Pathogen-driven CCR5/C5aR heterodimerization initiates a JNK2/JIP1-dependent signaling pathway that protects fromToxoplasma gondii infection (2008)
- Authors:
- Autor USP: CAMARGO, MARISTELA MARTINS DE - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Molecular Immunology
- Volume/Número/Paginação/Ano: v. 45, n. 16, 2008
- Conference titles: International Complement Workshop
-
ABNT
MACHADO, Fabiana et al. Pathogen-driven CCR5/C5aR heterodimerization initiates a JNK2/JIP1-dependent signaling pathway that protects fromToxoplasma gondii infection. Molecular Immunology. Chicago: Instituto de Ciências Biomédicas, Universidade de São Paulo. . Acesso em: 18 abr. 2024. , 2008 -
APA
Machado, F., Esper, L., Dias, A., Johswich, K., Bafica, A., Camargo, M. M. de, et al. (2008). Pathogen-driven CCR5/C5aR heterodimerization initiates a JNK2/JIP1-dependent signaling pathway that protects fromToxoplasma gondii infection. Molecular Immunology. Chicago: Instituto de Ciências Biomédicas, Universidade de São Paulo. -
NLM
Machado F, Esper L, Dias A, Johswich K, Bafica A, Camargo MM de, Klos A, Köhl J, Aliberti J. Pathogen-driven CCR5/C5aR heterodimerization initiates a JNK2/JIP1-dependent signaling pathway that protects fromToxoplasma gondii infection. Molecular Immunology. 2008 ; 45( 16):[citado 2024 abr. 18 ] -
Vancouver
Machado F, Esper L, Dias A, Johswich K, Bafica A, Camargo MM de, Klos A, Köhl J, Aliberti J. Pathogen-driven CCR5/C5aR heterodimerization initiates a JNK2/JIP1-dependent signaling pathway that protects fromToxoplasma gondii infection. Molecular Immunology. 2008 ; 45( 16):[citado 2024 abr. 18 ] - Existe vida após o doutorado? Parte II
- Characterization of hematological and immunological parameters during cub clinical phase of ehrlichia canis infection in dogs
- Immunology with a Brazilian twist [editorial]
- Changes in histone acetylation and methylation that are important for persistent but not transient expression. of CCR4 in human CD4+ T cells
- HIV infection and antiretroviral therapy lead to unfolded protein response activation
- Regulation of TH1/2 differentiation is controlled by p38 map kinase and MSK1/2 circuit
- A via unfolded protein response em linfócitos B humanos: Na homeostasia e na patologia
- RNA interference of MSK1 during differentiation of TH1/2 subsets
- Fever as an evolutionary agent to select immune complexes interfaces
- Silenciamento da MSK1 por siRNA durante a diferenciação TH1/2
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas