PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
34021643-4	2021	RESULTS: Here, we observed that the activity of Rad 51 is lower in SCNT eggs than in conventional IVF and found a significantly lower level of DSBs in SCNT embryos during reprogramming.	dsbs	143-147	RAD51 recombinase	Mus musculus	48-54
33864208-9	2021	RAD51 immunofluorescence eight hours post-cisplatin was positive in damaged cell types in both WT and Puma-/- mice, demonstrating induction of the homologous recombination pathway.	Cisplatin	42-51	RAD51 recombinase	Mus musculus	0-5
33792683-11	2021	In conclusion, our results showed that DNA DSBs in the fully-grown oocytes can initiate ssBIR and be amplified by Rad51 or DNA replication.	dsbs	43-47	RAD51 recombinase	Mus musculus	114-119
33507295-7	2021	Mechanistically, compared with KPT-330 alone, K+CS suppresses the expression of CRM1, Rad51, and thymidylate synthase proteins, leading to more efficient inhibition of CRM1-mediated nuclear export, impairment of DNA-damage repair, reduced pyrimidine synthesis, cell-cycle arrest in S-phase, and cell apoptosis.	k+cs	46-50	RAD51 recombinase	Mus musculus	86-91
32800233-0	2020	Chronic exposure to environmentally relevant concentration of fluoride alters Ogg1 and Rad51 expressions in mice: Involvement of epigenetic regulation.	Fluorides	62-70	RAD51 recombinase	Mus musculus	87-92
32800233-2	2020	In the present study, we assessed F induced oxidative stress through monitoring biochemical parameters and looked into the effect of chronic F exposure on two crucial DNA repair genes Ogg1 and Rad51 having important role against ROS induced DNA damages.	ros	229-232	RAD51 recombinase	Mus musculus	193-198
32709853-3	2020	We found that DAG produced replication-dependent DNA lesions decorated with RPA32, RAD51, and gammaH2AX foci.	Dianhydrogalactitol	14-17	RAD51 recombinase	Mus musculus	83-88
32644042-4	2020	Further mechanistic studies indicate that farrerol functions through stimulating the recruitment of RAD51 to DSB sites.	farrerol	42-50	RAD51 recombinase	Mus musculus	100-105
32393889-2	2020	Through insertion of a non-sequence-specific single-stranded DNA-binding domain from Rad51 protein between Cas9 nickase and the deaminases, serial hyper cytidine base editors were generated with substantially increased activity and an expanded editing window towards the protospacer adjacent motif in both cell lines and mouse embryos.	Cytidine	153-161	RAD51 recombinase	Mus musculus	85-90
32460033-0	2020	Meiosis-Specific C19orf57/4930432K21Rik/BRME1 Modulates Localization of RAD51 and DMC1 to DSBs in Mouse Meiotic Recombination.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	90-94	RAD51 recombinase	Mus musculus	72-77
32079355-3	2020	Quantitative high-performance liquid chromatography analysis reveals that RECA contains a significantly high proportion of glycosides than the aglycones with madecassoside as the highest component, followed by asiaticoside.	Glycosides	123-133	RAD51 recombinase	Mus musculus	74-78
32079355-3	2020	Quantitative high-performance liquid chromatography analysis reveals that RECA contains a significantly high proportion of glycosides than the aglycones with madecassoside as the highest component, followed by asiaticoside.	madecassoside	158-171	RAD51 recombinase	Mus musculus	74-78
32079355-3	2020	Quantitative high-performance liquid chromatography analysis reveals that RECA contains a significantly high proportion of glycosides than the aglycones with madecassoside as the highest component, followed by asiaticoside.	asiaticoside	210-222	RAD51 recombinase	Mus musculus	74-78
31844045-6	2019	Consistent with the role of RAD51 in fork regression, ATAD5 depletion inhibits slowdown of fork progression and native 5-bromo-2"-deoxyuridine signal induced by hydroxyurea.	Hydroxyurea	161-172	RAD51 recombinase	Mus musculus	28-33
30930246-3	2019	Pharmacological targeting of SCD1 is particularly toxic due to the accumulation of saturated fatty acids, which exacerbates ER stress, triggers apoptosis, impairs RAD51-mediated DNA repair, and achieves a remarkable therapeutic outcome with 25%-100% cure rate in xenograft mouse models.	Fatty Acids	83-104	RAD51 recombinase	Mus musculus	163-168
30773277-6	2019	Moreover, functional studies revealed increased amounts of spontaneous replication fork stalling and chromosomal aberrations, as well as fewer camptothecin (CPT)-induced RAD51 foci in subject-derived cell lines.	Camptothecin	143-155	RAD51 recombinase	Mus musculus	170-175
30773277-6	2019	Moreover, functional studies revealed increased amounts of spontaneous replication fork stalling and chromosomal aberrations, as well as fewer camptothecin (CPT)-induced RAD51 foci in subject-derived cell lines.	Camptothecin	157-160	RAD51 recombinase	Mus musculus	170-175
