A parent-of-origin effect determines the susceptibility of a non-informative F1 population to Trypanosoma cruzi infection in vivo (2013)
- Authors:
- USP affiliated authors: SILVA, JOÃO SANTANA DA - FMRP ; ZAMBONI, DARIO SIMÕES - FMRP
- Unidade: FMRP
- DOI: 10.1371/journal.pone.0056347
- Subjects: DOENÇA DE CHAGAS (GENÉTICA); HIBRIDIZAÇÃO; TRYPANOSOMA CRUZI; CROMOSSOMO X
- Language: Inglês
- Imprenta:
- Publisher place: San Francisco
- Date published: 2013
- Source:
- Este periódico é de acesso aberto
- Este artigo é de acesso aberto
- URL de acesso aberto
- Cor do Acesso Aberto: gold
- Licença: cc-by
-
ABNT
SILVA, Grace Kelly da et al. A parent-of-origin effect determines the susceptibility of a non-informative F1 population to Trypanosoma cruzi infection in vivo. PLoS One, v. 8, n. 2, p. e56347-1 - e56347-10, 2013Tradução . . Disponível em: https://doi.org/10.1371/journal.pone.0056347. Acesso em: 27 dez. 2025. -
APA
Silva, G. K. da, Cunha, L. D. da, Horta, C. V., Silva, A. L. N., Gutierrez, F. R. S., Silva, J. S. da, & Zamboni, D. S. (2013). A parent-of-origin effect determines the susceptibility of a non-informative F1 population to Trypanosoma cruzi infection in vivo. PLoS One, 8( 2), e56347-1 - e56347-10. doi:10.1371/journal.pone.0056347 -
NLM
Silva GK da, Cunha LD da, Horta CV, Silva ALN, Gutierrez FRS, Silva JS da, Zamboni DS. A parent-of-origin effect determines the susceptibility of a non-informative F1 population to Trypanosoma cruzi infection in vivo [Internet]. PLoS One. 2013 ; 8( 2): e56347-1 - e56347-10.[citado 2025 dez. 27 ] Available from: https://doi.org/10.1371/journal.pone.0056347 -
Vancouver
Silva GK da, Cunha LD da, Horta CV, Silva ALN, Gutierrez FRS, Silva JS da, Zamboni DS. A parent-of-origin effect determines the susceptibility of a non-informative F1 population to Trypanosoma cruzi infection in vivo [Internet]. PLoS One. 2013 ; 8( 2): e56347-1 - e56347-10.[citado 2025 dez. 27 ] Available from: https://doi.org/10.1371/journal.pone.0056347 - Ros-dependent NLRP3-inflammasome activation is critical for restriction of Leishmania amazonensis infection
- Critical role of ASC inflammasomes in host innate resistance to Trypanosoma cruzi infection
- NOD/RIP2 signaling contribute to development of a TH1 response and resistance against L. major infection
- Apoptosis-associated speck–like protein containing a caspase recruitment domain inflammasomes mediate IL-1β response and host resistance to Trypanosoma cruzi infection
- IFN-γ plays a unique role in protection against low virulent Trypanosoma cruzi strain
- Cutting edge: nucleotide binding oligomerization domain 1-dependent responses account for murine resistance against trypanosoma cruzi infection
- Resistance to Leishmania spp. is mediated by the inflammasome induced duo: IL- 1β and nitric oxide
- NOD1/NOD2/RIP2 signaling in response to non-peptidoglycan containing pathogen contribute to development of a TH1-biased response and resistance against L. major infection
- Interplay between reactive oxygen species and the inflammasome are crucial for restriction of Neospora caninum replication
- The inflammatose contributes for restriction of leishmania (Leishmania) amazonensis infection in macrophages and in vivo
Informações sobre o DOI: 10.1371/journal.pone.0056347 (Fonte: oaDOI API)
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