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Article: Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations.

Zhou, Qing / Greene, Lloyd A

2023 Volume 15, Issue 22

Abstract: Dpep is a cell-penetrating peptide targeting transcription factors ATF5, CEBPB, and CEBPD, and that selectively promotes the apoptotic death of multiple tumor cell types in vitro and in vivo. As such, it is a potential therapeutic. To better understand ... ...

Abstract	Dpep is a cell-penetrating peptide targeting transcription factors ATF5, CEBPB, and CEBPD, and that selectively promotes the apoptotic death of multiple tumor cell types in vitro and in vivo. As such, it is a potential therapeutic. To better understand its mechanism of action, we used PLATE-seq to compare the transcriptomes of six cancer cell lines of diverse origins before and after Dpep exposure. This revealed a context-dependent pattern of regulated genes that was unique to each line, but that exhibited a number of elements that were shared with other lines. This included the upregulation of pro-apoptotic genes and tumor suppressors as well as the enrichment of genes associated with responses to hypoxia and interferons. Downregulated transcripts included oncogenes and dependency genes, as well as enriched genes associated with different phases of the cell cycle and with DNA repair. In each case, such changes have the potential to lie upstream of apoptotic cell death. We also detected the regulation of unique as well as shared sets of transcription factors in each line, suggesting that Dpep may initiate a cascade of transcriptional responses that culminate in cancer cell death. Such death thus appears to reflect context-dependent, yet shared, disruption of multiple cellular pathways as well as of individual survival-relevant genes.
Language	English
Publishing date	2023-11-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15225318
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Article ; Online: Targeting Transcription Factors ATF5, CEBPB and CEBPD with Cell-Penetrating Peptides to Treat Brain and Other Cancers.

Greene, Lloyd A / Zhou, Qing / Siegelin, Markus D / Angelastro, James M

Cells

2023 Volume 12, Issue 4

Abstract: Developing novel therapeutics often follows three steps: target identification, design of strategies to suppress target activity and drug development to implement the strategies. In this review, we recount the evidence identifying the basic leucine ... ...

Abstract	Developing novel therapeutics often follows three steps: target identification, design of strategies to suppress target activity and drug development to implement the strategies. In this review, we recount the evidence identifying the basic leucine zipper transcription factors ATF5, CEBPB, and CEBPD as targets for brain and other malignancies. We describe strategies that exploit the structures of the three factors to create inhibitory dominant-negative (DN) mutant forms that selectively suppress growth and survival of cancer cells. We then discuss and compare four peptides (CP-DN-ATF5, Dpep, Bpep and ST101) in which DN sequences are joined with cell-penetrating domains to create drugs that pass through tissue barriers and into cells. The peptide drugs show both efficacy and safety in suppressing growth and in the survival of brain and other cancers in vivo, and ST101 is currently in clinical trials for solid tumors, including GBM. We further consider known mechanisms by which the peptides act and how these have been exploited in rationally designed combination therapies. We additionally discuss lacunae in our knowledge about the peptides that merit further research. Finally, we suggest both short- and long-term directions for creating new generations of drugs targeting ATF5, CEBPB, CEBPD, and other transcription factors for treating brain and other malignancies.
MeSH term(s)	Humans ; Cell-Penetrating Peptides/pharmacology ; Neoplasms ; Brain/metabolism ; Drug Development ; CCAAT-Enhancer-Binding Protein-delta ; Activating Transcription Factors/metabolism ; CCAAT-Enhancer-Binding Protein-beta
Chemical Substances	Cell-Penetrating Peptides ; CEBPD protein, human ; CCAAT-Enhancer-Binding Protein-delta (142662-43-9) ; ATF5 protein, human ; Activating Transcription Factors ; CEBPB protein, human ; CCAAT-Enhancer-Binding Protein-beta
Language	English
Publishing date	2023-02-11
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12040581
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Article ; Online: Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance.