30668564-5	2019	From leptotene to early pachytene, exogenous damage triggered the massive presence of gammaH2AX throughout the nucleus, which was associated with DNA repair mediated by HR components (DMC1 and RAD51).	pachytene	24-33	RAD51 recombinase	Mus musculus	193-198
30183475-6	2019	We show that MEC1 cells, are susceptible to 4,4"-Diisothiocyano-2,2"-stilbenedisulfonic acid (DIDS), a specific RAD51 inhibitor.	4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid	44-92	RAD51 recombinase	Mus musculus	112-117
30183475-6	2019	We show that MEC1 cells, are susceptible to 4,4"-Diisothiocyano-2,2"-stilbenedisulfonic acid (DIDS), a specific RAD51 inhibitor.	4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid	94-98	RAD51 recombinase	Mus musculus	112-117
30422982-4	2018	Overexpression of RAD51 also promoted increased resistance against hydrogen peroxide treatment, while the single-knockout epimastigotes for RAD51 exhibited increased sensitivity to this oxidant agent, which indicates a role for this gene in the repair of DNA oxidative lesions.	Hydrogen Peroxide	67-84	RAD51 recombinase	Mus musculus	18-23
30422982-6	2018	Also, RAD51 single-knockout epimastigotes showed a similar growth rate to that exhibited by wild-type ones after treatment with hydroxyurea, but an increased sensitivity to methyl methane sulfonate.	Hydroxyurea	128-139	RAD51 recombinase	Mus musculus	6-11
30422982-6	2018	Also, RAD51 single-knockout epimastigotes showed a similar growth rate to that exhibited by wild-type ones after treatment with hydroxyurea, but an increased sensitivity to methyl methane sulfonate.	Methyl Methanesulfonate	173-197	RAD51 recombinase	Mus musculus	6-11
30422982-8	2018	Besides that, RAD51-overexpressing parasites infecting mice also presented increased infectivity and higher resistance against benznidazole.	benzonidazole	127-139	RAD51 recombinase	Mus musculus	14-19
29151191-6	2018	The protein expressions of ATM, CHK-2, P53, E2F1, P73, BAX, Caspase-9, and Caspase-3 were significantly increased, while expressions of RAD51 were down-regulated after SiNP exposure by days 15.	sinp	168-172	RAD51 recombinase	Mus musculus	136-141
29080451-0	2018	Curcumin sensitizes lymphoma cells to DNA damage agents through regulating Rad51-dependent homologous recombination.	Curcumin	0-8	RAD51 recombinase	Mus musculus	75-80
29080451-6	2018	In addition, curcumin decreased the expression of Rad51, which suggests curcumin induces DNA damage through regulating Rad51-dependant homologous recombination.	Curcumin	13-21	RAD51 recombinase	Mus musculus	50-55
29080451-6	2018	In addition, curcumin decreased the expression of Rad51, which suggests curcumin induces DNA damage through regulating Rad51-dependant homologous recombination.	Curcumin	13-21	RAD51 recombinase	Mus musculus	119-124
29080451-6	2018	In addition, curcumin decreased the expression of Rad51, which suggests curcumin induces DNA damage through regulating Rad51-dependant homologous recombination.	Curcumin	72-80	RAD51 recombinase	Mus musculus	50-55
29080451-6	2018	In addition, curcumin decreased the expression of Rad51, which suggests curcumin induces DNA damage through regulating Rad51-dependant homologous recombination.	Curcumin	72-80	RAD51 recombinase	Mus musculus	119-124
29080451-7	2018	Rad51-dependant homologous recombination is a vital DNA repair pathway for cancer cells to resist anti-tumoral DNA damage drugs, therefore, we studied the effect of curcumin on the sensitizing lymphoma cells to various chemotherapeutic drugs.	Curcumin	165-173	RAD51 recombinase	Mus musculus	0-5
29080451-11	2018	Taken together, these results demonstrate that curcumin induces DNA damage through regulating Rad51-dependant homologous recombination and triggers caspase3-dependent apoptosis, more importantly, curcumin sensitizes lymphoma cells to various DNA damage drugs.	Curcumin	47-55	RAD51 recombinase	Mus musculus	94-99
28846983-8	2017	At 24h after treatment, MMC induced significant increase in oxidative stress, gamma-H2AX foci and expression of RAD51 and KU80 in testicular cells.	Mitomycin	24-27	RAD51 recombinase	Mus musculus	112-117
29085508-6	2017	Western blot analysis revealed that triptolide up-regulated Rad51 and nuclear proliferating cell nuclear antigen.	triptolide	36-46	RAD51 recombinase	Mus musculus	60-65
28912486-6	2017	Interestingly, caffeine treatment inhibited the formation of Rad51 or Rad54 foci, but not the formation of gammaH2AX and Exo1 foci, which led to incomplete HR in ssDNA, thus increasing DNA damage sensitivity.	Caffeine	15-23	RAD51 recombinase	Mus musculus	61-66
28461573-7	2017	Treatment with the RAD51 inhibitor 4,4"-diisothiocyanatostilbene-2, 2"-disulfonic acid also strongly inhibited T1D development in NOD mice.	4,4"-diisothiocyanatostilbene-2, 2"-disulfonic acid	35-86	RAD51 recombinase	Mus musculus	19-24
27785022-7	2016	Apoptosis likely occurred as a consequence of DNA damage (detected as gamma-H2AX and RAD51 foci) caused by increase in reactive oxygen species associated with loss of mitochondrial membrane potential.	Reactive Oxygen Species	119-142	RAD51 recombinase	Mus musculus	85-90
27358111-9	2016	Augmented HR appears to underpin temozolomide resistance in the recurrent lines, as these cells were cross-resistant to other agents that induced replication-associated DSBs, exhibited faster resolution of damage-induced Rad51 foci, and displayed higher levels of sister chromatid exchanges (SCE).	Temozolomide	33-45	RAD51 recombinase	Mus musculus	221-226
26951384-0	2016	Endoplasmic reticulum stress-inducing drugs sensitize glioma cells to temozolomide through downregulation of MGMT, MPG, and Rad51.	Temozolomide	70-82	RAD51 recombinase	Mus musculus	124-129
26951384-3	2016	O(6)-methylguanine DNA methyltransferase (MGMT), N-methylpurine DNA glycosylase (MPG), and Rad51 are DNA damage repair proteins that mediate resistance to temozolomide in glioblastoma.	Temozolomide	155-167	RAD51 recombinase	Mus musculus	91-96
27286262-6	2016	In addition, TMZ+JLK1486 treatment caused decreased RAD51 levels, impairing DNA damage repair.	Temozolomide	13-16	RAD51 recombinase	Mus musculus	52-57
27286262-6	2016	In addition, TMZ+JLK1486 treatment caused decreased RAD51 levels, impairing DNA damage repair.	JLK 1486	17-24	RAD51 recombinase	Mus musculus	52-57
27225532-7	2016	However, the alteration of histone deacetylation and miR-193b-3p and Rad51 expression in response to LDIR was restored by pretreatment with N-acetyl-cyctein.	n-acetyl-cyctein	140-156	RAD51 recombinase	Mus musculus	69-74
26719576-8	2016	Dinaciclib abolishes ABT-888-induced BRCA1 and RAD51 foci and potentiates DNA damage, indicated by increased gammaH2AX foci.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	21-24	RAD51 recombinase	Mus musculus	47-52
30188106-0	2016	INFLUENCE OF HDAC INHIBITOR SODIUM BUTYRATE ON THE EXPRESSION OF DNA REPAIR GENES Rad51 AND XRCC5 IN mEras-Waf1+/+ AND mEras-Waf1-/-.	Butyric Acid	28-43	RAD51 recombinase	Mus musculus	82-87
30188106-5	2016	When cells were treated with DNA-damaging agent adriamycin, there was an additional accumulation of Rad51 foci in the nuclei.	Doxorubicin	48-58	RAD51 recombinase	Mus musculus	100-105
30188106-6	2016	However, sodium butyrate reduced considerably the content of Rad51 and Ku80 proteins both in mEras-Waf1+/+ and mEras-Waf1-/- cells as well as in the cells treated by adriamycin.	Butyric Acid	9-24	RAD51 recombinase	Mus musculus	61-66
30188106-6	2016	However, sodium butyrate reduced considerably the content of Rad51 and Ku80 proteins both in mEras-Waf1+/+ and mEras-Waf1-/- cells as well as in the cells treated by adriamycin.	Doxorubicin	166-176	RAD51 recombinase	Mus musculus	61-66
30188106-7	2016	RT-PCR and immunobloting data show that inhibitory effect of sodium butyrate takes place at the level of Rad51 and XRCC5 gene transcription and the content of Rad51 and Ku80 proteins.	Butyric Acid	61-76	RAD51 recombinase	Mus musculus	105-110
30188106-7	2016	RT-PCR and immunobloting data show that inhibitory effect of sodium butyrate takes place at the level of Rad51 and XRCC5 gene transcription and the content of Rad51 and Ku80 proteins.	Butyric Acid	61-76	RAD51 recombinase	Mus musculus	159-164
25677620-4	2015	Similarly, here, we show that ferulic acid reduces HR repair, inhibits RAD 51 foci formation, and accumulates gamma-H2AX in breast cancer cells.	ferulic acid	30-42	RAD51 recombinase	Mus musculus	71-77
25621047-8	2015	Although the incidence of double-strand breaks (DSBs) was increased in the olaparib-treated JF-305 cells, the RAD51 foci were well formed at the sites of gamma-H2AX recruitment, indicating an activated HR mechanism.	olaparib	75-83	RAD51 recombinase	Mus musculus	110-115
25463395-5	2015	Compared to wild-type cells, heterozygous mRad51(+/wt-GFP) embryonic stem cells showed increased sensitivity to DNA damage induced by ionizing radiation and mitomycin C.	Mitomycin	157-168	RAD51 recombinase	Mus musculus	42-48
25448685-7	2014	Ovarian ATM, XRCC6, PRKDC, RAD51 and PARP1 proteins were increased (P<0.05) by DMBA exposure in lean mice.	9,10-Dimethyl-1,2-benzanthracene	82-86	RAD51 recombinase	Mus musculus	27-32
25448685-8	2014	A blunted DMBA-induced increase (P<0.05) in XRCC6, PRKDC, RAD51 and BRCA1 was observed in ovaries from obese mice, relative to lean counterparts.	9,10-Dimethyl-1,2-benzanthracene	10-14	RAD51 recombinase	Mus musculus	61-66
25218467-8	2014	In all, the results demonstrate the utility of the Tet-On 3G system in DT40 research and underpin a model in which BRC4 role on cell proliferation and chromosome repair arises primarily from its suppressive role on RAD51 functions.	tetramethylenedisulfotetramine	51-54	RAD51 recombinase	Mus musculus	215-220
