| Protein Name: | Nuclear factor NF-kappa-B (P19838) |
|---|---|
| Gene Name: | NFKB1 |
| Description: | Nuclear factor NF-kappa-B p105 subunit (DNA-binding factor KBF1) (EBP- 1) [Contains: Nuclear factor NF-kappa-B p50 subunit] |
| PDB ID: | 1MDI |
| Protein Family: | |
| Protein Category: | Cytosolic Protein | Transcription Factor |
This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Acetylsalicylic acid | Apoptosis | Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells [ ADR Type 1 ] | Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells |
| Amphotericin B | Neurotoxicity | The activation of transcription factor NF-kappaB was apparently required for AMB-induced iNOS mRNA expression@ as the latter was abolished by NF-kappaB inhibitors@which might be at least partly responsible for AMB neurotoxicity [ ADR Type 2 ] | Amphotericin B potentiates the activation of inducible nitric oxide synthase and causes nitric oxide-dependent mitochondrial dysfunction in cytokine-treated rodent |
| Dexamethasone | Pulmonary Inflammation | Treatment with dexamethasone at -3 h prior to silica instillation@ at the time of instillation (0 h)@ and +1.5 h postinstillation resulted in both a reduction in NF-kappa B expression (by 70%) at 3 h postinstillation and corresponding reductions in LDCL@ BAL cell count@ and BAL neutrophils@which is associated with silica-induced pulmonary inflammation. [ ADR Type 5 ] | Silica-induced pulmonary inflammation in rats: activation of NF-kappa B and its suppression by dexamethasone |
| Paclitaxel | Apoptosis | Paclitaxel-induced G2/M cell cycle arrest;NF-kappaB-inducible genes protect cancer cells against paclitaxel as MDA-MB-231 breast cancer cells modified to overexpress IkappaBalpha required lower concentrations of paclitaxel to arrest at the G2/M phase of the cell cycle and underGO apoptosis when compared to parental cells [ ADR Type 2 ] | Paclitaxel sensitivity of breast cancer cells with constitutively active NF-kappaB is enhanced by IkappaBalpha super-repressor |
| Paclitaxel | Apoptosis Of Breast Cancer Cells | Constitutive activation of NF-kappaB leads to overexpression of the anti-apoptotic genes c-inhibitor of apoptosis 2 (c-IAP2) and manganese superoxide dismutase (Mn-SOD) in breast cancer cells@which increase paclitaxel-induced apoptosis of breast cancer cells. [ ADR Type 2 ] | Paclitaxel sensitivity of breast cancer cells with constitutively active NF-kappaB is enhanced by IkappaBalpha super-repressor |
| SIlica | Pulmonary Inflammation | NF-kappa B activation was measurable at 3 h postinstillation of silica@ and this activation continued throughout the 18-h time course@which is associated with silica-induced pulmonary inflammation [ ADR Type 5 ] | Silica-induced pulmonary inflammation in rats: activation of NF-kappa B and its suppression by dexamethasone |
This panel provides information on drug category
| Toxicity | Source |
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