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
- Nad+ Adp-Ribosyltransferase Activity
- Transcription Factor Binding
- Zinc Ion Binding
- Enzyme Binding
- Protein Kinase Binding
- Identical Protein Binding
- Poly(A) Rna Binding
- Protein N-Terminus Binding
- Nad Binding
Biological Processes:
- Negative Regulation Of Transcription From Rna Polymerase Ii Promoter
- Nucleotide-Excision Repair, Dna Damage Recognition
- Nucleotide-Excision Repair, Dna Duplex Unwinding
- Double-Strand Break Repair Via Homologous Recombination
- Dna Repair
- Nucleotide-Excision Repair, Preincision Complex Stabilization
- Nucleotide-Excision Repair, Preincision Complex Assembly
- Nucleotide-Excision Repair, Dna Incision, 3'-To Lesion
- Nucleotide-Excision Repair, Dna Incision, 5'-To Lesion
- Double-Strand Break Repair
- Transcription From Rna Polymerase Ii Promoter
- Protein Adp-Ribosylation
- Cellular Response To Dna Damage Stimulus
- Mitochondrion Organization
- Transforming Growth Factor Beta Receptor Signaling Pathway
- Response To Gamma Radiation
- Positive Regulation Of Cardiac Muscle Hypertrophy
- Regulation Of Smad Protein Complex Assembly
- Protein Autoprocessing
- Protein Sumoylation
- Signal Transduction Involved In Regulation Of Gene Expression
- Macrophage Differentiation
- Mitochondrial Dna Metabolic Process
- Cellular Response To Insulin Stimulus
- Positive Regulation Of Intracellular Estrogen Receptor Signaling Pathway
- Nucleotide-Excision Repair, Dna Incision
- Cellular Response To Oxidative Stress
- Protein Modification Process
- Dna Damage Response, Detection Of Dna Damage
- Mitochondrial Dna Repair
- Regulation Of Dna Methylation
- Positive Regulation Of Transcription From Rna Polymerase Ii Promoter
- Dna Ligation Involved In Dna Repair
- Positive Regulation Of Mitochondrial Depolarization
- Positive Regulation Of Smad Protein Import Into Nucleus
- Protein Poly-Adp-Ribosylation
- Global Genome Nucleotide-Excision Repair
- Cellular Response To Zinc Ion
- Positive Regulation Of Neuron Death
- Regulation Of Oxidative Stress-Induced Neuron Intrinsic Apoptotic Signaling Pathway
- Regulation Of Cellular Protein Localization
- Response To Aldosterone
- Negative Regulation Of Telomere Maintenance Via Telomere Lengthening
- Cellular Response To Beta-Amyloid
- Positive Regulation Of Myofibroblast Differentiation
- Atp Generation From Poly-Adp-D-Ribose
- Positive Regulation Of Transcription Regulatory Region Dna Binding
- Negative Regulation Of Atp Biosynthetic Process
- Lagging Strand Elongation
Drug Bank:
- Nicotinamide
- Olaparib