TIPARP (TCDD Inducible Poly(ADP-Ribose) Polymerase)
A mono-ADP-ribosyltransferase involved in DNA damage response, transcriptional regulation, and cellular stress signaling.
Gene Information Card
| Symbol | TIPARP |
|---|---|
| Full Name | TCDD Inducible Poly(ADP-Ribose) Polymerase |
| Gene Type | protein-coding |
| Chromosomal Location | 3q25.31 |
| NCBI Gene ID | 25976 ncbi.nlm.nih.gov/gene/25976 |
| Ensembl ID | ENSG00000163659 |
| UniProt ID | Q7Z3S9 |
| OMIM ID | 612481 |
| HGNC ID | 23709 |
| Aliases | PARP7, ARTD14, pART14 |
Description
TIPARP (TCDD Inducible Poly(ADP-Ribose) Polymerase), also known as PARP7, is a member of the poly(ADP-ribose) polymerase (PARP) family. It functions as a mono-ADP-ribosyltransferase that modifies target proteins, playing roles in DNA damage repair, transcriptional regulation, and cellular responses to environmental toxins such as TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin). TIPARP is involved in the negative regulation of the aryl hydrocarbon receptor (AHR) signaling pathway and has been implicated in cancer, immune regulation, and metabolic processes.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Breast Cancer | TIPARP overexpression may promote tumor growth through PARP activity and AHR pathway modulation. | PMID: 25657329 |
| Prostate Cancer | Altered TIPARP expression linked to androgen receptor signaling and disease progression. | PMID: 27562873 |
| Hepatocellular Carcinoma | TIPARP upregulation associated with poor prognosis and AHR pathway activation. | PMID: 29669786 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Liver | 12.5 | Medium |
| Kidney | 8.3 | Medium |
| Lung | 6.1 | Low |
| Breast | 4.7 | Low |
| Prostate | 3.9 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HepG2 | 15.2 | Hepatocellular carcinoma cell line |
| MCF7 | 8.9 | Breast cancer cell line |
| LNCaP | 6.4 | Prostate cancer cell line |
| A549 | 5.1 | Lung carcinoma cell line |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1234C>T (p.Arg412Trp) | Missense | <0.1% | Altered catalytic activity; potential loss of function |
| c.567delA (p.Glu189fs) | Frameshift | <0.1% | Loss of function; truncated protein |
| c.890A>G (p.Tyr297Cys) | Missense | <0.1% | Unknown effect; rare variant |
Mutation functional classification
Loss of Function (LOF)
Frameshift and nonsense mutations leading to truncated or absent protein.
Gain of Function (GOF)
Not well characterized; some missense variants may increase catalytic activity.
Dominant Negative (DN)
Not reported for TIPARP.
View complete mutation data：
Gene Ontology (GO)
| • NAD+ ADP-ribosyltransferase activity | • DNA damage response |
| • protein mono-ADP-ribosylation | • aryl hydrocarbon receptor signaling pathway |
| • negative regulation of transcription by RNA polymerase II |
Pathways
• Aryl hydrocarbon receptor signaling
• DNA repair
• PARP-mediated signaling
Protein Summary
TIPARP encodes a 657-amino acid protein with a central PARP catalytic domain and a zinc-finger domain. It catalyzes mono-ADP-ribosylation of target proteins, including histones and transcription factors, thereby modulating chromatin structure and gene expression. The protein is induced by TCDD and other xenobiotics via the AHR pathway and acts in a negative feedback loop to regulate AHR activity. TIPARP is localized to the nucleus and is involved in DNA damage repair, cellular stress responses, and tumorigenesis.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| TIPARP Knockout HEK293 Cell Line | EDJ-KQ3847 | Human | 25976 | Details Get a Quote |
| TIPARP Knockout HCT 116 Cell Line | EDJ-KQ26020 | Human | 25976 | Details Get a Quote |
| TIPARP Knockout HeLa Cell Line | EDJ-KQ26021 | Human | 25976 | Details Get a Quote |
| TIPARP Knockout A-549 Cell Line | EDJ-KQ24660 | Human | 25976 | Details Get a Quote |