25110436-0	2014	RAD51 potentiates synergistic effects of chemotherapy with PCI-24781 and cis-diamminedichloroplatinum on gastric cancer.	abexinostat	59-68	RAD51 recombinase	Mus musculus	0-5
25110436-0	2014	RAD51 potentiates synergistic effects of chemotherapy with PCI-24781 and cis-diamminedichloroplatinum on gastric cancer.	Cisplatin	73-101	RAD51 recombinase	Mus musculus	0-5
25110436-11	2014	Depletion of RAD51 augmented the biological functions of PCI-24781, CDDP and the combination treatment, whereas overexpressing RAD51 had the opposite effects.	Cisplatin	68-72	RAD51 recombinase	Mus musculus	13-18
25110436-14	2014	CONCLUSION: These data suggest that RAD51 potentiates the synergistic effects of chemotherapy with PCI-24781 and CDDP on GC.	abexinostat	99-108	RAD51 recombinase	Mus musculus	36-41
25110436-14	2014	CONCLUSION: These data suggest that RAD51 potentiates the synergistic effects of chemotherapy with PCI-24781 and CDDP on GC.	Cisplatin	113-117	RAD51 recombinase	Mus musculus	36-41
24577941-0	2014	The use of Olaparib (AZD2281) potentiates SN-38 cytotoxicity in colon cancer cells by indirect inhibition of Rad51-mediated repair of DNA double-strand breaks.	olaparib	11-19	RAD51 recombinase	Mus musculus	109-114
24577941-0	2014	The use of Olaparib (AZD2281) potentiates SN-38 cytotoxicity in colon cancer cells by indirect inhibition of Rad51-mediated repair of DNA double-strand breaks.	olaparib	21-28	RAD51 recombinase	Mus musculus	109-114
24577941-0	2014	The use of Olaparib (AZD2281) potentiates SN-38 cytotoxicity in colon cancer cells by indirect inhibition of Rad51-mediated repair of DNA double-strand breaks.	Irinotecan	42-47	RAD51 recombinase	Mus musculus	109-114
24577941-5	2014	Furthermore, olaparib potentiated S-phase-specific double-strand DNA breaks (DSB) induced by SN-38, which is followed by Rad51 recruitment.	olaparib	13-21	RAD51 recombinase	Mus musculus	121-126
24577941-5	2014	Furthermore, olaparib potentiated S-phase-specific double-strand DNA breaks (DSB) induced by SN-38, which is followed by Rad51 recruitment.	Irinotecan	93-98	RAD51 recombinase	Mus musculus	121-126
24577941-6	2014	siRNA-mediated knockdown of Rad51, but not Mre11 or Rad50, increased the sensitivity to olaparib and/or SN-38 treatment in colon cancer cells.	olaparib	88-96	RAD51 recombinase	Mus musculus	28-33
24577941-6	2014	siRNA-mediated knockdown of Rad51, but not Mre11 or Rad50, increased the sensitivity to olaparib and/or SN-38 treatment in colon cancer cells.	Irinotecan	104-109	RAD51 recombinase	Mus musculus	28-33
24577941-8	2014	In conclusion, olaparib shows a synergistic effect in colon cancer cells in combination with SN-38 or irinotecan, potentiated by the Rad51-mediated HR pathway, irrespective of the Mre11-mediated failure of the MRN complex.	olaparib	15-23	RAD51 recombinase	Mus musculus	133-138
24682826-7	2014	We further revealed that Spironolactone impairs Rad51 foci formation, sensitizes cancer cells to DNA damaging agents, to Poly (ADP-ribose) polymerase (PARP) inhibitors and cross-linking agents and inhibits tumor growth in xenografts, in mice.	Spironolactone	25-39	RAD51 recombinase	Mus musculus	48-53
24244429-8	2013	Our results establish a novel mechanism underlying the cooperative antileukemic activities of these drug combinations in which panobinostat suppresses expression of BRCA1, CHK1, and RAD51 to enhance cytarabine and daunorubicin sensitivities in AML cells.	Panobinostat	127-139	RAD51 recombinase	Mus musculus	182-187
24244429-8	2013	Our results establish a novel mechanism underlying the cooperative antileukemic activities of these drug combinations in which panobinostat suppresses expression of BRCA1, CHK1, and RAD51 to enhance cytarabine and daunorubicin sensitivities in AML cells.	Daunorubicin	214-226	RAD51 recombinase	Mus musculus	182-187
23666627-0	2013	Caffeine suppresses homologous recombination through interference with RAD51-mediated joint molecule formation.	Caffeine	0-8	RAD51 recombinase	Mus musculus	71-76
23666627-3	2013	Biochemical and structural biology experiments revealed that caffeine interfered with a pivotal step in homologous recombination, homologous joint molecule formation, through increasing interactions of the RAD51 nucleoprotein filament with non-homologous DNA.	Caffeine	61-69	RAD51 recombinase	Mus musculus	206-211
23010348-9	2012	The combination of FK228 and cisplatin-induced apoptosis and activated aberrant DNA damage responses demonstrated by increased expression of pH2AX, RAD51 and 53BP1.	romidepsin	19-24	RAD51 recombinase	Mus musculus	148-153
23010348-9	2012	The combination of FK228 and cisplatin-induced apoptosis and activated aberrant DNA damage responses demonstrated by increased expression of pH2AX, RAD51 and 53BP1.	Cisplatin	29-38	RAD51 recombinase	Mus musculus	148-153
