Ignet

Gene Information

Gene symbol: RAD51

Gene name: RAD51 homolog (S. cerevisiae)

HGNC ID: 9817

Synonyms: HsRad51, HsT16930, BRCC5

Related Genes

#	Gene Symbol	Number of hits
1	ATM	1 hits
2	BAX	1 hits
3	BRCA1	1 hits
4	BRCA2	1 hits
5	CAT	1 hits
6	CDKN1A	1 hits
7	COL1A1	1 hits
8	COL4A4	1 hits
9	DMC1	1 hits
10	MND1	1 hits
11	MYC	1 hits
12	PCNA	1 hits
13	PDIK1L	1 hits
14	POU4F1	1 hits
15	PSMC3IP	1 hits
16	RAD50	1 hits
17	RAD51L1	1 hits
18	RAD52	1 hits
19	RPS27A	1 hits
20	SOD1	1 hits
21	THY1	1 hits
22	TP53	1 hits
23	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	9398851	Partial rescue of the prophase I defects of Atm-deficient mice by p53 and p21 null alleles.
2	9398851	Atm is required for proper assembly of Rad51 onto the chromosomal axial elements during meiosis.
3	9398851	In addition, p53, p21 and Bax are elevated in testes from Atm-deficient mice.
4	9398851	To determine whether these elevated protein levels are important factors in the meiotic disruption of Atm-deficient mice, we analysed the meiotic phenotype of Atm/p53 or Atm/p21 double mutants.
5	9398851	Previous results demonstrated that mice homozygous for a null mutation in Rad51 (ref. 6) display an early embryonic lethal phenotype that can be partly rescued by removing p53 and/or p21.
6	9398851	Because Atm-deficient mice are viable but completely infertile, our studies suggest that the Rad51 assembly defects and elevated levels of p53, p21 and Bax represent tissue-specific responses to the absence of Atm.
7	9398851	Partial rescue of the prophase I defects of Atm-deficient mice by p53 and p21 null alleles.
8	9398851	Atm is required for proper assembly of Rad51 onto the chromosomal axial elements during meiosis.
9	9398851	In addition, p53, p21 and Bax are elevated in testes from Atm-deficient mice.
10	9398851	To determine whether these elevated protein levels are important factors in the meiotic disruption of Atm-deficient mice, we analysed the meiotic phenotype of Atm/p53 or Atm/p21 double mutants.
11	9398851	Previous results demonstrated that mice homozygous for a null mutation in Rad51 (ref. 6) display an early embryonic lethal phenotype that can be partly rescued by removing p53 and/or p21.
12	9398851	Because Atm-deficient mice are viable but completely infertile, our studies suggest that the Rad51 assembly defects and elevated levels of p53, p21 and Bax represent tissue-specific responses to the absence of Atm.
13	9398851	Partial rescue of the prophase I defects of Atm-deficient mice by p53 and p21 null alleles.
14	9398851	Atm is required for proper assembly of Rad51 onto the chromosomal axial elements during meiosis.
15	9398851	In addition, p53, p21 and Bax are elevated in testes from Atm-deficient mice.
16	9398851	To determine whether these elevated protein levels are important factors in the meiotic disruption of Atm-deficient mice, we analysed the meiotic phenotype of Atm/p53 or Atm/p21 double mutants.
17	9398851	Previous results demonstrated that mice homozygous for a null mutation in Rad51 (ref. 6) display an early embryonic lethal phenotype that can be partly rescued by removing p53 and/or p21.
18	9398851	Because Atm-deficient mice are viable but completely infertile, our studies suggest that the Rad51 assembly defects and elevated levels of p53, p21 and Bax represent tissue-specific responses to the absence of Atm.
19	10918303	BRCA1 contains several functional domains that interact directly or indirectly with a variety of molecules, including tumor suppressors (p53, RB, BRCA2 and ATM), oncogenes (c-Myc, casein kinase II and E2F), DNA damage repair proteins (RAD50 and RAD51), cell-cycle regulators (cyclins and cyclin-dependent kinases), transcriptional activators and repressors (RNA polymerase II, RHA, histone deacetylase complex and CtIP) and others.
20	11106738	We did not detect Rad51/Dmc1 foci in meiotic chromosome spreads, indicating DSBs are not formed.
21	11106738	Cisplatin-induced DSBs restored Rad51/Dmc1 foci and promoted synapsis.
22	11106738	Other mouse mutants that arrest during meiotic prophase (Atm -/-, Dmc1 -/-, mei1, and Morc(-/-)) showed altered Spo11 protein localization and expression.
