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Article ; Online: Trust in Science: a novel research partnership model in Latin America.

Gloger, Israel S / Felice, Rosana / Madauss, Kevin P

2021 Volume 20, Issue 8, Page(s) 571–572

MeSH term(s)	Academies and Institutes/standards ; Biomedical Research/standards ; Humans ; Public-Private Sector Partnerships/standards ; Trust
Language	English
Publishing date	2021-04-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2062954-0
ISSN	1474-1784 ; 1474-1776
ISSN (online)	1474-1784
ISSN	1474-1776
DOI	10.1038/d41573-021-00065-z
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Zs.A 5564: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Correction: Inhibitors of Rho kinases (ROCK) induce multiple mitotic defects and synthetic lethality in BRCA2-deficient cells.

Martino, Julieta / Siri, Sebastián Omar / Calzetta, Nicolás Luis / Paviolo, Natalia Soledad / Garro, Cintia / Pansa, Maria F / Carbajosa, Sofía / Brown, Aaron C / Bocco, José Luis / Gloger, Israel / Drewes, Gerard / Madauss, Kevin P / Soria, Gastón / Gottifredi, Vanesa

eLife

2023 Volume 12

Language	English
Publishing date	2023-11-14
Publishing country	England
Document type	Published Erratum
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.94414
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Article ; Online: Inhibitors of Rho kinases (ROCK) induce multiple mitotic defects and synthetic lethality in BRCA2-deficient cells.

eLife

2023 Volume 12

Abstract: The trapping of Poly-ADP-ribose polymerase (PARP) on DNA caused by PARP inhibitors (PARPi) triggers acute DNA replication stress and synthetic lethality (SL) in BRCA2-deficient cells. Hence, DNA damage is accepted as a prerequisite for SL in BRCA2- ... ...

Abstract	The trapping of Poly-ADP-ribose polymerase (PARP) on DNA caused by PARP inhibitors (PARPi) triggers acute DNA replication stress and synthetic lethality (SL) in BRCA2-deficient cells. Hence, DNA damage is accepted as a prerequisite for SL in BRCA2-deficient cells. In contrast, here we show that inhibiting ROCK in BRCA2-deficient cells triggers SL independently from acute replication stress. Such SL is preceded by polyploidy and binucleation resulting from cytokinesis failure. Such initial mitosis abnormalities are followed by other M phase defects, including anaphase bridges and abnormal mitotic figures associated with multipolar spindles, supernumerary centrosomes and multinucleation. SL was also triggered by inhibiting Citron Rho-interacting kinase, another enzyme that, similarly to ROCK, regulates cytokinesis. Together, these observations demonstrate that cytokinesis failure triggers mitotic abnormalities and SL in BRCA2-deficient cells. Furthermore, the prevention of mitotic entry by depletion of Early mitotic inhibitor 1 (EMI1) augmented the survival of BRCA2-deficient cells treated with ROCK inhibitors, thus reinforcing the association between M phase and cell death in BRCA2-deficient cells. This novel SL differs from the one triggered by PARPi and uncovers mitosis as an Achilles heel of BRCA2-deficient cells.
MeSH term(s)	Anaphase ; DNA Damage ; Mitosis ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerases/metabolism ; Synthetic Lethal Mutations ; rho-Associated Kinases/antagonists & inhibitors ; BRCA2 Protein/genetics ; Humans
Chemical Substances	Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; rho-Associated Kinases (EC 2.7.11.1) ; BRCA2 Protein
Language	English
Publishing date	2023-04-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.80254
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Article ; Online: Author Correction: Novel scaffolds for inhibition of Cruzipain identified from high-throughput screening of anti-kinetoplastid chemical boxes.

Salas-Sarduy, Emir / Landaburu, Lionel Urán / Karpiak, Joel / Madauss, Kevin P / Cazzulo, Juan José / Agüero, Fernán / Alvarez, Vanina Eder

Scientific reports

2018 Volume 8, Issue 1, Page(s) 8743

Abstract: A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper. ...

Abstract	A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
Language	English
Publishing date	2018-06-04
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-26961-w
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Article ; Online: Novel scaffolds for inhibition of Cruzipain identified from high-throughput screening of anti-kinetoplastid chemical boxes.