Banerjee, Debarshi / Boboila, Shuobo / Okochi, Shunpei / Angelastro, James M / Kadenhe-Chiweshe, Angela V / Lopez, Gonzalo / Califano, Andrea / Connolly, Eileen P / Greene, Lloyd A / Yamashiro, Darrell J

Cancer research communications

2024 Volume 3, Issue 12, Page(s) 2518–2530

Abstract: MYCN-amplified neuroblastoma often presents as a highly aggressive metastatic disease with a poor prognosis. Activating transcription factor 5 (ATF5) is implicated in neural cell differentiation and cancer cell survival. Here, we show that ATF5 is highly ...

Abstract	MYCN-amplified neuroblastoma often presents as a highly aggressive metastatic disease with a poor prognosis. Activating transcription factor 5 (ATF5) is implicated in neural cell differentiation and cancer cell survival. Here, we show that ATF5 is highly expressed in patients with stage 4 high-risk neuroblastoma, with increased expression correlating with a poorer prognosis. We demonstrated that ATF5 promotes the metastasis of neuroblastoma cell lines in vivo. Functionally, ATF5 depletion significantly reduced xenograft tumor growth and metastasis of neuroblastoma cells to the bone marrow and liver. Mechanistically, ATF5 endows tumor cells with resistance to anoikis, thereby increasing their survival in systemic circulation and facilitating metastasis. We identified the proapoptotic BCL-2 modifying factor (BMF) as a critical player in ATF5-regulated neuroblastoma anoikis. ATF5 suppresses BMF under suspension conditions at the transcriptional level, promoting anoikis resistance, whereas BMF knockdown significantly prevents ATF5 depletion-induced anoikis. Therapeutically, we showed that a cell-penetrating dominant-negative ATF5 peptide, CP-d/n-ATF5, inhibits neuroblastoma metastasis to the bone marrow and liver by inducing anoikis sensitivity in circulating tumor cells. Our study identified ATF5 as a metastasis promoter and CP-d/n-ATF5 as a potential antimetastatic therapeutic agent for neuroblastoma. Significance: This study shows that resistance to anoikis in neuroblastoma is mediated by ATF5 and offers a rationale for targeting ATF5 to treat metastatic neuroblastoma.
MeSH term(s)	Humans ; Anoikis/genetics ; Cyclic AMP Response Element-Binding Protein ; Neuroblastoma/drug therapy ; Antineoplastic Agents/pharmacology ; Activating Transcription Factors
Chemical Substances	Cyclic AMP Response Element-Binding Protein ; Antineoplastic Agents ; Activating Transcription Factors
Language	English
Publishing date	2024-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-23-0154
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Article ; Online: Stress-induced phospho-ubiquitin formation causes parkin degradation.

Kovalchuke, Lyudmila / Mosharov, Eugene V / Levy, Oren A / Greene, Lloyd A

Scientific reports

2019 Volume 9, Issue 1, Page(s) 11682

Abstract: Mutations in the E3 ubiquitin ligase parkin are the most common known cause of autosomal recessive Parkinson's disease (PD), and parkin depletion may play a role in sporadic PD. Here, we sought to elucidate the mechanisms by which stress decreases parkin ...

