PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11422444-7	2001	The c2-ceramide treatment also increases levels of c-jun, c-fos and p53 mRNA in primary cortical neuron cultures, but this is independent of p38 activation.	N-acetylsphingosine	4-15	tumor protein p53	Homo sapiens	68-71	
31480728-0	2019	C2-Ceramide-Induced Rb-Dominant Senescence-Like Phenotype Leads to Human Breast Cancer MCF-7 Escape from p53-Dependent Cell Death.	N-acetylsphingosine	0-11	tumor protein p53	Homo sapiens	105-108	
31480728-4	2019	The growth assessment showed that C2-ceramide caused significant growth inhibition and apoptosis in MDA-MB-231 cells through down-regulating the expression of mutant p53 whereas up-regulating the expression of pro-apoptotic Bad, and the proteolytic activation of caspase-3.	N-acetylsphingosine	34-45	tumor protein p53	Homo sapiens	166-169	
18845789-4	2009	By contrast, treatment of cells with C2-ceramide (a potent PP2A activator) or expression of the PP2A catalytic subunit (PP2A/C) inhibits Bcl2 phosphorylation, leading to increased p53/Bcl2 binding and apoptotic cell death.	N-acetylsphingosine	37-48	tumor protein p53	Homo sapiens	180-183	
11422444-8	2001	Our study further elucidates the time-courses of MAPK cascade modulation, and of c-jun, c-fos and p53 activation during c2-ceramide-induced neuronal apoptosis.	N-acetylsphingosine	120-131	tumor protein p53	Homo sapiens	98-101	
9535218-3	1998	Treatment of cells with p53 or MnSOD antisense oligonucleotides prior to stimulation with oxLDL, C2-ceramide, TNF-alpha, or H2O2 caused an inhibition of the expression of the respective protein together with a marked reduction of apoptosis.	N-acetylsphingosine	97-108	tumor protein p53	Homo sapiens	24-27	
10360645-6	1999	Similarly, cell proliferation was abolished by C2-ceramide (5-20 microM) only in wild-type p53 cells.	N-acetylsphingosine	47-58	tumor protein p53	Homo sapiens	91-94	
10360645-7	1999	FACS-analysis revealed that C2-ceramide induced massive p53-dependent apoptosis (40-50% after 12-24 h) and cell cycle analysis showed a transient G1 arrest in p53-deficient tumour cells 12-24 h after C2-ceramide exposure.	N-acetylsphingosine	28-39	tumor protein p53	Homo sapiens	56-59	
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	N-acetylsphingosine	58-69	tumor protein p53	Homo sapiens	187-190	
8946936-4	1996	However, a cell-cycle arrest in G0/G1 phase was observed in Raji cells after the treatment with C2-ceramide, which was accompanied by the dephosphorylation of retinoblastoma (RB) gene products and decreased expression of p53 proteins.	N-acetylsphingosine	96-107	tumor protein p53	Homo sapiens	221-224