Salas-Sarduy, Emir / Landaburu, Lionel Urán / Karpiak, Joel / Madauss, Kevin P / Cazzulo, Juan José / Agüero, Fernán / Alvarez, Vanina Eder

Scientific reports

2017 Volume 7, Issue 1, Page(s) 12073

Abstract: American Trypanosomiasis or Chagas disease is a prevalent, neglected and serious debilitating illness caused by the kinetoplastid protozoan parasite Trypanosoma cruzi. The current chemotherapy is limited only to nifurtimox and benznidazole, two drugs ... ...

Abstract	American Trypanosomiasis or Chagas disease is a prevalent, neglected and serious debilitating illness caused by the kinetoplastid protozoan parasite Trypanosoma cruzi. The current chemotherapy is limited only to nifurtimox and benznidazole, two drugs that have poor efficacy in the chronic phase and are rather toxic. In this scenario, more efficacious and safer drugs, preferentially acting through a different mechanism of action and directed against novel targets, are particularly welcome. Cruzipain, the main papain-like cysteine peptidase of T. cruzi, is an important virulence factor and a chemotherapeutic target with excellent pre-clinical validation evidence. Here, we present the identification of new Cruzipain inhibitory scaffolds within the GlaxoSmithKline HAT (Human African Trypanosomiasis) and Chagas chemical boxes, two collections grouping 404 non-cytotoxic compounds with high antiparasitic potency, drug-likeness, structural diversity and scientific novelty. We have adapted a continuous enzymatic assay to a medium-throughput format and carried out a primary screening of both collections, followed by construction and analysis of dose-response curves of the most promising hits. Using the identified compounds as a starting point a substructure directed search against CHEMBL Database revealed plausible common scaffolds while docking experiments predicted binding poses and specific interactions between Cruzipain and the novel inhibitors.
MeSH term(s)	Antiprotozoal Agents/chemistry ; Antiprotozoal Agents/pharmacology ; Chagas Disease/drug therapy ; Chagas Disease/parasitology ; Cysteine Endopeptidases/chemistry ; Cysteine Endopeptidases/metabolism ; High-Throughput Screening Assays/methods ; Host-Parasite Interactions/drug effects ; Humans ; Kinetoplastida/drug effects ; Kinetoplastida/enzymology ; Kinetoplastida/physiology ; Molecular Docking Simulation ; Molecular Structure ; Nifurtimox/chemistry ; Nifurtimox/pharmacology ; Nitroimidazoles/chemistry ; Nitroimidazoles/pharmacology ; Protein Domains ; Protozoan Proteins/antagonists & inhibitors ; Protozoan Proteins/chemistry ; Protozoan Proteins/metabolism ; Trypanosoma cruzi/drug effects ; Trypanosoma cruzi/enzymology ; Trypanosoma cruzi/physiology
Chemical Substances	Antiprotozoal Agents ; Nitroimidazoles ; Protozoan Proteins ; Cysteine Endopeptidases (EC 3.4.22.-) ; cruzipain (EC 3.4.22.51) ; Nifurtimox (M84I3K7C2O) ; benzonidazole (YC42NRJ1ZD)
Language	English
Publishing date	2017-09-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-12170-4
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Article ; Online: AKT inhibition impairs PCNA ubiquitylation and triggers synthetic lethality in homologous recombination-deficient cells submitted to replication stress.

Villafañez, Florencia / García, Iris Alejandra / Carbajosa, Sofia / Pansa, María Florencia / Mansilla, Sabrina / Llorens, María Candelaria / Angiolini, Virginia / Guantay, Laura / Jacobs, Heinz / Madauss, Kevin P / Gloger, Israel / Gottifredi, Vanesa / Bocco, Jose Luis / Soria, Gaston

Oncogene

2019 Volume 38, Issue 22, Page(s) 4310–4324

Abstract: Translesion DNA synthesis (TLS) and homologous recombination (HR) cooperate during S-phase to safeguard replication forks integrity. Thus, the inhibition of TLS becomes a promising point of therapeutic intervention in HR-deficient cancers, where TLS ... ...