Abstract	Mutations in the E3 ubiquitin ligase parkin are the most common known cause of autosomal recessive Parkinson's disease (PD), and parkin depletion may play a role in sporadic PD. Here, we sought to elucidate the mechanisms by which stress decreases parkin protein levels using cultured neuronal cells and the PD-relevant stressor, L-DOPA. We find that L-DOPA causes parkin loss through both oxidative stress-independent and oxidative stress-dependent pathways. Characterization of the latter reveals that it requires both the kinase PINK1 and parkin's interaction with phosphorylated ubiquitin (phospho-Ub) and is mediated by proteasomal degradation. Surprisingly, autoubiquitination and mitophagy do not appear to be required for such loss. In response to stress induced by hydrogen peroxide or CCCP, parkin degradation also requires its association with phospho-Ub, indicating that this mechanism is broadly generalizable. As oxidative stress, metabolic dysfunction and phospho-Ub levels are all elevated in PD, we suggest that these changes may contribute to a loss of parkin expression.
MeSH term(s)	Animals ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/analogs & derivatives ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology ; Cell Differentiation ; Cell Line, Tumor ; Embryo, Mammalian ; Gene Expression Regulation ; Humans ; Hydrogen Peroxide/pharmacology ; Levodopa/pharmacology ; Models, Biological ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; PC12 Cells ; Parkinsonian Disorders/genetics ; Parkinsonian Disorders/metabolism ; Parkinsonian Disorders/pathology ; Phosphorylation/drug effects ; Primary Cell Culture ; Proteasome Endopeptidase Complex/drug effects ; Proteasome Endopeptidase Complex/metabolism ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Proteolysis ; Rats ; Ubiquitin/genetics ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Ubiquitin ; Levodopa (46627O600J) ; Carbonyl Cyanide m-Chlorophenyl Hydrazone (555-60-2) ; carbonylcyanide 4-chlorophenylhydrazone (946-76-9) ; Hydrogen Peroxide (BBX060AN9V) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2019-08-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-47952-5
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Article ; Online: An investigation into the stability and degradation of plastics in aquatic environments using a large-scale field-deployment study.

Theobald, Beatrix / Risani, Regis / Donaldson, Lloyd / Bridson, James H / Kingsbury, Joanne M / Pantos, Olga / Weaver, Louise / Lear, Gavin / Pochon, Xavier / Zaiko, Anastasija / Smith, Dawn A / Anderson, Ross / Davy, Ben / Davy, Steph / Doake, Fraser / Masterton, Hayden / Audrezet, François / Maday, Stefan D M / Wallbank, Jessica A /

Barbier, Maxime / Greene, Angelique F / Parker, Kate / Harris, Jessica / Northcott, Grant L / Abbel, Robert

The Science of the total environment

2024 Volume 917, Page(s) 170301

Abstract: The fragmentation of plastic debris is a key pathway to the formation of microplastic pollution. These disintegration processes depend on the materials' physical and chemical characteristics, but insight into these interrelationships is still limited, ... ...

Abstract	The fragmentation of plastic debris is a key pathway to the formation of microplastic pollution. These disintegration processes depend on the materials' physical and chemical characteristics, but insight into these interrelationships is still limited, especially under natural conditions. Five plastics of known polymer/additive compositions and processing histories were deployed in aquatic environments and recovered after six and twelve months. The polymer types used were linear low density polyethylene (LLDPE), oxo-degradable LLDPE (oxoLLDPE), poly(ethylene terephthalate) (PET), polyamide-6 (PA6), and poly(lactic acid) (PLA). Four geographically distinct locations across Aotearoa/New Zealand were chosen: three marine sites and a wastewater treatment plant (WWTP). Accelerated UV-weathering under controlled laboratory conditions was also carried out to evaluate artificial ageing as a model for plastic degradation in the natural environment. The samples' physical characteristics and surface microstructures were studied for each deployment location and exposure time. The strongest effects were found for oxoLLDPE upon artificial ageing, with increased crystallinity, intense surface cracking, and substantial deterioration of its mechanical properties. However, no changes to the same extent were found after recovery of the deployed material. In the deployment environments, the chemical nature of the plastics was the most relevant factor determining their behaviours. Few significant differences between the four aquatic locations were identified, except for PA6, where indications for biological surface degradation were found only in seawater, not the WWTP. In some cases, artificial ageing reasonably mimicked the changes which some plastic properties underwent in aquatic environments, but generally, it was no reliable model for natural degradation processes. The findings from this study have implications for the understanding of the initial phases of plastic degradation in aquatic environments, eventually leading to microplastics formation. They can also guide the interpretation of accelerated laboratory ageing for the fate of aquatic plastic pollution, and for the testing of aged plastic samples.
Language	English
Publishing date	2024-01-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	121506-1
ISSN	1879-1026 ; 0048-9697
ISSN (online)	1879-1026
ISSN	0048-9697
DOI	10.1016/j.scitotenv.2024.170301
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Article: Cell-Penetrating CEBPB and CEBPD Leucine Zipper Decoys as Broadly Acting Anti-Cancer Agents.

