ArticleMolecular and cellular biochemistry2003
Nicotinamide- and caspase-mediated inhibition of poly(ADP-ribose) polymerase are associated with p53-independent cell cycle (G2) arrest and apoptosis.
Article in Molecular and cellular biochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- NADNature reviews. Molecular cell biology · 2021Review
- SIRT1 regulates macrophage self-renewal.The EMBO journal · 2017Article
- Nicotinamide induces apoptosis of F9 mouse teratocarcinoma stem cells by downregulation of SATB1 expression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins.Neurotoxicity research · 2011Review
- Proteasome-mediated degradation of Tob is pivotal for triggering UV-induced apoptosis.Oncogene · 2009Article
- Identification of metabolites with anticancer properties by computational metabolomics.Molecular cancer · 2008Article
- Melatonin maintains mitochondrial membrane potential and attenuates activation of initiator (casp-9) and effector caspases (casp-3/casp-7) and PARP in UVR-exposed HaCaT keratinocytes.Journal of pineal research · 2008Article
- Niacin restriction upregulates NADPH oxidase and reactive oxygen species (ROS) in human keratinocytes.Free radical biology & medicine · 2008Article
- Plasticity of basal ganglia neurocircuitries following perinatal asphyxia: effect of nicotinamide.Experimental brain research · 2007Article
- Role of TAB1 in nitric oxide-induced p38 activation in insulin-producing cells.International journal of biological sciences · 2006Article
- Inhibition of SIRT1 catalytic activity increases p53 acetylation but does not alter cell survival following DNA damage.Molecular and cellular biology · 2006Article
- Role of MKK3 and p38 MAPK in cytokine-induced death of insulin-producing cells.The Biochemical journal · 2006Article
- Poly(ADP-ribose) polymerase (PARP-1) and p53 independently function in regulating double-strand break repair in primate cells.Nucleic acids research · 2004Article
- Oil A induces apoptosis of pancreatic cancer cells via caspase activation, redistribution of cell cycle and GADD expression.World journal of gastroenterology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose) polymerase (PARP), which is activated by DNA strand breaks, is involved in DNA repair and replication but, during apoptosis, undergoes early caspase-mediated cleavage. Activation of programmed cell death in response to DNA damage may rely on functional p53 protein. Tumor cells are commonly deficient in this oncogene product resulting in resistance to many cytostatic drugs. Here we report that nicotinamide-induced inhibition of poly(ADP-ribosyl)ation and cytokine-induced nitric oxide production both result in a transient increase in p53 levels in pancreatic tumor RINm5F cells. These treatments also induce disruption of the mitochondrial membrane potential (delta psi(m)), as revealed using the mitochondrial probe JC-1, followed by PARP cleavage and apoptosis all of which are inhibited by the anti-apoptotic protein Bcl-2. Moreover, PARP-inhibition by nicotinamide or 3-aminobenzamide induces apoptosis and/or cell cycle arrest at the G2 checkpoint in all of four tested tumor cell lines of both mesenchymal and epithelial origin including mouse NIH-3T3 cells and p53 deficient human HeLa and Jurkat cells. Bcl-2 counteracts cytokine-, but not nicotinamide-induced G2 arrest. These findings indicate that both chemical and caspase-mediated inhibition of PARP activity, possibly by interfering with DNA replication and repair, may promote a p53-independent G2 arrest and apoptosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.