Abstract	Translesion DNA synthesis (TLS) and homologous recombination (HR) cooperate during S-phase to safeguard replication forks integrity. Thus, the inhibition of TLS becomes a promising point of therapeutic intervention in HR-deficient cancers, where TLS impairment might trigger synthetic lethality (SL). The main limitation to test this hypothesis is the current lack of selective pharmacological inhibitors of TLS. Herein, we developed a miniaturized screening assay to identify inhibitors of PCNA ubiquitylation, a key post-translational modification required for efficient TLS activation. After screening a library of 627 kinase inhibitors, we found that targeting the pro-survival kinase AKT leads to strong impairment of PCNA ubiquitylation. Mechanistically, we found that AKT-mediated modulation of Proliferating Cell Nuclear Antigen (PCNA) ubiquitylation after UV requires the upstream activity of DNA PKcs, without affecting PCNA ubiquitylation levels in unperturbed cells. Moreover, we confirmed that persistent AKT inhibition blocks the recruitment of TLS polymerases to sites of DNA damage and impairs DNA replication forks processivity after UV irradiation, leading to increased DNA replication stress and cell death. Remarkably, when we compared the differential survival of HR-proficient vs HR-deficient cells, we found that the combination of UV irradiation and AKT inhibition leads to robust SL induction in HR-deficient cells. We link this phenotype to AKT ability to inhibit PCNA ubiquitylation, since the targeted knockdown of PCNA E3-ligase (RAD18) and a non-ubiquitylable (PCNA K164R) knock-in model recapitulate the observed SL induction. Collectively, this work identifies AKT as a novel regulator of PCNA ubiquitylation and provides the proof-of-concept of inhibiting TLS as a therapeutic approach to selectively kill HR-deficient cells submitted to replication stress.
MeSH term(s)	Cell Death/genetics ; Cell Line ; Cell Line, Tumor ; DNA/genetics ; DNA Damage/genetics ; DNA Replication/genetics ; DNA-Directed DNA Polymerase/genetics ; HCT116 Cells ; HEK293 Cells ; Homologous Recombination/genetics ; Humans ; Proliferating Cell Nuclear Antigen/genetics ; Proto-Oncogene Proteins c-akt/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitination/genetics
Chemical Substances	PCNA protein, human ; Proliferating Cell Nuclear Antigen ; DNA (9007-49-2) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
Language	English
Publishing date	2019-01-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-019-0724-7
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Zs.A 2218: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article: The evolution of progesterone receptor ligands.

Madauss, Kevin P / Stewart, Eugene L / Williams, Shawn P

Medicinal research reviews

2007 Volume 27, Issue 3, Page(s) 374–400

Abstract: Progesterone is one of the first nuclear receptor hormones to be described functionally and subsequently approached as a drug target. Because progesterone (1) affects both menstruation and gestation via the progesterone receptor (PR), research aimed at ... ...

Abstract	Progesterone is one of the first nuclear receptor hormones to be described functionally and subsequently approached as a drug target. Because progesterone (1) affects both menstruation and gestation via the progesterone receptor (PR), research aimed at modulating its activity is usually surrounded by controversy. However, ligands for PR were developed into drugs, and their evolution can be crudely divided into three periods: (1) drug-like steroids that mimic the gestational properties of progesterone; (2) drug-like steroids with different properties from progesterone and expanded therapeutic applications; and (3) non-steroidal PR ligands with improved selectivity and modulator properties and further expanded therapeutic applications. Although the latter have yet to see widespread clinical applications, their development is founded on a half century of research, and they represent the future for this drug target.
MeSH term(s)	Contraceptives, Oral/therapeutic use ; Furans/metabolism ; Humans ; Indoles/metabolism ; Ligands ; Models, Molecular ; Oxazines/metabolism ; Progestins/antagonists & inhibitors ; Progestins/metabolism ; Progestins/therapeutic use ; Quinolines/metabolism ; Receptors, Progesterone/metabolism ; Steroids/metabolism ; Steroids/therapeutic use
Chemical Substances	Contraceptives, Oral ; Furans ; Indoles ; Ligands ; Oxazines ; Progestins ; Quinolines ; Receptors, Progesterone ; Steroids
Language	English
Publishing date	2007-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603210-2
ISSN	0198-6325
ISSN	0198-6325
DOI	10.1002/med.20083
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Zs.A 1764: Show issues

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Article ; Online: Polo-like Kinase 1 Inhibition as a Therapeutic Approach to Selectively Target BRCA1-Deficient Cancer Cells by Synthetic Lethality Induction.

