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Métodos Terapéuticos y Terapias MTCI
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1.
Curr Protein Pept Sci ; 23(10): 684-696, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36121086

RESUMEN

As an important pectin enzyme, pectin methylesterase (PME) can hydrolyze methyl esters, release methanol and reduce esterification. It is essential in regulating pollen tube development, root extension, and fruit ripening. Pectin methylesterase inhibitors (PMEI) can specifically bind PME and inhibit its activity, which jointly determines the esterification degree of pectin. PMEI has important application prospects in plant pest control, fruits and vegetable processing fields. In this paper, the gene families, crystal structures, molecular recognition, and applications in plants and industry are reviewed for the PME and PMEI systems. Finally, the semi-rational design of PMEI is discussed and discussed prospected.


Asunto(s)
Hidrolasas de Éster Carboxílico , Pectinas , Hidrolasas de Éster Carboxílico/genética , Hidrolasas de Éster Carboxílico/metabolismo , Pectinas/química , Pectinas/metabolismo , Plantas/metabolismo , Inhibidores Enzimáticos/química
2.
Infect Genet Evol ; 75: 103981, 2019 11.
Artículo en Inglés | MEDLINE | ID: mdl-31369863

RESUMEN

Peste des petits ruminants virus (PPRV) is a morbillivirus which causes severe disease in ruminants. Since interferons (IFNs) serve as the important defense line against viral infection, we have investigated the roles of types I and III IFNs in PPRV infection in vitro. Upon PPRV infection, IFN-λ3 was strongly induced, while IFN-ß and IFN-λ2 were moderately induced at transcriptional level in human embryonic kidney 293 T (HEK293T) cells. Although the transcription of type I and III IFNs were triggered, the production of functional IFN products was not detected. Importantly, the replication of PPRV was strongly inhibited in HEK293T cells treated by the exogenous IFNs (IFN-α-2b, IFN-ß and IFN-λ3). Consistently, these IFNs significantly activate a panel of IFN-stimulated genes (ISGs). The inhibition of JAK-STAT pathway by JAK I inhibitor can abrogate the anti-PPRV activity of IFNs. Thus, our study shall contribute to better understanding of the complex PPRV-host interactions and provide rationale for therapeutic development of IFN-based treatment against PPRV infection.


Asunto(s)
Interferones/genética , Interferones/farmacología , Peste de los Pequeños Rumiantes/genética , Virus de la Peste de los Pequeños Rumiantes/fisiología , Animales , Regulación de la Expresión Génica/efectos de los fármacos , Células HEK293 , Interacciones Microbiota-Huesped , Humanos , Quinasas Janus/genética , Peste de los Pequeños Rumiantes/tratamiento farmacológico , Peste de los Pequeños Rumiantes/virología , Virus de la Peste de los Pequeños Rumiantes/efectos de los fármacos , Factores de Transcripción STAT/genética , Transducción de Señal/efectos de los fármacos , Replicación Viral/efectos de los fármacos
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