The role of NF-κB in the regulation of cell stress responses

Wang, Tieli; Zhang, Xia; Li, Jian Jian

doi:10.1016/s1567-5769(02)00058-9

Cited by 302 publications

(198 citation statements)

References 92 publications

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“…This study found that iNOS induction and excess NO production by thrombin are mediated primarily by NF-B activation. NF-B exists in the cytoplasm of unstimulated cells in a quiescent form bound to its inhibitor (52). Thrombin was found to activate the p65/p50 NF-B DNA binding complex and to induce the nuclear translocation of the p65 protein.…”

Section: Discussionmentioning

confidence: 99%

Thrombin Induces Nitric-oxide Synthase via Gα12/13-coupled Protein Kinase C-dependent I-κBα Phosphorylation and JNK-mediated I-κBα Degradation

Kang

Choi

Cho

et al. 2003

Journal of Biological Chemistry

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An imbalance between thrombin and antithrombin III contributed to vascular hyporeactivity in sepsis, which can be attributed to excess NO production by inducible nitricoxide synthase (iNOS). In view of the importance of the thrombin-activated coagulation pathway and excess NO as the culminating factors in vascular hyporeactivity, this study investigated the effects of thrombin on the induction of iNOS and NO production in macrophages. Thrombin induced iNOS protein in the Raw264.

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Section: Discussionmentioning

confidence: 99%

Thrombin Induces Nitric-oxide Synthase via Gα12/13-coupled Protein Kinase C-dependent I-κBα Phosphorylation and JNK-mediated I-κBα Degradation

Kang

Choi

Cho

et al. 2003

Journal of Biological Chemistry

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“…Oxidative stress activates many stress signaling pathways by direct modification of signaling proteins, including mitogen-activated protein kinases, AP-1, and NF-B transcription factors (12)(13)(14). Alternatively, ROS activate stress signaling pathways indirectly via damaging effects on macromolecules (Fig.…”

Section: Osmosensingmentioning

confidence: 99%

Hyperosmolality triggers oxidative damage in kidney cells

Kültz

2004

Proc. Natl. Acad. Sci. U.S.A.

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“…NF-κB is bound by its inhibitor IκB in the cytosol. Under stimulating signals, IκB gets phosphorylated and degraded, allowing NF-κB to translocate to the nucleus for transcription of target genes (12). Interaction between PARP-1 and NF-κB is implicated in the end-organ damage associated with diabetes mellitus.…”

mentioning

confidence: 99%

Recurrent hypoinsulinemic hyperglycemia in neonatal rats increases PARP-1 and NF-κB expression and leads to microglial activation in the cerebral cortex

et al. 2015

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Background: Hyperglycemia is a common metabolic problem in extremely low-birth-weight preterm infants. Neonatal hyperglycemia is associated with increased mortality and brain injury. Glucose-mediated oxidative injury may be responsible. Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme involved in DNA repair and cell survival. However, PARP-1 overactivation leads to cell death. NF-κB is coactivated with PARP-1 and regulates microglial activation. The effects of recurrent hyperglycemia on PARP-1/NF-κB expression and microglial activation are not well understood. Methods: Rat pups were subjected to recurrent hypoinsulinemic hyperglycemia of 2 h duration twice daily from postnatal (P) day 3-P12 and killed on P13. mRNA and protein expression of PARP-1/NF-κB and their downstream effectors were determined in the cerebral cortex. Microgliosis was determined using CD11 immunohistochemistry. results: Recurrent hyperglycemia increased PARP-1 expression confined to the nucleus and without causing PARP-1 overactivation and cell death. NF-κB mRNA expression was increased, while IκB mRNA expression was decreased. inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) mRNA expressions were decreased. Hyperglycemia significantly increased the number of microglia. conclusion: Recurrent hyperglycemia in neonatal rats is associated with upregulation of PARP-1 and NF-κB expression and subsequent microgliosis but not neuronal cell death in the cerebral cortex.

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The role of NF-κB in the regulation of cell stress responses

Cited by 302 publications

References 92 publications

Thrombin Induces Nitric-oxide Synthase via Gα12/13-coupled Protein Kinase C-dependent I-κBα Phosphorylation and JNK-mediated I-κBα Degradation

Thrombin Induces Nitric-oxide Synthase via Gα12/13-coupled Protein Kinase C-dependent I-κBα Phosphorylation and JNK-mediated I-κBα Degradation

Hyperosmolality triggers oxidative damage in kidney cells

Recurrent hypoinsulinemic hyperglycemia in neonatal rats increases PARP-1 and NF-κB expression and leads to microglial activation in the cerebral cortex

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