Carbajosa, Sofía / Pansa, María Florencia / Paviolo, Natalia S / Castellaro, Andrés M / Andino, Diego L / Nigra, Ayelén D / García, Iris Alejandra / Racca, Ana C / Rodriguez-Berdini, Lucía / Angiolini, Virginia / Guantay, Laura / Villafañez, Florencia / Federico, María Belén / Rodríguez-Baili, María Celeste / Caputto, Beatriz L / Drewes, Gerard / Madauss, Kevin P / Gloger, Israel / Fernandez, Elmer /

Gil, Germán A / Bocco, José Luis / Gottifredi, Vanesa / Soria, Gastón

Clinical cancer research : an official journal of the American Association for Cancer Research

2019 Volume 25, Issue 13, Page(s) 4049–4062

Abstract: Purpose: BRCA1 and BRCA2 deficiencies are widespread drivers of human cancers that await the development of targeted therapies. We aimed to identify novel synthetic lethal relationships with therapeutic potential using BRCA-deficient isogenic ... ...

Abstract	Purpose: BRCA1 and BRCA2 deficiencies are widespread drivers of human cancers that await the development of targeted therapies. We aimed to identify novel synthetic lethal relationships with therapeutic potential using BRCA-deficient isogenic backgrounds. Experimental design: We developed a phenotypic screening technology to simultaneously search for synthetic lethal (SL) interactions in BRCA1- and BRCA2-deficient contexts. For validation, we developed chimeric spheroids and a dual-tumor xenograft model that allowed the confirmation of SL induction with the concomitant evaluation of undesired cytotoxicity on BRCA-proficient cells. To extend our results using clinical data, we performed retrospective analysis on The Cancer Genome Atlas (TCGA) breast cancer database. Results: The screening of a kinase inhibitors library revealed that Polo-like kinase 1 (PLK1) inhibition triggers strong SL induction in BRCA1-deficient cells. Mechanistically, we found no connection between the SL induced by PLK1 inhibition and PARP inhibitors. Instead, we uncovered that BRCA1 downregulation and PLK1 inhibition lead to aberrant mitotic phenotypes with altered centrosomal duplication and cytokinesis, which severely reduced the clonogenic potential of these cells. The penetrance of PLK1/BRCA1 SL interaction was validated using several isogenic and nonisogenic cellular models, chimeric spheroids, and mice xenografts. Moreover, bioinformatic analysis revealed high-PLK1 expression in BRCA1-deficient tumors, a phenotype that was consistently recapitulated by inducing BRCA1 deficiency in multiple cell lines as well as in BRCA1-mutant cells. Conclusions: We uncovered an unforeseen addiction of BRCA1-deficient cancer cells to PLK1 expression, which provides a new means to exploit the therapeutic potential of PLK1 inhibitors in clinical trials, by generating stratification schemes that consider this molecular trait in patient cohorts.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; BRCA1 Protein/deficiency ; BRCA2 Protein/deficiency ; BRCA2 Protein/genetics ; Cell Cycle/drug effects ; Cell Cycle/genetics ; Cell Cycle Proteins/antagonists & inhibitors ; Cell Line, Tumor ; Cells, Cultured ; Chromosome Aberrations ; DNA Damage ; Disease Models, Animal ; Gene Expression ; Gene Knockdown Techniques ; Humans ; Mice ; Protein Kinase Inhibitors/pharmacology ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Proto-Oncogene Proteins/antagonists & inhibitors ; Synthetic Lethal Mutations/drug effects ; Xenograft Model Antitumor Assays ; Polo-Like Kinase 1
Chemical Substances	BRCA1 Protein ; BRCA1 protein, human ; BRCA2 Protein ; BRCA2 protein, human ; Cell Cycle Proteins ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2019-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-18-3516
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Zs.A 4223: Show issues

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Article: NK cells with decreased expression of multiple activating receptors is a dominant phenotype in pediatric patients with acute lymphoblastic leukemia.

Valenzuela-Vázquez, Lucero / Nuñez-Enriquez, Juan Carlos / Sánchez-Herrera, Jacqueline / Medina-Sanson, Aurora / Pérez-Saldivar, María Luisa / Jiménez-Hernández, Elva / Martiín-Trejo, Jorge Alfonso / Del Campo-Martínez, María de Los Ángeles / Flores-Lujano, Janet / Amador-Sánchez, Raquel / Mora-Ríos, Félix Gustavo / Peñaloza-González, José Gabriel / Duarte-Rodríguez, David Aldebarán / Torres-Nava, José Refugio / Espinosa-Elizondo, Rosa Martha / Cortés-Herrera, Beatriz / Flores-Villegas, Luz Victoria / Merino-Pasaye, Laura Elizabeth / Almeida-Hernández, Carolina /

