Evidence map›Paper›PMID 17997992›Full record

ArticleFree radical biology & medicine2008

Niacin restriction upregulates NADPH oxidase and reactive oxygen species (ROS) in human keratinocytes.

Claudia A Benavente, Elaine L Jacobson

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 65 citations in OpenAlex.

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  10. Metabolome-Wide Association Study of Deployment to Balad, Iraq or Bagram, Afghanistan.Journal of occupational and environmental medicine · 2019
    Article
  11. Role of Nicotinamide in Genomic Stability and Skin Cancer Chemoprevention.International journal of molecular sciences · 2019
    Review
  12. Review
  13. Diverse therapeutic efficacies and more diverse mechanisms of nicotinamide.Metabolomics : Official journal of the Metabolomic Society · 2019
    Review
  14. Article
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  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Claudia A BenaventeArizona Cancer Center, University of Arizona, Tucson, AZ 85724, USA.
Elaine L Jacobson
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
VITAMIN A, AND ITS PRECURSORS AND DERIVATIVES AS THERAPEUTIC MODALITIESP01CA027502 · NCI · UNIVERSITY OF ARIZONA · PI EINSPAHR, JANINE G · 1985 to 2015
$36.3M
ALTERATION OF NAD METABOLISM BY CHEMICAL CARCINOGENSR01CA043894 · NCI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI JACOBSON, MYRON K · 1986 to 2008
$2.8M
Endogenous photosensitizers in skin carcinogenesisR01CA106677 · NCI · UNIVERSITY OF ARIZONA · PI JACOBSON, ELAINE L · 2005 to 2009
$1.6M
NCI NIH HHS CA106677NCI NIH HHS CA27502NCI NIH HHS CA43894NCI NIH HHS P01 CA027502NCI NIH HHS P30 CA023074NCI NIH HHS R01 CA043894NCI NIH HHS R01 CA106677NIEHS NIH HHS ES06694NIEHS NIH HHS P30 ES006694
6 · The paper itself

Abstract

NAD(+) is a substrate for many enzymes, including poly(ADP-ribose) polymerases and sirtuins, which are involved in fundamental cellular processes including DNA repair, stress responses, signaling, transcription, apoptosis, metabolism, differentiation, chromatin structure, and life span. Because these molecular processes are important early in cancer development, we developed a model to identify critical NAD-dependent pathways potentially important in early skin carcinogenesis. Removal of niacin from the cell culture medium allowed control of intracellular NAD. Unlike many nonimmortalized human cells, HaCaT keratinocytes, which are immortalized and have a mutant p53 and aberrant NF-kB activity, become severely NAD depleted but divide indefinitely under these conditions. Niacin-deficient HaCaTs develop a decreased growth rate due to an increase in apoptotic cells and an arrest in the G(2)/M phase of the cell cycle. Long-term survival mechanisms in niacin-deficient HaCats involve accumulation of reactive oxygen species and increased DNA damage. These alterations result, at least in part, from increased expression and activity of NADPH oxidase, whose downstream effects can be reversed by nicotinamide or NADPH oxidase inhibitors. Our data support the hypothesis that glutamine is a likely alternative energy source during niacin deficiency and we suggest a model for NADPH generation important in ROS production.

Indexed as

Cell CycleCell ProliferationCells, CulturedDNA DamageGlutaminaseHumansKeratinocytesNADNADPH OxidasesNiacinOxidation-ReductionReactive Oxygen SpeciesSignal TransductionSkin NeoplasmsUp-RegulationGlutaminaseNADNADPH OxidasesNiacinReactive Oxygen Species

Identifiers

PMID17997992
PMCPMC2323356
OpenAlexW1988505861

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.