| Protein Name: | Beta-2-microglobulin (P61769) |
|---|---|
| Gene Name: | B2M |
| Description: | Beta-2-microglobulin precursor [Contains: Beta-2-microglobulin variant pI 53] |
| PDB ID: | 1A1M |
| Protein Family: | |
| Protein Category: |
This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Carbamazepine | Impair Renal Function | Treatment with high-dose carboplatin in patients accompany with an increase in urinary beta 2 microglobulin@which leads to impaired renal function and further loss of renal function [ ADR Type 1 ] | Renal dysfunction following high-dose carboplatin treatment |
| Ifosfamide | Aminoaciduria | Proximal tubular toxicity was indicated by increased urine beta 2 microglobulin excretion@ which leads to generalised aminoaciduria. [ ADR Type 1 ] | Nephrotoxicity after ifosfamide |
| Ifosfamide | Glycosuria | Proximal tubular toxicity was indicated by increased urine beta 2 microglobulin excretion@ which leads to glycosuria [ ADR Type 1 ] | Nephrotoxicity after ifosfamide |
| Ifosfamide | Hypophosphataemia | Proximal tubular toxicity was indicated by increased urine beta 2 microglobulin excretion@ which leads to phosphaturia and hypophosphataemia. [ ADR Type 1 ] | Nephrotoxicity after ifosfamide |
| Phylloquinone | Morphological Changes | Immunocytochemical investigations performed on menadione-exposed cells revealed that some surface proteins (collagen IV@ sialo-proteins@ beta 2 microglobulin and fibronectin) and adhesion molecules (vinculin) underwent changes in their expression over the bleb surface@which demonstrate that cytoskeletal structures and the microfilament system in particular@represent important targets in menadione-induced morphological changes in cultured cells. [ ADR Type 5 ] | Cytoskeleton as a target in menadione-induced oxidative stress in cultured mammalian cells: alterations underlying surface bleb formation |
This panel provides information on drug category
| Toxicity | Source |
|---|