PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19765187-7 2009 Treatment with either l-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 39-43 BCL2-associated X protein Mus musculus 124-127 15111020-10 2004 Striatal Bcl-2 was significantly decreased, while Bax was increased in MPTP treated mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 71-75 BCL2-associated X protein Mus musculus 50-53 18675323-5 2008 Therefore, we used Affymetrix and qRT-PCR technology to characterize temporal mRNA changes in striatum in response to MPTP in genetically MPTP-sensitive, C57BL/6J, and MPTP-resistant Swiss Webster and BCL2-associated X protein (Bax)-/- mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 118-122 BCL2-associated X protein Mus musculus 201-226 32585786-10 2004 Striatal Bcl-2 was significantly decreased, while Bax was increased in MPTP treated mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 71-75 BCL2-associated X protein Mus musculus 50-53 17076657-0 2006 Recombinant human granulocyte colony-stimulating factor protects against MPTP-induced dopaminergic cell death in mice by altering Bcl-2/Bax expression levels. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 73-77 BCL2-associated X protein Mus musculus 136-139 17076657-7 2006 G-CSF significantly prevented MPTP-induced loss of tyrosine hydroxylase-positive neurons (p < 0.05), increased Bcl-2 protein and decreased Bax protein expression. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 30-34 BCL2-associated X protein Mus musculus 142-145 12718432-2 2003 Three days to 12 weeks after MPTP treatment, a detectable reduction of tyrosine hydroxylase immunoreactivity in the amacrine cells was observed, with an increase of Bcl-2 expression in the Muller glial cells, and a de novo expression of Bad and Bax in the retinal ganglion cells, optic nerve fibers and plexiform layers. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 29-33 BCL2-associated X protein Mus musculus 245-248 32386222-8 2020 The CPO-A treatment attenuated or restored (P < 0.05) these changes and inhibited (P < 0.05) the MPTP-induced activation of P38 mitogen-activated protein kinase (P38MAPK) and P53, along with the downstream expression of BCL-2 associated X protein (BAX) in the SN. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 97-101 BCL2-associated X protein Mus musculus 220-246 11698144-0 2001 Sequential up-regulation of the c-fos, c-jun and bax genes in the cortex, striatum and cerebellum induced by a single injection of a low dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 145-189 BCL2-associated X protein Mus musculus 49-52 11698144-0 2001 Sequential up-regulation of the c-fos, c-jun and bax genes in the cortex, striatum and cerebellum induced by a single injection of a low dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 191-195 BCL2-associated X protein Mus musculus 49-52 33925146-5 2021 MPTP and NE52-QQ57 co-treatment in mice significantly decreased pro-apoptotic marker Bax protein levels and increased anti-apoptotic marker Bcl-2 protein levels in the SNpc and striatum. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 0-4 BCL2-associated X protein Mus musculus 85-88 12402257-5 2002 MPTP caused an increase in the level of the proapoptotic protein Bax, which was prevented by giving mice PFT-alpha and Z-1-117. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 0-4 BCL2-associated X protein Mus musculus 65-68 12200191-7 2002 Evidence has emerged to suggest that Bcl-2, Bax, JNK, and caspases are implicated in neurotoxic effects due to in vivo MPTP administration to mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 119-123 BCL2-associated X protein Mus musculus 44-47 11698144-1 2001 We investigated whether single injection of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) (20 mg/kg) will alter the expression of pro-apoptotic genes, namely, the c-fos, c-jun, and bax, in the striatum, cortex, and cerebellum of adult male C57BL/6 mice using reverse transcription-polymerase chain reaction assay. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 44-89 BCL2-associated X protein Mus musculus 188-191 11698144-1 2001 We investigated whether single injection of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) (20 mg/kg) will alter the expression of pro-apoptotic genes, namely, the c-fos, c-jun, and bax, in the striatum, cortex, and cerebellum of adult male C57BL/6 mice using reverse transcription-polymerase chain reaction assay. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 91-95 BCL2-associated X protein Mus musculus 188-191 11226327-0 2001 Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 60-105 BCL2-associated X protein Mus musculus 0-3 11226327-3 2001 In adult mice, there is an up-regulation of Bax in the SNpc after MPTP administration and a decrease in Bcl-2. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 66-70 BCL2-associated X protein Mus musculus 44-47 11226327-5 2001 We also show that mutant mice lacking Bax are significantly more resistant to MPTP than their wild-type littermates. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 78-82 BCL2-associated X protein Mus musculus 38-41 11226327-6 2001 This study demonstrates that Bax plays a critical role in the MPTP neurotoxic process and suggests that targeting Bax may provide protective benefit in the treatment of Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 62-66 BCL2-associated X protein Mus musculus 29-32 11226327-6 2001 This study demonstrates that Bax plays a critical role in the MPTP neurotoxic process and suggests that targeting Bax may provide protective benefit in the treatment of Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 62-66 BCL2-associated X protein Mus musculus 114-117 8929984-0 1996 Increase in bax expression in substantia nigra following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment of mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 57-101 BCL2-associated X protein Mus musculus 12-15 8929984-0 1996 Increase in bax expression in substantia nigra following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment of mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 103-107 BCL2-associated X protein Mus musculus 12-15 8929984-3 1996 Intraperitoneal MPTP injections in mice resulted in a significant increase in bax mRNA by about two- and three-fold after 3 and 6 days, respectively. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 16-20 BCL2-associated X protein Mus musculus 78-81 8929984-5 1996 Our results indicate a pathophysiological significance of bax, which promotes programmed cell death, in MPTP neurotoxicity. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 104-108 BCL2-associated X protein Mus musculus 58-61 32495646-8 2020 The BCL-2/Bax ratio significantly increased in the MPTP + EE compared to the MPTP + SC group. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 51-55 BCL2-associated X protein Mus musculus 10-13 32495646-8 2020 The BCL-2/Bax ratio significantly increased in the MPTP + EE compared to the MPTP + SC group. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 77-81 BCL2-associated X protein Mus musculus 10-13 31175966-6 2019 IGF-1 pretreatment also reversed the changes of Bcl-2 and Bax protein expressions in SN in MPTP mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 91-95 BCL2-associated X protein Mus musculus 58-61 31690718-10 2019 Moreover, MPTP led to DNA fragmentation, caspase-3 activation, lipid peroxidation and BAX expression in Wt mice, in the absence of caspase-8 cleavage, suggesting intrinsic apoptosis. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 10-14 BCL2-associated X protein Mus musculus 86-89 32333598-12 2020 CONCLUSIONS In the mouse model of MPTP-induced PD, 2-aminoquinoline reduced motor deficiencies, inhibited MPP+ activated astrocyte apoptosis, and regulated the Bax/Bcl-2 ratio by targeting p-JNK. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 34-38 BCL2-associated X protein Mus musculus 160-163 29264673-5 2018 Moreover, ODN blocked the inhibition of the anti-apoptotic gene Bcl-2, and the stimulation of the pro-apoptotic genes Bax and caspase-3, induced by MPTP in the substantia nigra pars compacta. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 148-152 BCL2-associated X protein Mus musculus 118-121 27017962-7 2016 Meanwhile, the Bcl2/Bax ratio was decreased significantly by MPTP in the striatum and SN of MtFt knockout (MtFt-/-) mice compared with controls. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 61-65 BCL2-associated X protein Mus musculus 20-23 29588573-7 2018 Vit also enhanced the activation of PI3K and Akt and suppressed the ratio of Bax/Bcl-2 and caspase-3 activity in MPTP-treated mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 113-117 BCL2-associated X protein Mus musculus 77-80 28190476-10 2017 The MPTP-induced changes of Bcl-2, Bax and caspase 3 protein expressions in the striatum could be reversed by icariin pretreatment. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 4-8 BCL2-associated X protein Mus musculus 35-38 27317935-5 2016 However, in DA-p53KO mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that the induction of Bax and p53 up-regulated modulator of apoptosis (PUMA) mRNA and protein levels by MPTP were diminished in both striatum and substantia nigra of these mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 54-98 BCL2-associated X protein Mus musculus 138-141 27317935-5 2016 However, in DA-p53KO mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that the induction of Bax and p53 up-regulated modulator of apoptosis (PUMA) mRNA and protein levels by MPTP were diminished in both striatum and substantia nigra of these mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 100-104 BCL2-associated X protein Mus musculus 138-141 27317935-5 2016 However, in DA-p53KO mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that the induction of Bax and p53 up-regulated modulator of apoptosis (PUMA) mRNA and protein levels by MPTP were diminished in both striatum and substantia nigra of these mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 220-224 BCL2-associated X protein Mus musculus 138-141 27317935-9 2016 Our results further support the role of programmed cell death mediated by p53 in this animal model of PD and identify Bax, BAD and PUMA genes as downstream targets of p53 in modulating DA neuronal death in the in vivo MPTP-induced PD model. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 218-222 BCL2-associated X protein Mus musculus 118-121 27317935-10 2016 We deleted p53 gene in dopaminergic neurons in late developmental stages and found that DA specific p53 deletion is protective in acute MPTP animal model possibly through blocking MPTP-induced BAX and PUMA up-regulation. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 136-140 BCL2-associated X protein Mus musculus 193-196 27317935-10 2016 We deleted p53 gene in dopaminergic neurons in late developmental stages and found that DA specific p53 deletion is protective in acute MPTP animal model possibly through blocking MPTP-induced BAX and PUMA up-regulation. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 180-184 BCL2-associated X protein Mus musculus 193-196 27619562-7 2016 Instead, inhibition of Drp1 mitochondrial translocation diminished MPTP-induced p53, BAX and PUMA mitochondrial translocation. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 67-71 BCL2-associated X protein Mus musculus 85-88 25730317-8 2016 In addition, lutein repressed the MPTP-induced neuronal damage/apoptosis by inhibiting the activation of pro-apoptotic markers (Bax, caspases-3, 8 and 9) and enhancing anti-apoptotic marker (Bcl-2) expressions. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 34-38 BCL2-associated X protein Mus musculus 128-131 26484597-3 2016 Treatment with samples significantly ameliorated the depletion of both DA and TH-, Bcl-2- and Bax-positive neurons in MPTP-induced PD mice, DF1 showed the highest activity. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 118-122 BCL2-associated X protein Mus musculus 94-97 25976060-7 2016 Indeed, treatment of miR-124 agomir in MPTP-treated mice inhibited Bim expression, thus suppressing Bax translocation to mitochondria. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 39-43 BCL2-associated X protein Mus musculus 100-103 25645943-4 2015 Previous reports have indicated those knockout mice with Bcl-2 associated protein X (Bax) or caspase-2, two mitochondrial outer membrane permeabilization inducers, are resistant to MPTP administration, suggesting that mitochondria are involved in MPP(+)-triggered apoptosis. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 181-185 BCL2-associated X protein Mus musculus 57-83 25645943-4 2015 Previous reports have indicated those knockout mice with Bcl-2 associated protein X (Bax) or caspase-2, two mitochondrial outer membrane permeabilization inducers, are resistant to MPTP administration, suggesting that mitochondria are involved in MPP(+)-triggered apoptosis. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 181-185 BCL2-associated X protein Mus musculus 85-88 24995576-5 2014 The administration of MPTP (30 mg/kg for four successive days) significantly induced motor impairments as determined by behavioral studies (narrow beam test, catalepsy and akinesia), lowered dopamine levels and up-regulated the expressions of the inflammatory and apoptotic markers (tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, inducible nitric oxide synthase, glial fibrillary acidic protein, cyclooxygenase-2 and Bax). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 22-26 BCL2-associated X protein Mus musculus 433-436 25857436-8 2015 RESULTS: Our histological findings revealed that MPTP administration enhanced Bax/Bcl2 ratio and microglial cells activation reflecting induction of apoptosis and inflammation, respectively. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 49-53 BCL2-associated X protein Mus musculus 78-81 24686337-7 2014 Furthermore, pharmacological BAX channel inhibition is able to prevent LMP, restore lysosomal levels, reverse AP accumulation, and attenuate mitochondrial permeabilization and overall nigrostriatal degeneration caused by MPTP, both in vitro and in vivo. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 221-225 BCL2-associated X protein Mus musculus 29-32 24262283-10 2013 Expressions of Bax and Bcl2 along with GFAP did show significant variations (p < 0.05) on MPTP treatment when compared to control animals and the changes were found to be reversed significantly (p < 0.05) after treatment with asiaticoside. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 93-97 BCL2-associated X protein Mus musculus 15-18 24095822-6 2013 MPTP treatment leads to enhanced oxidative stress, induction of apoptosis (upregulates the expression of Bax, proapoptotic protein and downregulates the expression of anti-apoptotic marker Bcl-2), and loss of dopominergic neurons which results in motor impairments. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 0-4 BCL2-associated X protein Mus musculus 105-108 23877198-6 2013 In addition, the Bax/Bcl-2 gene and protein expression ratios were significantly increased in the MPTP-exposed mice, and this effect was reversed by selegiline. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 98-102 BCL2-associated X protein Mus musculus 17-20