21900962-4	2012	Here, we show that DTIC increases expression of Rad51, but not Ku70, in a cultured B16-F10 mouse melanoma cell line in dose- and time-dependent manners.	Dacarbazine	19-23	RAD51 recombinase	Mus musculus	48-53
21900962-5	2012	On introducing Rad51 short interfering RNA (siRNA) with the hemagglutinating virus of Japan envelope (HVJ-E) to B16-F10 cells, DSBs induced by DTIC treatment were not efficiently repaired and resulted in enhanced apoptotic cell death.	dsbs	127-131	RAD51 recombinase	Mus musculus	15-20
21900962-5	2012	On introducing Rad51 short interfering RNA (siRNA) with the hemagglutinating virus of Japan envelope (HVJ-E) to B16-F10 cells, DSBs induced by DTIC treatment were not efficiently repaired and resulted in enhanced apoptotic cell death.	Dacarbazine	143-147	RAD51 recombinase	Mus musculus	15-20
21900962-6	2012	Colony formation of B16-F10 cells that received Rad51 siRNA was significantly decreased by DTIC treatment as compared with cells that received scramble siRNA.	Dacarbazine	91-95	RAD51 recombinase	Mus musculus	48-53
22008909-3	2012	Here we delivered Rad51 promoter-based constructs in vivo using linear polyethylenimine nanoparticles, in vivo jetPEI, to visualize and treat tumors in mice with HeLa xenografts.	Polyethyleneimine	71-87	RAD51 recombinase	Mus musculus	18-23
22384017-4	2012	Molecular analysis revealed that treatment with Dox, AN-7, and to a greater degree, AN-7 together with Dox increased tumor levels of gammaH2AX, the marker for DNA double-strand breaks and decreased the expression of Rad51, a protein needed for DNA repair.	Doxorubicin	48-51	RAD51 recombinase	Mus musculus	216-221
22384017-4	2012	Molecular analysis revealed that treatment with Dox, AN-7, and to a greater degree, AN-7 together with Dox increased tumor levels of gammaH2AX, the marker for DNA double-strand breaks and decreased the expression of Rad51, a protein needed for DNA repair.	Doxorubicin	103-106	RAD51 recombinase	Mus musculus	216-221
22384017-6	2012	In the myocardium, Dox-induced cardiomyopathy was associated with an increase in gammaH2AX expression and a reduction in Rad51 and MRE11 expression and increased apoptosis.	Doxorubicin	19-22	RAD51 recombinase	Mus musculus	121-126
22384017-7	2012	The addition of AN-7 to the Dox treatment protected the heart from Dox insults as was manifested by a decrease in gammaH2AX levels, an increase in Rad51 and MRE11 expression, and a diminution of cytochrome-c release.	Doxorubicin	28-31	RAD51 recombinase	Mus musculus	147-152
21917757-5	2011	In contrast, cotreatment of MM cell lines and primary CD138(+) cells with bortezomib and ABT-888 resulted in the sustained accumulation of unrepaired DNA DSBs with persistence of unubiquitylated gammaH2AX foci, lack of recruitment of BRCA1 and RAD51, and ensuing MM-cell death.	Bortezomib	74-84	RAD51 recombinase	Mus musculus	244-249
21917757-5	2011	In contrast, cotreatment of MM cell lines and primary CD138(+) cells with bortezomib and ABT-888 resulted in the sustained accumulation of unrepaired DNA DSBs with persistence of unubiquitylated gammaH2AX foci, lack of recruitment of BRCA1 and RAD51, and ensuing MM-cell death.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	89-92	RAD51 recombinase	Mus musculus	244-249
20926829-9	2010	Intriguingly, PARG(110)(-/-) cells accumulate more Rad51 foci in response to hydroxyurea, indicative of a defective repair of replication fork damage.	Hydroxyurea	77-88	RAD51 recombinase	Mus musculus	51-56
20231360-7	2010	Moreover, repair of mitomycin C (MMC)-induced DSBs and sister chromatid exchanges (SCEs), two RAD51-dependent processes, are 53BP1 independent.	Mitomycin	20-31	RAD51 recombinase	Mus musculus	94-99
20231360-7	2010	Moreover, repair of mitomycin C (MMC)-induced DSBs and sister chromatid exchanges (SCEs), two RAD51-dependent processes, are 53BP1 independent.	Mitomycin	33-36	RAD51 recombinase	Mus musculus	94-99
18987339-6	2009	Furthermore, we show that Recql5 functions nonredundantly with Rad51, a key factor for HR to protect mouse ES cells from CPT-induced cytotoxicity.	Camptothecin	121-124	RAD51 recombinase	Mus musculus	63-68
18606826-6	2008	While the RecA mutant was moderately more sensitive to UV irradiation and mitomycin C than the wild-type strain, the lack of RecA abolished allelic exchange in the mutant.	Mitomycin	74-85	RAD51 recombinase	Mus musculus	10-14
18266050-9	2008	Before an introduction into zygotes, single-stranded oligonucleotides were bound to RecA to enhance the homologous recombination.	single-stranded oligonucleotides	37-69	RAD51 recombinase	Mus musculus	84-88
17719855-4	2007	Augmentation of the endogenous pool of Rad51 by over-expression of transgene-encoded wildtype Rad51 enhances cell growth and gene targeting, but has minimal effects on cell survival to DNA damage induced by ionizing radiation (IR) or mitomycin C (MMC).	Mitomycin	247-250	RAD51 recombinase	Mus musculus	39-44
