Summary of PARP1
The PARP1 gene codes for an enzyme (PARP1) that is activated whenever your body detects DNA damage in its cells. This enzyme then binds to the damaged DNA to “mark” it so that other natural repair processes can come in and start fixing the damage [R, R, R].
Although being able to repair your DNA is obviously a good thing, there’s a catch: PARP1 activation also triggers your body’s inflammatory response [R, R, R].
The trade-off between DNA repair and increased inflammation means that your levels of the PARP1 enzyme have to be held in a delicate balance to ensure optimal health. Too little of it, and your body and brain will be more susceptible to common forms of cellular DNA damage, such as oxidative stress – but too much of it, and you will be more likely to experience chronic inflammation.
Some SNPs in the PARP1 gene, such as rs7515023, have been associated with overall cognitive ability -- most likely because they determine how vulnerable your brain is to oxidative stress and inflammation ('T' = better, 'C' = worse) [R].
>>> This gene is featured in SelfDecode's Cognitive Function DNA Wellness Report, along with 44 other key intelligence-related genes.
The Function of PARP1
Involved in the base excision repair (BER) pathway, by catalyzing the poly(ADP-ribosyl)ation of a limited number of acceptor proteins involved in chromatin architecture and in DNA metabolism. This modification follows DNA damages and appears as an obligatory step in a detection/signaling pathway leading to the reparation of DNA strand breaks (PubMed:17177976, PubMed:18172500, PubMed:19344625, PubMed:19661379, PubMed:23230272). Mediates the poly(ADP-ribosyl)ation of APLF and CHFR (PubMed:17396150). Positively regulates the transcription of MTUS1 and negatively regulates the transcription of MTUS2/TIP150. With EEF1A1 and TXK, forms a complex that acts as a T-helper 1 (Th1) cell-specific transcription factor and binds the promoter of IFN-gamma to directly regulate its transcription, and is thus involved importantly in Th1 cytokine production (PubMed:17177976). Required for PARP9 and DTX3L recruitment to DNA damage sites (PubMed:23230272). PARP1-dependent PARP9-DTX3L-mediated ubiquitination promotes the rapid and specific recruitment of 53BP1/TP53BP1, UIMC1/RAP80, and BRCA1 to DNA damage sites (PubMed:23230272). Mediates the poly(ADP-ribosyl)ation of histones in a HPF1-dependent manner (PubMed:27067600). Involved in the synthesis of ATP in the nucleus, together with NMNAT1, PARG and NUDT5 (PubMed:27257257). Nuclear ATP generation is required for extensive chromatin remodeling events that are energy-consuming (PubMed:27257257).
Protein names
Recommended name:
Poly [ADP-ribose] polymerase 1Short name:
ARTD1Alternative name(s):
PARP-1ADP-ribosyltransferase diphtheria toxin-like 1
NAD(+
ADPRT 1
Poly[ADP-ribose] synthase 1
- RS1136410 (PARP1) ??
- RS1805414 (PARP1) ??
- RS3219090 (PARP1) ??
- RS7515023 (PARP1) ??
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Top Gene-Substance Interactions
PARP1 Interacts with These Diseases
| Disease | Score |
Substances That Increase PARP1
| Substances | Interaction | Organism | Category |
Substances That Decrease PARP1
| Substances | Interaction | Organism | Category |
Advanced Summary
The PARP1 gene codes for an enzyme (PARP1) that is activated whenever your body detects DNA damage in its cells. This enzyme then binds to the damaged DNA to “mark” it so that other natural repair processes can come in and start fixing the damage [R, R, R].
Although being able to repair your DNA is obviously a good thing, there’s a catch: PARP1 activation also triggers your body’s inflammatory response [R, R, R].
The trade-off between DNA repair and increased inflammation means that your levels of the PARP1 enzyme have to be held in a delicate balance to ensure optimal health. Too little of it, and your body and brain will be more susceptible to common forms of cellular DNA damage, such as oxidative stress – but too much of it, and you will be more likely to experience chronic inflammation.
Some SNPs in the PARP1 gene, such as rs7515023, have been associated with overall cognitive ability -- most likely because they determine how vulnerable your brain is to oxidative stress and inflammation ('T' = better, 'C' = worse) [R].
>>> This gene is featured in SelfDecode's Cognitive Function DNA Wellness Report, along with 44 other key intelligence-related genes.
Conditions with Increased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
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Conditions with Decreased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
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Technical
The following transcription factors affect gene expression:
Gene Pathways:
Molecular Function:
- Dna Binding
- Dna Ligase (Atp) Activity
- Enzyme Binding
- Nad+ Adp-Ribosyltransferase Activity
- Nad Binding
- Poly(A) Rna Binding
- Protein Kinase Binding
- Protein N-Terminus Binding
- Transcription Factor Binding
- Zinc Ion Binding
- Identical Protein Binding
Biological Processes:
- Atp Generation From Poly-Adp-D-Ribose
- Cellular Response To Beta-Amyloid
- Cellular Response To Dna Damage Stimulus
- Cellular Response To Insulin Stimulus
- Cellular Response To Oxidative Stress
- Cellular Response To Zinc Ion
- Dna Damage Response, Detection Of Dna Damage
- Dna Ligation Involved In Dna Repair
- Dna Repair
- Double-Strand Break Repair
- Double-Strand Break Repair Via Homologous Recombination
- Global Genome Nucleotide-Excision Repair
- Lagging Strand Elongation
- Macrophage Differentiation
- Mitochondrial Dna Metabolic Process
- Mitochondrial Dna Repair
- Mitochondrion Organization
- Negative Regulation Of Atp Biosynthetic Process
- Negative Regulation Of Telomere Maintenance Via Telomere Lengthening
- Negative Regulation Of Transcription From Rna Polymerase Ii Promoter
- Nucleotide-Excision Repair, Dna Damage Recognition
- Nucleotide-Excision Repair, Dna Duplex Unwinding
- Nucleotide-Excision Repair, Dna Incision
- Nucleotide-Excision Repair, Dna Incision, 3'-To Lesion
- Nucleotide-Excision Repair, Dna Incision, 5'-To Lesion
- Nucleotide-Excision Repair, Preincision Complex Assembly
- Nucleotide-Excision Repair, Preincision Complex Stabilization
- Positive Regulation Of Cardiac Muscle Hypertrophy
- Positive Regulation Of Intracellular Estrogen Receptor Signaling Pathway
- Positive Regulation Of Mitochondrial Depolarization
- Positive Regulation Of Myofibroblast Differentiation
- Positive Regulation Of Neuron Death
- Positive Regulation Of Smad Protein Import Into Nucleus
- Positive Regulation Of Transcription From Rna Polymerase Ii Promoter
- Positive Regulation Of Transcription Regulatory Region Dna Binding
- Protein Adp-Ribosylation
- Protein Autoprocessing
- Protein Modification Process
- Protein Poly-Adp-Ribosylation
- Protein Sumoylation
- Regulation Of Cellular Protein Localization
- Regulation Of Dna Methylation
- Regulation Of Oxidative Stress-Induced Neuron Intrinsic Apoptotic Signaling Pathway
- Regulation Of Smad Protein Complex Assembly
- Response To Aldosterone
- Response To Gamma Radiation
- Signal Transduction Involved In Regulation Of Gene Expression
- Transcription From Rna Polymerase Ii Promoter
- Transforming Growth Factor Beta Receptor Signaling Pathway
Drug Bank:
- Nicotinamide
- Olaparib