cells by cytochrome c release from mitochondria into the cytosol, PARP cleavage and down regulation of Bcl-2
Kawano et al., Anticancer Res 2004 (MAP Kinase Signaling System) : The combination treatment activated caspase-3 and cleaved PARP , but it did not induce any notable change in the expression of Bcl-XL , Bcl-2 and Bax compared with each single treatment ... The combination treatment activated caspase-3 and cleaved PARP , but it did not induce any notable change in the expression of Bcl-XL, Bcl-2 and Bax compared with each single treatment
Lee et al., J Ethnopharmacol 2005 (Osteoarthritis) : Expression level of Bcl-2 , and caspase-3 and PARP activations were assayed by Western blot
Eom et al., Biol Pharm Bull 2008 (Brain Neoplasms...) : Berberine treatment also markedly enhanced apoptosis in T98G cells through the induction of a higher ratio of the Bax/Bcl-2 proteins, the disruption of mitochondrial membrane potential, and the activation of procaspase-9, caspase-9, caspase-3, and poly ( ADP-ribose ) polymerase ( PARP )
Jeon et al., Exp Mol Med 2008 (Seizures) : Protein levels of Bcl-2 , Bcl-X ( L ), Bax, and Bad showed no change, and cleavage of caspase-3 and PARP were not induced
Boosani et al., Invest Ophthalmol Vis Sci 2009 (Neovascularization, Pathologic) : alpha1 ( IV ) NC1 induced MREC apoptosis is mediated by inhibition of Bcl-2 and Bcl-x ( L ) expression and activation of caspase-3/PARP through FAK/p38-MAPK signaling
Quintás-Cardama et al., Invest New Drugs 2011 : Atiprimod induced cell growth inhibition of JAK2 ( V617F ) -positive cells was coupled with induction of apoptosis, as evidenced by heightened mitochondrial membrane potential and caspase-3 activity, as well as PARP cleavage, increased turnover of the anti-apoptotic X-linked mammalian inhibitor of apoptosis ( XIAP ) protein, and inhibition of the pro-apoptotic protein BCL-2 in a time- and dose dependent manner
Ha et al., Biochem Cell Biol 2012 (Colonic Neoplasms) : The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP , and procaspase-3 proteins in HT-29 cells
Bhattarai et al., Biol Pharm Bull 2012 (Carcinoma, Squamous Cell...) : Fomitoside-K could induce a dose and time dependent apoptosis in YD-10B cells as characterized by cell morphology, cell cycle arrest, inhibition of survivin, activation of poly ( ADP-ribose ) polymerase ( PARP ), caspase-3, -9 and an increased expression ratio of Bax/Bcl-2
Mou et al., Int J Biochem Cell Biol 2013 (Neoplasms) : Further studies with HCT8 cells showed that knockdown of FAM3B increased the protein levels of membrane bound Fas and Bax, reduced the expression of Bcl-2 , promoted the cleavage of caspases-8, -3, -9 and PARP, and the nuclear translocation of cleaved PARP
Ibrado et al., Cancer Res 1996 : In the present studies, we determined the effect of high intracellular levels of the antiapoptosis Bcl-2 or Bcl-xL protein on Yama protease activation and PARP degradation during Ara-C induced apoptosis ... In the present studies, we determined the effect of high intracellular levels of the antiapoptosis Bcl-2 or Bcl-xL protein on Yama protease activation and PARP degradation during Ara-C induced apoptosis ... High Bcl-2 and Bcl-xL levels in these cells also inhibited Yama protease activity, PARP degradation, and apoptosis due to clinically relevant concentrations of etoposide and mitoxantrone ... High Bcl-2 and Bcl-xL levels in these cells also inhibited Yama protease activity, PARP degradation, and apoptosis due to clinically relevant concentrations of etoposide and mitoxantrone
Bonfoco et al., Neuroreport 1996 : To explore further the protective mechanism ( s ) elicited by bcl-2 expression, we investigated whether BCL-2 could prevent NO-induced cleavage of poly-ADP-ribose-polymerase ( PARP ) , which is a substrate for interleukin-1 beta converting enzyme ( ICE ) -like proteases in 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
Kuo et al., Oncogene 1998 : In addition, analysis of basal PARP activity in control and several Bcl-2 overexpressing clones revealed that Bcl-2 down-regulated PARP activity under the condition without DNA damages
Yang et al., Immunopharmacology 1998 : Furthermore, enforced expression of Bcl-2 inhibited triptolide induced degradation of PARP and apoptosis