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Literature summary for 2.7.7.1 extracted from

  • Pan, L.Z.; Ahn, D.G.; Sharif, T.; Clements, D.; Gujar, S.A.; Lee, P.W.
    The NAD+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) is a p53 downstream target (2014), Cell Cycle, 13, 1041-1048.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
gene NMNAT2, semi-quantitative and real-time PCR enzyme expression analysis Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information H1299 human non-small lung cancer cell line, which lacks expression of endogenous p53 due to homozygous partial deletion of the p53 gene, is used to construct a stable cell line expressing wild-type p53 under the control of doxycycline. mRNA levels of NAD+ synthetic enzymes, including NAMPT, NMNAT1, NMNAT2, and NMNAT3, are compared in the presence or absence of p53 by semi-quantitative PCR: only the NMNAT2 mRNA level is significantly elevated by ectopic p53 expression. Although genes NMNAT1 and NMNAT3 are also induced, their expression levels are significantly lower than those of NMNAT?2 Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
Golgi apparatus
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Homo sapiens 5794
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Organism

Organism UniProt Comment Textmining
Homo sapiens Q9BZQ4 gene NMNAT2
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Source Tissue

Source Tissue Comment Organism Textmining
colon cancer cell
-
Homo sapiens
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H-1299 cell
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Homo sapiens
-
HCT-116 cell
-
Homo sapiens
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non-small cell lung cancer cell
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Homo sapiens
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U2-OS cell
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Homo sapiens
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Synonyms

Synonyms Comment Organism
nicotinamide mononucleotide adenylyltransferase 2
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Homo sapiens
NMNAT-2
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Homo sapiens

Expression

Organism Comment Expression
Homo sapiens NMNAT-2 expression is induced upon DNA damage in a p53-dependent manner. Two putative p53 binding sites are identified within the human NMNAT-2 gene, and both are functional in a p53-dependent manner, overview. DNA damage agents, actinomycin D and doxorubicin, and Nutlin-3a, a p53 stabilizer that disrupts interaction of p53 with its negative regulator MDM2, in a time-dependent manner in control but not in p53-knockdown U2-OS cells up

General Information

General Information Comment Organism
malfunction knockdown of NMNAT-2 significantly reduces cellular NAD+ levels and protects cells from p53-dependent cell death upon DNA damage. p53 knockdown abolishes NMNAT-2 expression upon actinomycin D treatment. In NMNAT-2-knockdown cells, actinomycin D treatment does not result in enhanced immunoreactivity Homo sapiens
metabolism gene expression of NAD+ synthesizing enzymes in the NAD+ salvage pathways can be modulated by p53 Homo sapiens
physiological function the enzyme is a target for the tumor suppressor p53, a major player in cancer signaling pathways, that is an important regulator of cellular metabolism. Determination of an important functional role of NMNAT-2 in p53-mediated signaling. Enzyme NMNAT-2 plays an important role in p53-mediated cell death upon DNA damage Homo sapiens