Zhou, Qing / Sun, Xiotian / Pasquier, Nicolas / Jefferson, Parvaneh / Nguyen, Trang T T / Siegelin, Markus D / Angelastro, James M / Greene, Lloyd A

Cancers

2021 Volume 13, Issue 10

Abstract: Transcription factors are key players underlying cancer formation, growth, survival, metastasis and treatment resistance, yet few drugs exist to directly target them. Here, we characterized the in vitro and in vivo anti-cancer efficacy of novel synthetic ...

Abstract	Transcription factors are key players underlying cancer formation, growth, survival, metastasis and treatment resistance, yet few drugs exist to directly target them. Here, we characterized the in vitro and in vivo anti-cancer efficacy of novel synthetic cell-penetrating peptides (Bpep and Dpep) designed to interfere with the formation of active leucine-zipper-based dimers by CEBPB and CEBPD, transcription factors implicated in multiple malignancies. Both peptides similarly promoted apoptosis of multiple tumor lines of varying origins, without such effects on non-transformed cells. Combined with other treatments (radiation, Taxol, chloroquine, doxorubicin), the peptides acted additively to synergistically and were fully active on Taxol-resistant cells. The peptides suppressed expression of known direct CEBPB/CEBPD targets
Language	English
Publishing date	2021-05-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13102504
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Article: An Experimental Study of a Mediterranean-style Diet Supplemented with Nuts and Extra-virgin Olive Oil for Cardiovascular Disease Risk Reduction: The Healthy Hearts Program (P12-021-19)

Willis, Amy / Braxton-lloyd, Kimberly / Greene, Michael

Current developments in nutrition. 2019 June 13, v. 3, no. Supplement_1

2019

Abstract: The primary objective of this 12-week, randomized, controlled trial was to assess the efficacy of a Mediterranean diet (MD) intervention in reducing cardiovascular disease (CVD) risk factors in a high-risk population in the southeastern United States. ... ...

Abstract	The primary objective of this 12-week, randomized, controlled trial was to assess the efficacy of a Mediterranean diet (MD) intervention in reducing cardiovascular disease (CVD) risk factors in a high-risk population in the southeastern United States. Adults (n = 30) with a BMI of > 24.9 and at least two additional CVD risk factors were randomized into one of two groups. The control group (n = 14) received nutrition education on the recommendations of the American Heart Association (AHA). The intervention group (n = 16) received education promoting patterns of a MD as well as dietary supplements of extra-virgin olive oil (EVOO) and mixed nuts. The primary outcome measure was change in systolic blood pressure from baseline to 6 and 12-weeks. Secondary outcome measures include changes in diastolic blood pressure; weight; BMI; fasted total cholesterol, HDLc, LDLc, TG, total cholesterol to HDLc ratio, blood glucose, and HOMA-IR. Nutrition knowledge and MD adherence were assessed at baseline, 6 and 12-weeks. The AHA group had decreases in HDLc, total cholesterol to HDLc ratio, and TG at baseline to 6-weeks, while the MD group had decreases in fat mass and BMR. The total population, experienced a decrease in weight, BMI, and TG from baseline to 6-weeks. At 12-weeks, decreases in weight, BMI, and % body fat were seen in the entire population compared to baseline. The MD group experienced trends towards significance in the differences in measures from baseline to 12-weeks in systolic blood pressure, TG, and total cholesterol to HDLc ratio. Group assignment played a significant role from baseline to 6-weeks in systolic blood pressure, HDLc, and LDLc levels. Nutrition knowledge influenced blood glucose and total cholesterol levels. MD adherence impacted total cholesterol and non-HDLc levels. Percent nut consumption had a significant impact on HDLc levels, % EVOO consumption significantly influenced LDLc values, and the nut/EVOO interaction was significant in both systolic pressure and HDLc levels. Increases in nutrition knowledge, MD adherence, and % nut and EVOO consumption were the most significant influences on measurement outcomes. Our results suggest that a MD can be implemented on a larger scale with potential positive impacts on CVD risk. Funding was provided by Mallon-Zallen Graduate Research Fellowship.
Keywords	adults ; at-risk population ; blood glucose ; body fat ; body mass index ; cardiovascular diseases ; cholesterol ; diastolic blood pressure ; dietary supplements ; extra-virgin olive oil ; heart ; Mediterranean diet ; nutrition education ; nutrition knowledge ; nuts ; risk factors ; risk reduction ; systolic blood pressure ; Southeastern United States
Language	English
Dates of publication	2019-0613
Publishing place	Oxford University Press
Document type	Article
ISSN	2475-2991
DOI	10.1093/cdn/nzz035.P12-021-19
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Contribution of avoidable mortality to life expectancy inequalities in Wales: a decomposition by age and by cause between 2002 and 2020.

