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Gene Information

Gene symbol: TIPARP

Gene name: TCDD-inducible poly(ADP-ribose) polymerase

HGNC ID: 23696

Synonyms: DKFZP434J214, DKFZp686N0351, DDF1, PARP7, PARP-7, PARP-1, pART14, RM1

Related Genes

# Gene Symbol Number of hits
1 ATM 1 hits
2 BRCA1 1 hits
3 BRCA2 1 hits
4 BRD4 1 hits
5 DCLRE1A 1 hits
6 ERCC1 1 hits
7 EXO1 1 hits
8 FANCA 1 hits
9 FOXM1 1 hits
10 MSH2 1 hits
11 PALB2 1 hits
12 PARP1 1 hits
13 PARP2 1 hits
14 RAD51C 1 hits
15 XPA 1 hits

Related Sentences

# PMID Sentence
1 33637776 BKM120 sensitizes BRCA-proficient triple negative breast cancer cells to olaparib through regulating FOXM1 and Exo1 expression.
2 33637776 BKM120 sensitizes BRCA-proficient triple negative breast cancer cells to olaparib through regulating FOXM1 and Exo1 expression.
3 33637776 Poly (ADP-ribose) polymerase (PARP) inhibitors offer a significant clinical benefit for triple-negative breast cancers (TNBCs) with BRCA1/2 mutation.
4 33637776 Poly (ADP-ribose) polymerase (PARP) inhibitors offer a significant clinical benefit for triple-negative breast cancers (TNBCs) with BRCA1/2 mutation.
5 33637776 Phosphoinositide 3-kinase (PI3K) inhibition sensitizes BRCA-proficient TNBC to PARP inhibition, which broadens the indication of PARP inhibitors.
6 33637776 Phosphoinositide 3-kinase (PI3K) inhibition sensitizes BRCA-proficient TNBC to PARP inhibition, which broadens the indication of PARP inhibitors.
7 33637776 Previously researches have reported that PI3K inhibition induced the defect of homologous recombination (HR) mediated repair by downregulating the expression of BRCA1/2 and Rad51.
8 33637776 Previously researches have reported that PI3K inhibition induced the defect of homologous recombination (HR) mediated repair by downregulating the expression of BRCA1/2 and Rad51.
9 33637776 Herein, we focused on DNA damage, DNA single-strand breaks (SSBs) repair and DNA double-strand breaks (DSBs) repair three aspects to investigate the mechanism of dual PI3K and PARP inhibition in DNA damage response.
10 33637776 Herein, we focused on DNA damage, DNA single-strand breaks (SSBs) repair and DNA double-strand breaks (DSBs) repair three aspects to investigate the mechanism of dual PI3K and PARP inhibition in DNA damage response.
11 33637776 We found that dual PI3K and PARP inhibition with BKM120 and olaparib significantly reduced the proliferation of BRCA-proficient TNBC cell lines MDA-MB-231 and MDA231-LM2.
12 33637776 We found that dual PI3K and PARP inhibition with BKM120 and olaparib significantly reduced the proliferation of BRCA-proficient TNBC cell lines MDA-MB-231 and MDA231-LM2.
13 33637776 Olaparib resulted in concomitant gain of PARP1, forkhead box M1 (FOXM1) and Exonuclease 1 (Exo1) while inhibited the activity of PARP.
14 33637776 Olaparib resulted in concomitant gain of PARP1, forkhead box M1 (FOXM1) and Exonuclease 1 (Exo1) while inhibited the activity of PARP.
15 33637776 BKM120 downregulated the expression of PARP1 and PARP2 to assist olaparib in blocking PARP mediated repair of DNA SSBs.
16 33637776 BKM120 downregulated the expression of PARP1 and PARP2 to assist olaparib in blocking PARP mediated repair of DNA SSBs.
17 33637776 Meanwhile, BKM120 inhibited the expression of BRAC1/2 and Rad51/52 to block HR mediated repair through the PI3K/Akt/NFκB/c-Myc signaling pathway and PI3K/Akt/ FOXM1/Exo1 signaling pathway.
18 33637776 Meanwhile, BKM120 inhibited the expression of BRAC1/2 and Rad51/52 to block HR mediated repair through the PI3K/Akt/NFκB/c-Myc signaling pathway and PI3K/Akt/ FOXM1/Exo1 signaling pathway.
19 33637776 FOXM1 and Exo1 are novel therapeutic targets that serves important roles in DNA damage response.
20 33637776 FOXM1 and Exo1 are novel therapeutic targets that serves important roles in DNA damage response.
21 34813314 Discovery of Potent and Novel Dual PARP/BRD4 Inhibitors for Efficient Treatment of Pancreatic Cancer.
22 34813314 Discovery of Potent and Novel Dual PARP/BRD4 Inhibitors for Efficient Treatment of Pancreatic Cancer.
23 34813314 Discovery of Potent and Novel Dual PARP/BRD4 Inhibitors for Efficient Treatment of Pancreatic Cancer.
24 34813314 Targeting poly(ADP-ribose) polymerase1/2 (PARP1/2) is a promising strategy for the treatment of pancreatic cancer with breast cancer susceptibility gene (BRCA) mutation.
25 34813314 Targeting poly(ADP-ribose) polymerase1/2 (PARP1/2) is a promising strategy for the treatment of pancreatic cancer with breast cancer susceptibility gene (BRCA) mutation.
26 34813314 Targeting poly(ADP-ribose) polymerase1/2 (PARP1/2) is a promising strategy for the treatment of pancreatic cancer with breast cancer susceptibility gene (BRCA) mutation.
27 34813314 Inducing the deficiency of homologous recombination (HR) repair is an effective way to broaden the indication of PARP1/2 inhibitor for more patients with pancreatic cancer.
28 34813314 Inducing the deficiency of homologous recombination (HR) repair is an effective way to broaden the indication of PARP1/2 inhibitor for more patients with pancreatic cancer.
29 34813314 Inducing the deficiency of homologous recombination (HR) repair is an effective way to broaden the indication of PARP1/2 inhibitor for more patients with pancreatic cancer.
30 34813314 Bromodomain-containing protein 4 (BRD4) repression has been reported to elevate HR deficiency.
31 34813314 Bromodomain-containing protein 4 (BRD4) repression has been reported to elevate HR deficiency.
32 34813314 Bromodomain-containing protein 4 (BRD4) repression has been reported to elevate HR deficiency.
33 34813314 Therefore, we designed, synthetized, and optimized a dual PARP/BRD4 inhibitor <b>III</b>-<b>16</b>, with a completely new structure and high selectivity against PARP1/2 and BRD4.
34 34813314 Therefore, we designed, synthetized, and optimized a dual PARP/BRD4 inhibitor <b>III</b>-<b>16</b>, with a completely new structure and high selectivity against PARP1/2 and BRD4.
35 34813314 Therefore, we designed, synthetized, and optimized a dual PARP/BRD4 inhibitor <b>III</b>-<b>16</b>, with a completely new structure and high selectivity against PARP1/2 and BRD4.
36 34813314 The advantages of <b>III</b>-<b>16</b> over Olaparib suggest that dual PARP/BRD4 inhibitors are novel and promising agents for the treatment of advanced pancreatic cancer.
37 34813314 The advantages of <b>III</b>-<b>16</b> over Olaparib suggest that dual PARP/BRD4 inhibitors are novel and promising agents for the treatment of advanced pancreatic cancer.
38 34813314 The advantages of <b>III</b>-<b>16</b> over Olaparib suggest that dual PARP/BRD4 inhibitors are novel and promising agents for the treatment of advanced pancreatic cancer.
39 35293552 The following genes were selected: BRCA1, PALB2, RAD51C, BRCA2, ATM, FANCA, MSH2, XPA, ERCC1, PARP1, and SNM1.
40 35293552 The following genes were selected: BRCA1, PALB2, RAD51C, BRCA2, ATM, FANCA, MSH2, XPA, ERCC1, PARP1, and SNM1.
41 35293552 The DNA expression of 2 genes assessed in pre-NACT biopsies (PALB2 and ERCC1) was lower in pCR than in non-pCR patients (P=0.005 and P=0.009, respectively).
42 35293552 The DNA expression of 2 genes assessed in pre-NACT biopsies (PALB2 and ERCC1) was lower in pCR than in non-pCR patients (P=0.005 and P=0.009, respectively).
43 35293552 The genes BRCA2 (P=0.009), ATM (P=0.004), FANCA (P=0.001), and PARP1 (P=0.011) showed a lower expression in post-NACT residual tumor samples (n=32) than in pre-NACT biopsy samples (n=98).
44 35293552 The genes BRCA2 (P=0.009), ATM (P=0.004), FANCA (P=0.001), and PARP1 (P=0.011) showed a lower expression in post-NACT residual tumor samples (n=32) than in pre-NACT biopsy samples (n=98).
45 35293552 The expression of 2 genes (PALB2 and ERCC1) was lower in pCR patients.
46 35293552 The expression of 2 genes (PALB2 and ERCC1) was lower in pCR patients.