Ignet

Gene Pair Information

Gene Pair: CDKN1A, BRCA1

Related Sentences

#	PMID	Sentence
1	9296497	Arrest of the cell cycle by the tumour-suppressor BRCA1 requires the CDK-inhibitor p21WAF1/CiP1.
2	9296497	The nuclear protein BRCA1 has the properties of a transcription factor, and can interact with the recombination and repair protein RAD51.
3	9296497	Here we show that BRCA1 transactivates expression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 in a p53-independent manner, and that BRCA1 inhibits cell-cycle progression into the S-phase following its transfection into human cancer cells.
4	9296497	BRCA1 does not inhibit S-phase progression in p21-/- cells, unlike p21+/+ cells, and tumour-associated, transactivation-deficient mutants of BRCA1 are defective in both transactivation of p21 and cell-cycle inhibition.
5	9321930	We found that multiple tumor suppressor genes (e.g., p53, DCC, APC, MCC, BRCA1, and WAF1/CIP1) were inactivated at different frequencies via various mechanisms [e.g., loss of heterozygosity (LOH), loss of expression (LOE), mutation, and inactivation by cellular binding protein].
6	9321930	Several important and novel findings are as following: LOH and LOE of the DCC gene, LOH, LOE, and possible mutation of the APC/MCC genes, LOH of the BRCA1 locus, and mutation of the WAF1/CIP1 gene.
7	9321930	For p53 tumor suppressor gene alone, multiple inactivation mechanisms (i.e., LOH, LOE, mutation, and amplification of the cellular inactivating protein MDM2) were identified.
8	9321930	In addition, we identified a number of novel mechanisms of tumor suppressor gene inactivation, in prostate cancer such as loss of mRNA expression of the DCC, APC, MCC and p53 gene, and mutator phenotype.
9	9321930	When we analyzed the relationship between DCC loss of expression and 12-LOX elevation in prostate cancer pati
10	9535786	Decreased BRCA1 expression levels may arrest the cell cycle through activation of p53 checkpoint in human sporadic breast tumors.
11	9535786	We also investigated possible relationships between BRCA1, p53, mdm-2 and p21(WAF1/CIP1) at the expression level. p53 expression was unaffected in almost all the specimens, mdm-2 was overexpressed in 18/35 specimens while 21/35 overexpressed p21.
12	9535786	Samples exhibiting reduced BRCA1 levels simultaneously overexpressed both p21 and mdm-2, showing that BRCA1, at certain levels, even reduced up to 2.7-fold, is functional and sufficient to upregulate p21, when p53 activity is inhibited by its negative regulator, the mdm-2.
13	9535786	On the contrary, specimens exhibiting more than 2.7-fold reduced BRCA1 levels, overexpressed p21 while mdm-2 expression was normal, allowing us to speculate that p21 transcriptional activation is due to p53 activity, in cases with dramatically decreased BRCA1 expression.
14	9535786	Our findings provide evidence, indicating that BRCA1 might affect cell cycle regulation and loss of BRCA1 function due to decreased expression leads to cell cycle arrest, through p53 and p21 genes.
15	9582019	BRCA1 physically associates with p53 and stimulates its transcriptional activity.
16	9582019	We show here that BRCA1 increases p53-dependent transcription from the p21WAF1/CIP1 and bax promoters.
17	9582019	We also show that BRCA1 and p53 proteins interact both in vitro and in vivo.
18	9582019	The interacting regions map, in vitro, to aa 224-500 of BRCA1 and the C-terminal domain of p53.
19	9582019	Tumor-derived transactivation-deficient BRCA1 mutants are defective in co-activation of p53-dependent transcription and a truncation mutant of BRCA1 that retains the p53-interacting region acts as a dominant inhibitor of p53-dependent transcription.
20	9582019	BRCA1 and p53 cooperatively induce apoptosis of cancer cells.
21	9582019	The results indicate that BRCA1 and p53 may coordinately regulate gene expression in their role as tumor suppressors.
22	9674697	Western blotting analysis revealed that pre-treatment of MDA-MB-453 cells with SF inhibited the ADR-induced decreases in the levels of Bcl-XL, an anti-apoptotic protein related to Bcl-2; and the dose-response and time course characteristics for SF-mediated increases in the Bcl-XL protein levels of ADR-treated cells were consistent with the degrees of protection against apoptosis observed under the same conditions.
23	9674697	In contrast to Bcl-XL, SF blocked ADR-induced increases in c-Myc and inhibited the expression of p21WAF1/CIP1 and of the BRCA1 protein in MDA-MB-453 cells.
24	9926942	The second BRCT domain of BRCA1 proteins interacts with p53 and stimulates transcription from the p21WAF1/CIP1 promoter.
25	9926942	Inherited mutations in the breast and ovarian cancer susceptibility gene BRCA1 are associated with high risk for developing breast and ovarian cancers.
26	9926942	BRCA1 associates with p53 and stimulates transcription in both p53 dependent and p53-independent manners.
27	9926942	BRCA1 splice variants BRCA1a (p110) and BRCA1b (p100) associates with CBP/p300 co-activators.
28	9926942	Here we show that BRCA1a and BRCA1b proteins stimulate p53-dependent transcription from the p21WAF1/CIP1 promoter.
29	9926942	In addition, the C-terminal second BRCA1 (BRCT) domain is sufficient for p53 mediated transactivation of the p21 promoter.
30	9926942	Previous studies emphasized the importance of the BRCT domain, which shows homology with p53 binding protein (53BP1), in transcriptional activation, growth inhibition and tumor suppression.
31	9926942	These results demonstrate for the first time the presence of a second p53 interaction domain in BRCA1 proteins and suggests that BRCA1a and BRCA1b proteins, like BRCA1, function as p53 co-activators.
32	9926942	These results suggest that one of the mechanisms by which BRCA1 proteins function is through recruitment of CBP/p300 associated HAT/FAT activity for acetylation of p53 to specific promoters resulting in transcriptional activation.