Currie, Jonny / Schilling, Hayden T / Evans, Lloyd / Boyce, Tammy / Lester, Nathan / Greene, Giles / Little, Kirsty / Humphreys, Ciarán / Huws, Dyfed / Yeoman, Andrew / Lewis, Sally / Paranjothy, Shantini

Journal of public health (Oxford, England)

2022 Volume 45, Issue 3, Page(s) 762–770

Abstract: Objectives: To explore the contribution of avoidable mortality to life expectancy inequalities in Wales during 2002-2020.: Design: Observational study.: Setting: Wales, 2002-20, including early data from the COVID-19 pandemic.: Methods: We used ...

Abstract	Objectives: To explore the contribution of avoidable mortality to life expectancy inequalities in Wales during 2002-2020. Design: Observational study. Setting: Wales, 2002-20, including early data from the COVID-19 pandemic. Methods: We used routine statistics for 2002-2020 on population and deaths in Wales stratified by age, sex, deprivation quintile and cause of death. We estimated the contribution of avoidable causes of death and specific age-categories using the Arriaga decomposition method to highlight priorities for action. Results: Life expectancy inequalities rose 2002-20 amongst both sexes, driven by serial decreases in life expectancy amongst the most deprived quintiles. The contributions of amenable and preventable mortality to life expectancy inequalities changed relatively little between 2002 and 2020, with larger rises in non-avoidable causes. Key avoidable mortality conditions driving the life expectancy gap in the most recent period of 2018-2020 for females were circulatory disease, cancers, respiratory disease and alcohol- and drug-related deaths, and also injuries for males. Conclusions: Life expectancy inequalities widened during 2002-20, driven by deteriorating life expectancy in the most deprived quintiles. Sustained investment in prevention post-COVID-19 is needed to address growing health inequity in Wales; there remains a role for the National Health Service in ensuring equitable healthcare access to alongside wider policies that promote equity.
MeSH term(s)	Male ; Female ; Humans ; Cause of Death ; Wales/epidemiology ; Pandemics ; State Medicine ; COVID-19 ; Life Expectancy ; Mortality
Language	English
Publishing date	2022-11-15
Publishing country	England
Document type	Observational Study ; Journal Article
ZDB-ID	2142082-8
ISSN	1741-3850 ; 1741-3842
ISSN (online)	1741-3850
ISSN	1741-3842
DOI	10.1093/pubmed/fdac133
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Article ; Online: Dominant-negative ATF5 rapidly depletes survivin in tumor cells.

Sun, Xiaotian / Angelastro, James M / Merino, David / Zhou, Qing / Siegelin, Markus D / Greene, Lloyd A

Cell death & disease

2019 Volume 10, Issue 10, Page(s) 709

Abstract: Survivin (BIRC5, product of the BIRC5 gene) is highly expressed in many tumor types and has been widely identified as a potential target for cancer therapy. However, effective anti-survivin drugs remain to be developed. Here we report that both vector- ... ...

