ArticleOncogene2005
Caspase-dependent processing activates the proapoptotic activity of deleted in breast cancer-1 during tumor necrosis factor-alpha-mediated death signaling.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- The splicing factor CCAR1 regulates the Fanconi anemia/BRCA pathway.Molecular cell · 2024Article
- Mechanistic insights into the dual role of CCAR2/DBC1 in cancer.Experimental & molecular medicine · 2023Review
- Unraveling the Dichotomy of Enigmatic Serine Protease HtrA2.Frontiers in molecular biosciences · 2022Review
- A novel form of Deleted in breast cancer 1 (DBC1) lacking the N-terminal domain does not bind SIRT1 and is dynamically regulated in vivo.Scientific reports · 2019Article
- DBC1 Regulates p53 Stability via Inhibition of CBP-Dependent p53 Polyubiquitination.Cell reports · 2019Article
- The Proteomic Profile of Deleted in Breast Cancer 1 (DBC1) Interactions Points to a Multifaceted Regulation of Gene Expression.Molecular & cellular proteomics : MCP · 2016Article
- DBC1/CCAR2 is involved in the stabilization of androgen receptor and the progression of osteosarcoma.Scientific reports · 2015Article
- Inflammation negatively regulates FOXP3 and regulatory T-cell function via DBC1.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Review
- DBC1 functions as a tumor suppressor by regulating p53 stability.Cell reports · 2015Article
- High DBC1 (CCAR2) expression in gallbladder carcinoma is associated with favorable clinicopathological factors.International journal of clinical and experimental pathology · 2015Article
- SIRT1 expression is associated with a poor prognosis, whereas DBC1 is associated with favorable outcomes in gastric cancer.Cancer medicine · 2014Article
- CCAR2 deficiency augments genotoxic stress-induced apoptosis in the presence of melatonin in non-small cell lung cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Nuclear cytoplasmic trafficking of proteins is a major response of human fibroblasts to oxidative stress.Journal of proteome research · 2014Article
- DBC1 is over-expressed and associated with poor prognosis in colorectal cancer.International journal of clinical oncology · 2014Article
- DBC1/CCAR2 and CCAR1 Are Largely Disordered Proteins that Have Evolved from One Common Ancestor.BioMed research international · 2014Article
- Role of multifunctional transcription factor TFII-I and putative tumour suppressor DBC1 in cell cycle and DNA double strand damage repair.British journal of cancer · 2013Article
- Multi-omic data integration links deleted in breast cancer 1 (DBC1) degradation to chromatin remodeling in inflammatory response.Molecular & cellular proteomics : MCP · 2013Article
- Carboxamide SIRT1 inhibitors block DBC1 binding via an acetylation-independent mechanism.Cell cycle (Georgetown, Tex.) · 2013Article
- A Functional Proteomics Perspective of DBC1 as a Regulator of Transcription.Journal of proteomics & bioinformatics · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Deleted in breast cancer-1 (DBC-1) was initially cloned from a homozygously deleted region in breast and other cancers on human chromosome 8p21, although no function is known for the protein product it encodes. We identified the generation of amino-terminally truncated versions of DBC-1 during tumor necrosis factor (TNF)-alpha-mediated apoptosis. Full-length 150 kDa DBC-1 underwent caspase-dependent processing during TNF-alpha-mediated death signaling, to produce p120 DBC-1 and p66 DBC-1 carboxy-terminal fragments. Endogenous DBC-1 localized to the nucleus in healthy cells, but localized to the cytoplasm during TNF-alpha-mediated apoptosis, consistent with the loss of the amino-terminus containing the nuclear localization signal. Overexpression of an amino-terminal truncated DBC-1, resembling p120 DBC-1, caused mitochondrial clustering, mitochondrial matrix condensation, and sensitized cells to TNF-alpha-mediated apoptosis. The carboxy-terminal coiled-coil domain of DBC-1 was responsible for the cytoplasmic and mitochondrial localization, and for the death-promoting activity of DBC-1. Thus, caspase-dependent processing of DBC-1 may act as a feed-forward mechanism to promote apoptosis and possibly also tumor suppression. DBC-1, like its homolog cell cycle and apoptosis regulatory protein-1 (CARP-1), may function in the regulation of apoptosis.
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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.