23	11106738	We did not detect Rad51/Dmc1 foci in meiotic chromosome spreads, indicating DSBs are not formed.
24	11106738	Cisplatin-induced DSBs restored Rad51/Dmc1 foci and promoted synapsis.
25	11106738	Other mouse mutants that arrest during meiotic prophase (Atm -/-, Dmc1 -/-, mei1, and Morc(-/-)) showed altered Spo11 protein localization and expression.
26	11359908	Both human and mouse cells express an alternatively spliced variant of BRCA1, BRCA1-Delta11, which lacks exon 11 in its entirety, including putative nuclear localization signals.
27	11359908	Our results demonstrate that full-length murine Brca1 is identical to human BRCA1 with respect to its cell cycle regulation, DNA damage-induced phosphorylation, nuclear localization, and association with Rad51.
28	11359908	Surprisingly, we show that endogenous Brca1-Delta11 localizes to discrete nuclear foci indistinguishable from those found in wild-type cells, despite the fact that Brca1-Delta11 lacks previously defined nuclear localization signals.
29	11359908	However, we further show that DNA damage-induced phosphorylation of Brca1-Delta11 is significantly reduced compared to full-length Brca1, and that gamma irradiation-induced Rad51 focus formation is impaired in cells in which only Brca1-Delta11 is expressed.
30	11359908	Both human and mouse cells express an alternatively spliced variant of BRCA1, BRCA1-Delta11, which lacks exon 11 in its entirety, including putative nuclear localization signals.
31	11359908	Our results demonstrate that full-length murine Brca1 is identical to human BRCA1 with respect to its cell cycle regulation, DNA damage-induced phosphorylation, nuclear localization, and association with Rad51.
32	11359908	Surprisingly, we show that endogenous Brca1-Delta11 localizes to discrete nuclear foci indistinguishable from those found in wild-type cells, despite the fact that Brca1-Delta11 lacks previously defined nuclear localization signals.
33	11359908	However, we further show that DNA damage-induced phosphorylation of Brca1-Delta11 is significantly reduced compared to full-length Brca1, and that gamma irradiation-induced Rad51 focus formation is impaired in cells in which only Brca1-Delta11 is expressed.
34	12581656	Expression of Y-family polymerases is often induced by DNA damage, and their recruitment to the replication fork is mediated by beta-clamp, clamp loader, single-strand-DNA-binding protein and RecA in Escherichia coli, and by ubiquitin-modified proliferating cell nuclear antigen in yeast.
35	15834424	The Hop2 and Mnd1 proteins act in concert with Rad51 and Dmc1 in meiotic recombination.
36	15834424	Rad51 and Dmc1 recombinases are the major players in these processes.
37	15834424	Disruption of meiosis-specific HOP2 or MND1 genes leads to severe defects in homologous synapsis and an early-stage recombination failure resulting in sterility.
38	15834424	Here we show that mouse Hop2 can efficiently form D-loops, the first recombination intermediates, but this activity is abrogated upon association with Mnd1.
39	15834424	Furthermore, the Hop2-Mnd1 heterodimer physically interacts with Rad51 and Dmc1 recombinases and stimulates their activity up to 35-fold.
40	15834424	Our data reveal an interplay among Hop2, Mnd1 and Rad51 and Dmc1 in the formation of the first recombination intermediates during meiosis.
41	15834424	The Hop2 and Mnd1 proteins act in concert with Rad51 and Dmc1 in meiotic recombination.
42	15834424	Rad51 and Dmc1 recombinases are the major players in these processes.
43	15834424	Disruption of meiosis-specific HOP2 or MND1 genes leads to severe defects in homologous synapsis and an early-stage recombination failure resulting in sterility.
44	15834424	Here we show that mouse Hop2 can efficiently form D-loops, the first recombination intermediates, but this activity is abrogated upon association with Mnd1.
45	15834424	Furthermore, the Hop2-Mnd1 heterodimer physically interacts with Rad51 and Dmc1 recombinases and stimulates their activity up to 35-fold.
