Table 1 Proteins differentially expressed in AZT-treated K562 cells.
Spot Identification (Figure 1) | Protein | Gene name | SWISS-PROT accession number | MW (expt/pred) | pI (expt/pred) | Trend in AZT-treated cells | Observations and reported functions a |
|---|---|---|---|---|---|---|---|
1 | HSP-60 | HSPD1 | P10809 | 61187/62000 | 5.70/5.75 | Absent | Chaperone that accelerates the maturation of pro-caspase by upstream activator proteases during apoptosis |
2 | PDI-A3 | GRP58 | P30101 | 57146/63000 | 5.98/5.80 | Increased 4.0 -fold | Chaperone in the endoplasmic reticulum lumen, may regulate signalling by sequestering inactive and activated Stat3 |
3 | NDPK-A | NME1 | P15531 | 17309/21000 | 5.83/5.90 | Present in AZT-treated cells; Absent in control cells | Found in reduced amount in tumor cells of high metastasic potential. May have distinct if not opposite roles in different tumors |
4 | Stathmin (onco-protein 18; phospho-protein p19) | STMN1 | P16949 | 17161/19000 | 5.77/5.90 | Increased 1.4-fold | Microtubule-destabilizing proteins up-regulated in neoplastic cells; down-regulation in malignant cells interferes with their progression through cell cycle and abrogates their transformed phenotype |
5 | Cu,Zn-SOD | SOD1 | P00441 | 16023/19000 | 5.70/5.75 | Absent | Cellular protective function against oxidative stress. Defects in SOD1 are the cause of familial amyotrophic lateral sclerosis (FALS) also called amyotrophic lateral sclerosis 1 (ALS1 or ALS). |