The non-canonical NF-κB pathway and its contribution to β-cell failure in diabetes (2018)
- Authors:
- Autor USP: ORTIS, FERNANDA - ICB
- Unidade: ICB
- DOI: 10.1530/JME-16-0183
- Subjects: BIOLOGIA CELULAR; LINFÓCITOS B; DIABETES MELLITUS; CITOCINAS; INFLAMAÇÃO; PROTEÍNAS QUINASES; PROLIFERAÇÃO CELULAR; ILHOTAS DE LANGERHANS
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Journal of Molecular Endocrinology
- ISSN: 1479-6813
- Volume/Número/Paginação/Ano: v. 61, n. 2, p. F1–F6, 2018
- Este periódico é de acesso aberto
- Este artigo NÃO é de acesso aberto
-
ABNT
MEYEROVICH, Kira e ORTIS, Fernanda e CARDOZO, Alessandra Kupper. The non-canonical NF-κB pathway and its contribution to β-cell failure in diabetes. Journal of Molecular Endocrinology, v. 61, n. 2, p. F1–F6, 2018Tradução . . Disponível em: https://doi.org/10.1530/JME-16-0183. Acesso em: 11 fev. 2026. -
APA
Meyerovich, K., Ortis, F., & Cardozo, A. K. (2018). The non-canonical NF-κB pathway and its contribution to β-cell failure in diabetes. Journal of Molecular Endocrinology, 61( 2), F1–F6. doi:10.1530/JME-16-0183 -
NLM
Meyerovich K, Ortis F, Cardozo AK. The non-canonical NF-κB pathway and its contribution to β-cell failure in diabetes [Internet]. Journal of Molecular Endocrinology. 2018 ; 61( 2): F1–F6.[citado 2026 fev. 11 ] Available from: https://doi.org/10.1530/JME-16-0183 -
Vancouver
Meyerovich K, Ortis F, Cardozo AK. The non-canonical NF-κB pathway and its contribution to β-cell failure in diabetes [Internet]. Journal of Molecular Endocrinology. 2018 ; 61( 2): F1–F6.[citado 2026 fev. 11 ] Available from: https://doi.org/10.1530/JME-16-0183 - The non-canonical NF-κB pathway is induced by cytokines in pancreatic beta cells and contributes to cell death and proinflammatory responses in vitro
- Endoplasmic reticulum stress and the unfolded protein response in pancreatic islet inflammation
- Transporte através de membranas celulares e tráfego intracelular
- Retículo endoplasmático e Complexo de Golgi
- Papel de BRG1 e Brm, reguladores globais de transcrição, na reversão fenotípica de células ST1 pela ação de glicocorticóides
- Membranas celulares
- Augmented β-Cell function and mass in glucocorticoid-treated rodents are associated with increased islet Ir-β/AKT/mTOR and decreased AMPK/ACC and AS160 signaling
- Metabolic memory of ß-cells controls insulin secretion and is mediated by CaMKII
- ARHGAP21 acts as an inhibitor of the glucose-stimulated insulin secretion process
- Prolactin protects against cytokine-induced beta-cell death by NFκB and JNK inhibition
Informações sobre o DOI: 10.1530/JME-16-0183 (Fonte: oaDOI API)
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