17719855-4	2007	Augmentation of the endogenous pool of Rad51 by over-expression of transgene-encoded wildtype Rad51 enhances cell growth and gene targeting, but has minimal effects on cell survival to DNA damage induced by ionizing radiation (IR) or mitomycin C (MMC).	Mitomycin	247-250	RAD51 recombinase	Mus musculus	94-99
17719855-8	2007	The results suggest that ATP hydrolysis by Rad51 is more important for some homologous recombination functions than it is for other aspects of DNA repair.	Adenosine Triphosphate	25-28	RAD51 recombinase	Mus musculus	43-48
16252008-5	2005	Moreover, we show that CPDs provoke accumulation of gamma-H2AX, P53bp1 and Rad51 foci as well as an increase in the amount of DSBs, which coincides with accumulation of cells in S phase.	Pyrimidine Dimers	23-27	RAD51 recombinase	Mus musculus	75-80
16236763-2	2005	In mammals, HR requires the activities of the RAD51 family (RAD51, RAD51B, RAD51C, RAD51D, XRCC2, XRCC3 and DMC1), each of which contains conserved ATP binding sequences (Walker Motifs A and B).	Adenosine Triphosphate	148-151	RAD51 recombinase	Mus musculus	46-51
16236763-2	2005	In mammals, HR requires the activities of the RAD51 family (RAD51, RAD51B, RAD51C, RAD51D, XRCC2, XRCC3 and DMC1), each of which contains conserved ATP binding sequences (Walker Motifs A and B).	Adenosine Triphosphate	148-151	RAD51 recombinase	Mus musculus	60-65
15928951-2	2005	We previously hypothesized that Mei1 is likely required for the formation of genetically programmed double-strand breaks (DSBs), the initiating event of meiotic recombination because in mutant spermatocytes (1) RAD51 foci are greatly reduced at zygonema; (2) RAD51 foci can be restored by cisplatin-induced DNA damage; and (3) phosphorylated H2AX is greatly reduced at leptonema.	Cisplatin	289-298	RAD51 recombinase	Mus musculus	211-216
15388331-8	2004	Three and four weeks after busulfan treatment, RAD51 and FasL expression decreased to nearly undetectable levels, indicating that meiotic spermatocytes and post-meiotic cells, respectively, were lost.	Busulfan	27-35	RAD51 recombinase	Mus musculus	47-52
14743204-4	2004	Here, we report that p53-/- mouse embryonic fibroblasts (MEFs) exhibit higher levels of the RAD51 protein and increased level of spontaneous RAD51 foci Agents that stall replication forks, for example, hydroxyurea (HU), potently induce HR repair and RAD51 foci.	Hydroxyurea	202-213	RAD51 recombinase	Mus musculus	141-146
14743204-4	2004	Here, we report that p53-/- mouse embryonic fibroblasts (MEFs) exhibit higher levels of the RAD51 protein and increased level of spontaneous RAD51 foci Agents that stall replication forks, for example, hydroxyurea (HU), potently induce HR repair and RAD51 foci.	Hydroxyurea	202-213	RAD51 recombinase	Mus musculus	141-146
15342939-8	2004	Rad51, xpc, and mdm-2 transcript levels were increased in male but not female HSCs exposed to 1,4-BQ.	1,4-bq	94-100	RAD51 recombinase	Mus musculus	0-5
14668445-4	2003	Here, we show that treatment of mutant males with cisplatin restores RAD51 loading, suggesting that mutant spermatocytes have intact recombinational repair mechanisms.	Cisplatin	50-59	RAD51 recombinase	Mus musculus	69-74
11923292-3	2002	By using a dominant negative approach, we generated a mouse embryonic stem cell line that expresses an ATP hydrolysis-defective RAD51 protein, hRAD51-K133R, at comparable levels to the endogenous wild-type RAD51 protein, whose expression is retained in these cells.	Adenosine Triphosphate	103-106	RAD51 recombinase	Mus musculus	128-133
11923292-3	2002	By using a dominant negative approach, we generated a mouse embryonic stem cell line that expresses an ATP hydrolysis-defective RAD51 protein, hRAD51-K133R, at comparable levels to the endogenous wild-type RAD51 protein, whose expression is retained in these cells.	Adenosine Triphosphate	103-106	RAD51 recombinase	Mus musculus	144-149
11698339-7	2001	Furthermore, MSH2(-/-) cells displayed an elevated spontaneous RAD51 focus-forming activity and a higher induction of RAD51 foci following camptothecin treatment.	Camptothecin	139-151	RAD51 recombinase	Mus musculus	118-123
11698339-9	2001	Therefore, our results suggest an involvement of MSH2 in the early events leading to correct RAD51 relocalization after the formation of DSBs specifically produced at the blocked replication fork.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	137-141	RAD51 recombinase	Mus musculus	93-98
11349014-4	2001	The recA mutants are sensitive to DNA-damaging agents and show increased susceptibility to metronidazole, the first lead compound active against the dormant M. tuberculosis complex.	Metronidazole	91-104	RAD51 recombinase	Mus musculus	4-8
