Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Mais filtros








Base de dados
Intervalo de ano de publicação
1.
ACS Chem Biol ; 13(10): 2862-2867, 2018 10 19.
Artigo em Inglês | MEDLINE | ID: mdl-30200762

RESUMO

P300/CBP-associated factor (PCAF) and general control nonderepressible 5 (GCN5) are closely related epigenetic proteins, each containing an acetyltransferase domain and a bromodomain. Consistent with reported roles for these proteins in immune function, we find that PCAF-deficient macrophages exhibit a markedly reduced ability to produce cytokines upon stimulation with lipopolysaccharide (LPS). Investigating the potential to target this pathway pharmacologically, we show that chemical inhibition of the PCAF/GCN5 bromodomains is insufficient to recapitulate the diminished inflammatory response of PCAF-deficient immune cells. However, by generating the first PCAF/GCN5 proteolysis targeting chimera (PROTAC), we identify small molecules able to degrade PCAF/GCN5 and to potently modulate the expression of multiple inflammatory mediators in LPS-stimulated macrophages and dendritic cells. Our data illustrate the power of the PROTAC approach in the context of multidomain proteins, revealing a novel anti-inflammatory therapeutic opportunity for targeting PCAF/GCN5.


Assuntos
Benzoatos/farmacologia , Piperidinas/farmacologia , Piridazinas/farmacologia , Fatores de Transcrição de p300-CBP/metabolismo , Proteínas Adaptadoras de Transdução de Sinal , Animais , Benzoatos/síntese química , Benzoatos/química , Diferenciação Celular/efeitos dos fármacos , Citocinas/metabolismo , Células Dendríticas/metabolismo , Humanos , Inflamação/induzido quimicamente , Inflamação/metabolismo , Lipopolissacarídeos , Macrófagos/metabolismo , Camundongos , Monócitos/metabolismo , Peptídeo Hidrolases/metabolismo , Piperidinas/síntese química , Piperidinas/química , Domínios Proteicos , Proteólise , Piridazinas/síntese química , Piridazinas/química , Estereoisomerismo , Ubiquitina-Proteína Ligases , Fatores de Transcrição de p300-CBP/química
2.
SLAS Discov ; 23(6): 532-545, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29699447

RESUMO

High-throughput screening (HTS) hits include compounds with undesirable properties. Many filters have been described to identify such hits. Notably, pan-assay interference compounds (PAINS) has been adopted by the community as the standard term to refer to such filters, and very useful guidelines have been adopted by the American Chemical Society (ACS) and subsequently triggered a healthy scientific debate about the pitfalls of draconian use of filters. Using an inhibitory frequency index, we have analyzed in detail the promiscuity profile of the whole GlaxoSmithKline (GSK) HTS collection comprising more than 2 million unique compounds that have been tested in hundreds of screening assays. We provide a comprehensive analysis of many previously published filters and newly described classes of nuisance structures that may serve as a useful source of empirical information to guide the design or growth of HTS collections and hit triaging strategies.


Assuntos
Descoberta de Drogas/métodos , Ensaios de Triagem em Larga Escala/métodos , Bibliotecas de Moléculas Pequenas/química , Bioensaio/métodos
3.
Curr Opin Drug Discov Devel ; 12(5): 666-81, 2009 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-19736625

RESUMO

The correct folding of proteins is a fundamental process in the normal physiological functioning of cells, and is mediated by cellular chaperones including members of the Hsp70 family. Many diseases are caused by a failure of cellular chaperones to adequately maintain correct protein folding, and has led to the development of a therapeutic strategy to upregulate the activity of cellular chaperones in order to ameliorate intrinsic folding deficits. A large range of pharmacological agents that can induce cellular chaperones and correct deficits associated with misfolded proteins are known. This review surveys the mechanisms and compounds that have been used to modulate cellular chaperones, and discusses the continuing challenges in translating this approach into clinical improvements in the treatment of protein misfolding disorders.


Assuntos
Desenho de Fármacos , Chaperonas Moleculares/metabolismo , Dobramento de Proteína , Deficiências na Proteostase/metabolismo , Animais , Terapia Genética , Proteínas de Choque Térmico HSP70/metabolismo , Proteínas de Choque Térmico HSP90/antagonistas & inibidores , Proteínas de Choque Térmico HSP90/metabolismo , Humanos , Hidroxilaminas/farmacologia , Chaperonas Moleculares/antagonistas & inibidores , Chaperonas Moleculares/genética , Estrutura Molecular , Conformação Proteica , Dobramento de Proteína/efeitos dos fármacos , Processamento de Proteína Pós-Traducional/efeitos dos fármacos , Deficiências na Proteostase/genética , Deficiências na Proteostase/terapia , Relação Estrutura-Atividade , Regulação para Cima
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA