Ignet

Gene Information

Gene symbol: TOP1

Gene name: topoisomerase (DNA) I

HGNC ID: 11986

Related Genes

#	Gene Symbol	Number of hits
1	ASNS	1 hits
2	C4A	1 hits
3	CASP3	1 hits
4	CDC73	1 hits
5	COL1A1	1 hits
6	CSF1	1 hits
7	CSF2	1 hits
8	CYP21A2	1 hits
9	HLA-A	1 hits
10	PARP1	1 hits
11	TIPARP	1 hits
12	TOP2A	1 hits
13	TYMS	1 hits

Related Sentences

#	PMID	Sentence
1	1327851	As a partial test of the hypothesis that the WS phenotype is due to a defect in DNA topoisomerase I (topo I) or DNA topoisomerase II (topo II) we exposed lymphoid cells from a healthy control to the topo I inhibitor camptothecin or to the topo II inhibitor 4'-(9-acridinylamino)methanesulfon-m-anisidine.
2	1750798	In this respect it has been suggested that the 5' flanking DNA of dermal collagen genes is particularly susceptible to the action of Scl-70 (topoisomerase I).
3	1750798	The association of autoantibodies with topoisomerase I provides a tentative link between the MHC and collagen gene expression.
4	1750798	For insulin dependent diabetes mellitus it has been shown that the MHC determined susceptibility to the disease is conferred by neutral residues (Val, Ser, Ala), at position 57 of the DQ beta chain, while Asp at this position correlates with resistance.
5	1750798	In this respect it has been suggested that the 5' flanking DNA of dermal collagen genes is particularly susceptible to the action of Scl-70 (topoisomerase I).
6	1750798	The association of autoantibodies with topoisomerase I provides a tentative link between the MHC and collagen gene expression.
7	1750798	For insulin dependent diabetes mellitus it has been shown that the MHC determined susceptibility to the disease is conferred by neutral residues (Val, Ser, Ala), at position 57 of the DQ beta chain, while Asp at this position correlates with resistance.
8	11264156	We conducted a phase II randomized trial of recombinant granculocyte-macrophage colony-stimulating factor (GM-CSF) administered before topotecan chemotherapy to determine whether it could prevent myelosuppression and to determine the antitumor activity of this topoisomerase I inhibitor in 53 patients with metastatic malignant melanoma and renal cell cancer.
9	15286835	Deficiencies in C4 allotypes have been associated with Mycobacterium leprae infection, erythema nodosum, systemic sclerosis with anti-topoisomerase I antibodies, intermediate congenital adrenal hyperplasia with DR5 genotype, diabetes mellitus type 1 with DR3,4 genotype, and diabetes mellitus with antibodies against islet cells.
10	15286835	Some reports associate C4A with thyroiditis after delivery as well as limited and systemic sclerosis without anti-topoisomerase I antibodies.
11	15286835	Deficiencies in C4 allotypes have been associated with Mycobacterium leprae infection, erythema nodosum, systemic sclerosis with anti-topoisomerase I antibodies, intermediate congenital adrenal hyperplasia with DR5 genotype, diabetes mellitus type 1 with DR3,4 genotype, and diabetes mellitus with antibodies against islet cells.
12	15286835	Some reports associate C4A with thyroiditis after delivery as well as limited and systemic sclerosis without anti-topoisomerase I antibodies.
13	16010439	Increased anticancer activity of the thymidylate synthase inhibitor BGC9331 combined with the topoisomerase I inhibitor SN-38 in human colorectal and breast cancer cells: induction of apoptosis and ROCK cleavage through caspase-3-dependent and -independent mechanisms.
14	16010439	Both drugs also augmented the proteolytic cleavage of the Rho-kinase ROCK-1 that was attenuated by the caspase-3 pathway inhibitor z-DEVD-fmk.
15	17314275	Human parafibromin binds to RNA polymerase II as part of a PAF1 transcriptional regulatory complex.
16	17314275	Because the subcellular localization of parafibromin is likely to be critical for its function with the nuclear PAF1 complex, we sought to experimentally define the nuclear localization signal (NLS) of parafibromin and examine its potential role in parafibromin function.
17	17314275	The NLS-mutant parafibromin is significantly impaired in its association with endogenous Paf1 and Leo1.
18	17314275	Inhibition of endogenous parafibromin expression by RNA interference inhibits the basal rate of apoptosis and apoptosis resulting from DNA damage induced by camptothecin, a topoisomerase I inhibitor.
19	17875716	In those clones, Top1 is reduced approximately 5-fold and Top2alpha compensates for Top1 deficiency.
20	17875716	Among them, asparagine synthetase (ASNS) expression was reduced in siTop1 cells and in cells with transient Top1 down-regulation.
21	17875716	Conversely, Top1 complementation increased ASNS, indicating a causal link between Top1 and ASNS expression.
22	17875716	In those clones, Top1 is reduced approximately 5-fold and Top2alpha compensates for Top1 deficiency.
23	17875716	Among them, asparagine synthetase (ASNS) expression was reduced in siTop1 cells and in cells with transient Top1 down-regulation.
24	17875716	Conversely, Top1 complementation increased ASNS, indicating a causal link between Top1 and ASNS expression.
25	17875716	In those clones, Top1 is reduced approximately 5-fold and Top2alpha compensates for Top1 deficiency.
26	17875716	Among them, asparagine synthetase (ASNS) expression was reduced in siTop1 cells and in cells with transient Top1 down-regulation.
27	17875716	Conversely, Top1 complementation increased ASNS, indicating a causal link between Top1 and ASNS expression.
28	19362586	PARP-1, the best characterized member of the PARP family, which currently comprises 18 members, is an abundant nuclear enzyme implicated in cellular responses to DNA injury provoked by genotoxic stress.
29	19362586	PARP-1 is essential to the repair of DNA single-strand breaks via the base excision repair pathway.
30	19362586	Inhibitors of PARP-1 have been shown to enhance the cytotoxic effects of ionizing radiation and DNA-damaging chemotherapy agents, such as the methylating agents and topoisomerase I inhibitors.
31	19362586	Recent in vitro and in vivo evidence suggests that PARP inhibitors could be used not only as chemo/radiotherapy sensitizers, but also as single agents to selectively kill cancers defective in DNA repair, specifically cancers with mutations in the breast cancer-associated genes (BRCA1 and BRCA2).