11106738-6	2000	Cisplatin-induced DSBs restored Rad51/Dmc1 foci and promoted synapsis.	Cisplatin	0-9	RAD51 recombinase	Mus musculus	32-37
11106738-6	2000	Cisplatin-induced DSBs restored Rad51/Dmc1 foci and promoted synapsis.	dsbs	18-22	RAD51 recombinase	Mus musculus	32-37
10843985-0	2000	The breast cancer susceptibility gene BRCA1 is required for subnuclear assembly of Rad51 and survival following treatment with the DNA cross-linking agent cisplatin.	Cisplatin	155-164	RAD51 recombinase	Mus musculus	83-88
9571148-2	1998	In this study, we investigated both in vitro and in vivo whether inhibition of the RAD51 gene by antisense oligonucleotides (ODNs) enhances the radiosensitivity of mouse malignant gliomas.	Oligonucleotides	107-123	RAD51 recombinase	Mus musculus	83-88
9417871-9	1997	We have now analyzed Rad51 nuclear foci induced in both primary and immortalized B cells by treatment with the DNA damaging agent, methyl methanesulfonate (MMS).	Methyl Methanesulfonate	131-154	RAD51 recombinase	Mus musculus	21-26
9417871-9	1997	We have now analyzed Rad51 nuclear foci induced in both primary and immortalized B cells by treatment with the DNA damaging agent, methyl methanesulfonate (MMS).	Methyl Methanesulfonate	156-159	RAD51 recombinase	Mus musculus	21-26
9417871-10	1997	We have found that, in LPS-cultured primary B cells, MMS treatment increases the fraction of cells containing Rad51 foci and induces formation of a very high number of foci per cell.	Methyl Methanesulfonate	53-56	RAD51 recombinase	Mus musculus	110-115
9424847-1	1997	Recombinant adenovirus expressing NS1 nonstructural protein of trick-borne encephalitis (TBE) virus (Rad 51) protected mice from many strains of TBE and Omsk hemorhagic fever (OHF) viruses, but virtually did not protect them from Negishi virus.	tbe	89-92	RAD51 recombinase	Mus musculus	101-107
9424847-6	1997	The prospects of using Rad 51 as a vaccine against TBE are discussed.	tbe	51-54	RAD51 recombinase	Mus musculus	23-29
9135082-5	1996	RESULTS: In the leptotene and zygotene stages, the Rad51 protein was present on chromatin loops of mouse testis chromosomes then the protein left the loops.	leptotene	16-25	RAD51 recombinase	Mus musculus	51-56
9135082-5	1996	RESULTS: In the leptotene and zygotene stages, the Rad51 protein was present on chromatin loops of mouse testis chromosomes then the protein left the loops.	zygotene	30-38	RAD51 recombinase	Mus musculus	51-56
7587590-2	1995	We observed the following dynamic changes in distribution of Rad51 during meiosis: (1) in early leptotene nuclei there are multiple, apparently randomly distributed, foci that by late leptonema become organized into tracks of foci.	leptotene	96-105	RAD51 recombinase	Mus musculus	61-66
8341671-4	1993	The Rad51 protein is structurally similar to Escherichia coli RecA protein, which is required in homologous recombination and SOS responses in bacteria.	sulfur monoxide	126-129	RAD51 recombinase	Mus musculus	4-9
8341671-7	1993	The mouse gene complemented a rad51 mutation of S. cerevisiae with sensitivity to methyl-methanesulfonate, which produces double-strand breaks of DNA.	Methyl Methanesulfonate	82-105	RAD51 recombinase	Mus musculus	30-35
7683155-10	1993	Most interestingly the properties of phospholipid and nucleic acid binding are markedly similar to those recently described for the bacterial DNA-binding proteins DnaA and recA.	Phospholipids	37-49	RAD51 recombinase	Mus musculus	172-176
8321120-2	1993	The recA gene was cloned from a B. abortus genomic DNA library by complementation of an Escherichia coli recA mutant in the presence of methyl methanesulfonate (MMS).	Methyl Methanesulfonate	136-159	RAD51 recombinase	Mus musculus	4-8
8321120-2	1993	The recA gene was cloned from a B. abortus genomic DNA library by complementation of an Escherichia coli recA mutant in the presence of methyl methanesulfonate (MMS).	Methyl Methanesulfonate	161-164	RAD51 recombinase	Mus musculus	4-8
8321120-7	1993	The RecA mutant was more sensitive than the parental strain to killing by MMS.	Methyl Methanesulfonate	74-77	RAD51 recombinase	Mus musculus	4-8
34936917-11	2022	The recombination markers, including DMC1 and RAD51, and crossover marker MLH1 were decreased during spermatogenesis after exposure to BDE-209.	decabromobiphenyl ether	135-142	RAD51 recombinase	Mus musculus	46-51
34844627-12	2021	In addition, HCQ activated ATM to enhance HR repair, a high-fidelity repair for DNA double-strand breaks (DSBs) in cells, while BKM120 inhibited HR repair by blocking the phosphorylation of ATM and the expression of BRCA1/2 and Rad51.	Hydroxychloroquine	13-16	RAD51 recombinase	Mus musculus	228-233
34844627-12	2021	In addition, HCQ activated ATM to enhance HR repair, a high-fidelity repair for DNA double-strand breaks (DSBs) in cells, while BKM120 inhibited HR repair by blocking the phosphorylation of ATM and the expression of BRCA1/2 and Rad51.	NVP-BKM120	128-134	RAD51 recombinase	Mus musculus	228-233