Abstract	Survivin (BIRC5, product of the BIRC5 gene) is highly expressed in many tumor types and has been widely identified as a potential target for cancer therapy. However, effective anti-survivin drugs remain to be developed. Here we report that both vector-delivered and cell-penetrating dominant-negative (dn) forms of the transcription factor ATF5 that promote selective death of cancer cells in vitro and in vivo cause survivin depletion in tumor cell lines of varying origins. dn-ATF5 decreases levels of both survivin mRNA and protein. The depletion of survivin protein appears to be driven at least in part by enhanced proteasomal turnover and depletion of the deubiquitinase USP9X. Survivin loss is rapid and precedes the onset of cell death triggered by dn-ATF5. Although survivin downregulation is sufficient to drive tumor cell death, survivin over-expression does not rescue cancer cells from dn-ATF5-promoted apoptosis. This indicates that dn-ATF5 kills malignant cells by multiple mechanisms that include, but are not limited to, survivin depletion. Cell-penetrating forms of dn-ATF5 are currently being developed for potential therapeutic use and the present findings suggest that they may pose an advantage over treatments that target only survivin.
MeSH term(s)	Activating Transcription Factors/administration & dosage ; Activating Transcription Factors/genetics ; Amino Acid Sequence ; Apoptosis/drug effects ; Cell Line, Tumor ; Drug Development/methods ; Genetic Vectors/administration & dosage ; Genetic Vectors/genetics ; HEK293 Cells ; Humans ; Proteasome Endopeptidase Complex/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Survivin/biosynthesis ; Survivin/genetics ; Survivin/metabolism ; Transfection ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	ATF5 protein, human ; Activating Transcription Factors ; BIRC5 protein, human ; RNA, Messenger ; Survivin ; USP9X protein, human ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2019-09-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-019-1872-y
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Article ; Online: Dominant-Negative ATF5 Compromises Cancer Cell Survival by Targeting CEBPB and CEBPD.

Sun, Xiaotian / Jefferson, Parvaneh / Zhou, Qing / Angelastro, James M / Greene, Lloyd A

Molecular cancer research : MCR

2019 Volume 18, Issue 2, Page(s) 216–228

Abstract: The basic leucine zipper transcription factor ATF5 is overexpressed in many tumor types and interference with its expression or function inhibits cancer cell survival. As a potential therapeutic approach to exploit these findings, we created dominant- ... ...

Abstract	The basic leucine zipper transcription factor ATF5 is overexpressed in many tumor types and interference with its expression or function inhibits cancer cell survival. As a potential therapeutic approach to exploit these findings, we created dominant-negative (DN) ATF5 forms lacking DNA-binding ability that retain the ATF5 leucine zipper, and thus associate with and sequester ATF5's requisite leucine zipper-binding partners. Preclinical studies with DN-ATF5, including a cell-penetrating form, show
MeSH term(s)	Activating Transcription Factors/genetics ; Activating Transcription Factors/metabolism ; CCAAT-Enhancer-Binding Protein-beta/genetics ; CCAAT-Enhancer-Binding Protein-beta/metabolism ; CCAAT-Enhancer-Binding Protein-delta/genetics ; CCAAT-Enhancer-Binding Protein-delta/metabolism ; Cell Line, Tumor ; Cell Survival/physiology ; Cytoskeletal Proteins/genetics ; Cytoskeletal Proteins/metabolism ; Gene Knockdown Techniques ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Transfection
Chemical Substances	ATF5 protein, human ; Activating Transcription Factors ; CCAAT-Enhancer-Binding Protein-beta ; CCDC6 protein, human ; CEBPB protein, human ; CEBPD protein, human ; Cytoskeletal Proteins ; CCAAT-Enhancer-Binding Protein-delta (142662-43-9)
Language	English
Publishing date	2019-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-19-0631
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