46	15834424	Our data reveal an interplay among Hop2, Mnd1 and Rad51 and Dmc1 in the formation of the first recombination intermediates during meiosis.
47	15834424	The Hop2 and Mnd1 proteins act in concert with Rad51 and Dmc1 in meiotic recombination.
48	15834424	Rad51 and Dmc1 recombinases are the major players in these processes.
49	15834424	Disruption of meiosis-specific HOP2 or MND1 genes leads to severe defects in homologous synapsis and an early-stage recombination failure resulting in sterility.
50	15834424	Here we show that mouse Hop2 can efficiently form D-loops, the first recombination intermediates, but this activity is abrogated upon association with Mnd1.
51	15834424	Furthermore, the Hop2-Mnd1 heterodimer physically interacts with Rad51 and Dmc1 recombinases and stimulates their activity up to 35-fold.
52	15834424	Our data reveal an interplay among Hop2, Mnd1 and Rad51 and Dmc1 in the formation of the first recombination intermediates during meiosis.
53	15834424	The Hop2 and Mnd1 proteins act in concert with Rad51 and Dmc1 in meiotic recombination.
54	15834424	Rad51 and Dmc1 recombinases are the major players in these processes.
55	15834424	Disruption of meiosis-specific HOP2 or MND1 genes leads to severe defects in homologous synapsis and an early-stage recombination failure resulting in sterility.
56	15834424	Here we show that mouse Hop2 can efficiently form D-loops, the first recombination intermediates, but this activity is abrogated upon association with Mnd1.
57	15834424	Furthermore, the Hop2-Mnd1 heterodimer physically interacts with Rad51 and Dmc1 recombinases and stimulates their activity up to 35-fold.
58	15834424	Our data reveal an interplay among Hop2, Mnd1 and Rad51 and Dmc1 in the formation of the first recombination intermediates during meiosis.
59	15942943	RAD51L1 is a tumor-suppressor gene belonging to the RAD51 family, already implicated in many tumors (uterine leiomyomas, pseudo-Meigs syndromes, pulmonary chondroid hamartomas) and involved in recombinational repair of DNA double-strand breaks.
60	15942943	BMP2 belongs to the TGFbeta superfamily, and the BMP2-BMP4 genes are involved in thymocyte differentiation by blocking progression from CD4-CD8- to CD4+CD8+ while maintaining a sufficient pool of immature precursors.
61	19120318	Moreover, antibody array showed that RAD51 and RAD52 were significantly decreased in AGE2-treated INS-1 cells.
62	19182373	By using Escherichia coli mutant strains, we observed that cyclohexyl-DHP exposure strongly reduced the survival rate of a cytosolic sodium dodecyl sulfate (SOD)-deficient strain (sodA sodB), significantly reduced the survival rates of DNA repair-deficient strains (recA and uvrB) and mildly reduced the survival rate of a catalase-deficient strain (katE katG) compared with the survival rate of the wild-type strain.
63	21112301	Hop2-Mnd1 is a meiotic recombination mediator that stimulates DNA strand invasion by both Dmc1 and Rad51.
64	21112301	The condensation of DNA is Hop2-Mnd1 concentration-dependent, reversible, and specific to the heterodimer, as neither Hop2 nor Mnd1 acting alone can facilitate this reaction.
65	22312291	Retinal morphological changes, endothelial markers (RECA), collagen IV (Col-IV), vascular endothelial growth factor (VEGF), and neuropathic changes (Thy-1 and Brn3a expression) of the retinal ganglion cells (RGCs) were investigated.
66	22312291	Numerous pathological changes (deceased expression of RECA, VEGF, Thy-1, and Brn3a as well as decreased Collagen IV and Müller cell content) were noted in the retinal vessels of diabetic rats; these changes were attenuated in diabetic animals that received ICA.
67	22312291	Retinal morphological changes, endothelial markers (RECA), collagen IV (Col-IV), vascular endothelial growth factor (VEGF), and neuropathic changes (Thy-1 and Brn3a expression) of the retinal ganglion cells (RGCs) were investigated.
68	22312291	Numerous pathological changes (deceased expression of RECA, VEGF, Thy-1, and Brn3a as well as decreased Collagen IV and Müller cell content) were noted in the retinal vessels of diabetic rats; these changes were attenuated in diabetic animals that received ICA.