ArticleExperimental cell research2007
Phosphatidylinositol 3-kinase/Akt signaling enhances nuclear localization and transcriptional activity of BRCA1.
Article in Experimental cell research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
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- Acetylation, Phosphorylation, Ubiquitination (Oh My!): Following Post-Translational Modifications on the Ubiquitin Road.Biomolecules · 2022Review
- A protein interaction landscape of breast cancer.Science (New York, N.Y.) · 2021Article
- BRCA1 subcellular localization regulated by PI3K signaling pathway in triple-negative breast cancer MDA-MB-231 cells and hormone-sensitive T47D cells.Open life sciences · 2020Article
- Functional Impacts of the BRCA1-mTORC2 Interaction in Breast Cancer.International journal of molecular sciences · 2019Article
- Elucidating the novel BRCA1 function as a non-genomic metabolic restraint in ER-positive breast cancer cell lines.Oncotarget · 2018Article
- Connection between Tumor Suppressor BRCA1 and PTEN in Damaged DNA Repair.Frontiers in oncology · 2014Review
- ROS-mediated activation of AKT induces apoptosis via pVHL in prostate cancer cells.Molecular and cellular biochemistry · 2013Article
- Article
- Missense variants of uncertain significance (VUS) altering the phosphorylation patterns of BRCA1 and BRCA2.PloS one · 2013Article
- Akt: a double-edged sword in cell proliferation and genome stability.Journal of oncology · 2012Article
- Histone methyltransferase EZH2 induces Akt-dependent genomic instability and BRCA1 inhibition in breast cancer.Cancer research · 2011Article
- AKT1/BRCA1 in the control of homologous recombination and genetic stability: the missing link between hereditary and sporadic breast cancers.Oncotarget · 2010Review
- Impact of RING and BRCT domain mutations on BRCA1 protein stability, localization and recruitment to DNA damage.Radiation research · 2010Article
- AKT regulates BRCA1 stability in response to hormone signaling.Molecular and cellular endocrinology · 2010Article
- Nucleocytoplasmic shuttling of p62/SQSTM1 and its role in recruitment of nuclear polyubiquitinated proteins to promyelocytic leukemia bodies.The Journal of biological chemistry · 2010Article
- Article
- Nuclear and mitochondrial signalling Akts in cardiomyocytes.Cardiovascular research · 2009Review
- Nuclear export of BRCA1 occurs during early S phase and is calcium-dependent.Cellular signalling · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Signaling pathways involved in regulating nuclear-cytoplasmic distribution of BRCA1 have not been previously reported. Here, we provide evidence that heregulin beta1-induced activation of the Akt pathway increases the nuclear content of BRCA1. First, treatment of T47D breast cancer cells with heregulin beta1 results in a two-fold increase in nuclear BRCA1 as assessed by FACS analysis, immunoblotting and immunofluorescence. This heregulin-induced increase in nuclear BRCA1 is blocked by siRNA-mediated down-regulation of Akt. Second, mutation of threonine 509 in BRCA1, the site of Akt phosphorylation, to an alanine, attenuates the ability of heregulin to induce BRCA1 nuclear accumulation. These data suggest that Akt-catalyzed phosphorylation of BRCA1 is required for the heregulin-regulated nuclear concentration of BRCA1. Because most functions ascribed to BRCA1 occur within the nucleus, we postulated that phosphorylation-dependent nuclear accumulation of BRCA1 would result in enhanced nuclear activity, specifically transcriptional activity, of BRCA1. This postulate is affirmed by our observation that the ability of BRCA1 to transactivate GADD45 promoter constructs was enhanced in T47D cells treated with heregulin beta1. Furthermore, the heterologous expression of BRCA1 in HCC1937 human breast cancer cells, which have constitutively active Akt, also induces GADD45 promoter activity, whereas the expression of BRCA1 in which threonine 509 has been mutated to an alanine is able to only minimally induce promoter activity. These findings implicate Akt in upstream events leading to BRCA1 nuclear localization and function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.