34696786-9	2021	PCI-24781 significantly inhibited tumor growth and downregulated DNA repair machinery (BRCA1, CHK1, RAD51, and O6-methylguanine-DNA- methyltransferase (MGMT)), increasing DNA double-strand breaks and causing apoptosis in the GBM cell lines, including an MGMT expressing cell line in vitro.	abexinostat	0-9	RAD51 recombinase	Mus musculus	100-105
34456631-12	2021	Cooverexpressing miR-34b-3p with RAD51 reversed the miR-34b-3p-induced changes in proliferation, the cell cycle, the expression of H2A.X, and that of apoptosis-related proteins.	mir-34b-3p	52-62	RAD51 recombinase	Mus musculus	33-38
34456631-16	2021	miR-34b-3p was identified as the target of HCG9, and RAD51 acted as a potential target of miR-34b-3p.	mir-34b-3p	90-100	RAD51 recombinase	Mus musculus	53-58
34221998-12	2021	Majority of fecal lipids including lysophosphatidylcholine and phosphatidylcholine were upregulated in CRPC FMT treated mice, accompanied with enhanced expressions of LPCAT1, RAD51, and DNA-PKcs in mice prostate.	Phosphatidylcholines	63-82	RAD51 recombinase	Mus musculus	175-180
35471225-11	2022	Meanwhile, tea polyphenols reduced DNA damage in diabetic oocytes which may be mediated by the increased expression of Rad51, related to DNA damage repair.	Polyphenols	15-26	RAD51 recombinase	Mus musculus	119-124
35140124-4	2022	RESULTS: Treatment with onalespib depleted CHK1 and RAD51, two key proteins of the HR pathway, and attenuated HR repair, sensitizing GSCs to the combination of radiation and temozolomide (TMZ).	(2,4-dihydroxy-5-isopropylphenyl)-(5-(4-methylpiperazin-1-ylmethyl)-1,3-dihydroisoindol-2-yl)methanone	24-33	RAD51 recombinase	Mus musculus	52-57
35365640-6	2022	We show the restoration of RAD51 foci in mutant cells when Topoisomerase I inhibitor-induced single strand breaks are converted into DSBs during DNA replication.	dsbs	133-137	RAD51 recombinase	Mus musculus	27-32
34998818-0	2022	E3 ubiquitin ligase RNF180 reduces sensitivity of triple-negative breast cancer cells to Gefitinib by downregulating RAD51.	Gefitinib	89-98	RAD51 recombinase	Mus musculus	117-122
6348525-5	1983	These tests were also used to demonstrate that dimethyl nitrosamine (DMNA) is activated by Aroclor-1254-induced rat-liver S9 fractions to genotoxic products, as measured by the low survival of a recA derivative compared with the repair-proficient wild-type strain.	Dimethylnitrosamine	47-67	RAD51 recombinase	Mus musculus	195-199
6348525-5	1983	These tests were also used to demonstrate that dimethyl nitrosamine (DMNA) is activated by Aroclor-1254-induced rat-liver S9 fractions to genotoxic products, as measured by the low survival of a recA derivative compared with the repair-proficient wild-type strain.	Dimethylnitrosamine	69-73	RAD51 recombinase	Mus musculus	195-199
6348525-5	1983	These tests were also used to demonstrate that dimethyl nitrosamine (DMNA) is activated by Aroclor-1254-induced rat-liver S9 fractions to genotoxic products, as measured by the low survival of a recA derivative compared with the repair-proficient wild-type strain.	Chlorodiphenyl (54% Chlorine)	91-103	RAD51 recombinase	Mus musculus	195-199
6348525-7	1983	Using a mixture of the repair-proficient parent and the recA derivative inoculated into mice that were subsequently treated with MMS, NMU or DMNA, we found that these chemicals induce a larger decrease in survival in the recA strain as compared with the wild-type in cells recovered from the liver and the spleen.	Methyl Methanesulfonate	129-132	RAD51 recombinase	Mus musculus	56-60
6348525-7	1983	Using a mixture of the repair-proficient parent and the recA derivative inoculated into mice that were subsequently treated with MMS, NMU or DMNA, we found that these chemicals induce a larger decrease in survival in the recA strain as compared with the wild-type in cells recovered from the liver and the spleen.	Methyl Methanesulfonate	129-132	RAD51 recombinase	Mus musculus	221-225
6348525-7	1983	Using a mixture of the repair-proficient parent and the recA derivative inoculated into mice that were subsequently treated with MMS, NMU or DMNA, we found that these chemicals induce a larger decrease in survival in the recA strain as compared with the wild-type in cells recovered from the liver and the spleen.	Dimethylnitrosamine	141-145	RAD51 recombinase	Mus musculus	56-60
6348525-7	1983	Using a mixture of the repair-proficient parent and the recA derivative inoculated into mice that were subsequently treated with MMS, NMU or DMNA, we found that these chemicals induce a larger decrease in survival in the recA strain as compared with the wild-type in cells recovered from the liver and the spleen.	Dimethylnitrosamine	141-145	RAD51 recombinase	Mus musculus	221-225