Ramírez-Colorado, Rosario / Solís-Labastida, Karina Anastacia / Medrano-López, Francisco / Pérez-Gómez, Jessica Arleet / Velázquez-Aviña, Martha Margarita / Martínez-Ríos, Annel / Aguilar-De Los Santos, Antonio / Santillán-Juárez, Jessica Denisse / Gurrola-Silva, Alma / García-Velázquez, Alejandra Jimena / Mata-Rocha, Minerva / Hernández-Echáurregui, Gabriela Alicia / Sepúlveda-Robles, Omar Alejandro / Rosas-Vargas, Haydeé / Mancilla-Herrera, Ismael / Jimenez-Morales, Silvia / Hidalgo-Miranda, Alfredo / Martinez-Duncker, Ivan / Waight, Jeremy D / Hance, Kenneth W / Madauss, Kevin P / Mejía-Aranguré, Juan Manuel / Cruz-Munoz, Mario Ernesto

Frontiers in oncology

2022 Volume 12, Page(s) 1023510

Abstract: NK cells have unique attributes to react towards cells undergoing malignant transformation or viral infection. This reactivity is regulated by activating or inhibitory germline encoded receptors. An impaired NK cell function may result from an aberrant ... ...

Abstract	NK cells have unique attributes to react towards cells undergoing malignant transformation or viral infection. This reactivity is regulated by activating or inhibitory germline encoded receptors. An impaired NK cell function may result from an aberrant expression of such receptors, a condition often seen in patients with hematological cancers. Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer worldwide and NK cells have emerged as crucial targets for developing immunotherapies. However, there are important gaps concerning the phenotype and behavior of NK cells during emergence of ALL. In this study we analyze the phenotype and function of NK cells from peripheral blood in pediatric patients with ALL at diagnosis. Our results showed that NK cells exhibited an altered phenotype highlighted by a significant reduction in the overall expression and percent representation of activating receptors compared to age-matched controls. No significant differences were found for the expression of inhibitory receptors. Moreover, NK cells with a concurrent reduced expression in various activating receptors, was the dominant phenotype among patients. An alteration in the relative frequencies of NK cells expressing NKG2A and CD57 within the mature NK cell pool was also observed. In addition, NK cells from patients displayed a significant reduction in the ability to sustain antibody-dependent cellular cytotoxicity (ADCC). Finally, an aberrant expression of activating receptors is associated with the phenomenon of leukemia during childhood.
Language	English
Publishing date	2022-11-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.1023510
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Article ; Online: The first X-ray crystal structure of the glucocorticoid receptor bound to a non-steroidal agonist.

Madauss, Kevin P / Bledsoe, Randy K / Mclay, Iain / Stewart, Eugene L / Uings, Iain J / Weingarten, Gordon / Williams, Shawn P

Bioorganic & medicinal chemistry letters

2008 Volume 18, Issue 23, Page(s) 6097–6099

Abstract: The amino-pyrazole 2,6-dichloro-N-ethyl benzamide 1 is a selective GR agonist with dexamethasone-like in vitro potency. Its X-ray crystal structure in the GR LBD (Glucocorticoid ligand-binding domain) is described and compared to other reported ... ...

Abstract	The amino-pyrazole 2,6-dichloro-N-ethyl benzamide 1 is a selective GR agonist with dexamethasone-like in vitro potency. Its X-ray crystal structure in the GR LBD (Glucocorticoid ligand-binding domain) is described and compared to other reported structures of steroidal GR agonists in the GR LBD (3E7C).
MeSH term(s)	Benzamides/chemical synthesis ; Benzamides/chemistry ; Benzamides/pharmacology ; Crystallography, X-Ray ; Dexamethasone/chemistry ; Dexamethasone/pharmacology ; Models, Molecular ; Molecular Conformation ; Molecular Structure ; Pyrazoles/chemical synthesis ; Pyrazoles/chemistry ; Pyrazoles/pharmacology ; Receptors, Glucocorticoid/agonists ; Structure-Activity Relationship
Chemical Substances	Benzamides ; Pyrazoles ; Receptors, Glucocorticoid ; amino-pyrazole 2,6-dichloro-N-ethyl benzamide ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2008-12-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2008.10.021
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