Table 2.
Effects of different somatic SNPs most commonly found in cancer on the intrinsic disorder-based interactivity of human CALR.
| SNPs | AA Substitutions | Predicted function | MoRF1 | MoRF2 | MoRF3 | MoRF4 | MoRF5 |
|---|---|---|---|---|---|---|---|
| wt | N/A | Wild type CALR | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 13 | V5M | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 79 | F27L | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 133 | D45Y | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 137 | F46Y | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 151 | L51V | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 168 | F56L | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 186 | K62N | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 185 | K62R | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 191 | K64T | Loss/Acetylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 201 | Q67H | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 298 | E100Q | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 365 | M122T | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 383 | Y128C | Loss/Binding Site | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 394 | F132L | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 562 | N188D | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 610 | P204S | – | 170–176 | 198–205 | 259–269 | 304–352 | 409–417 |
| 700 | E234K | Gain/Phosphorylation | 170–176 | 199–205 | 263–269 | 304–352 | 409–417 |
| 720 | E240D | Gain/Phosphorylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 731 | D244G | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 892 | E298Y | – | 170–176 | 198–204 | 257–296 | ||
| 899 | S300Y | – | 170–176 | 198–204 | 263–268 | 303–350 | 409–417 |
| 925 | D309Y | Gain/Phosphorylation | 170–176 | 198–204 | 304–350 | 409–417 | |
| 968 | S323F | – | 170–176 | 198–204 | 259–268 | 304–350 | 409–417 |
| 1003 | D335N | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 1022 | E341G | Gain/Glycosylation | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 1028 | G343D | – | 170–176 | 198–204 | 259–269 | 304–352 | 408–417 |
| 1103 | K368M | – | 170–176 | 198–204 | 259–269 | 304–352 | 408–417 |
| 1113 | E371D | – | 170–176 | 198–204 | 259–269 | 304–352 | 408–417 |
| 1121 | K374R | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 1137 | E379D | – | 170–176 | 198–204 | 259–269 | 304–352 | 408–417 |
| 1142 | E381G | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 1157 | E386G | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 1167 | E389D | – | 170–176 | 198–204 | 259–269 | 304–352 | 408–417 |
| 1192 | E398K | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 1207 | E403Y | – | 170–176 | 198–204 | 259–269 | 304–350 | |
| 1212 | D404E | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
| 1213 | E405Q | – | 170–176 | 198–204 | 259–269 | 304–352 | 408–417 |
| 1229 | P410L | – | 170–176 | 198–204 | 259–269 | 304–351 | 406–417 |
| 1240 | K414E | – | 170–176 | 198–204 | 259–269 | 304–352 | 408–417 |
| 1245 | D415E | – | 170–176 | 198–204 | 259–269 | 304–352 | 409–417 |
Information on SNP identification number (column 1) and description of the related AA substitution (columns 2), as well as predicted functional outputs (column 3) were taken from https://hive.biochemistry.gwu.edu/biomuta. Expected effects of SNPs on the interactivity of CALR were evaluated by the ANCHOR algorithm (Dosztányi et al., 2009; Mészáros et al., 2009). To this end, the AA sequence of each mutant identified in column 2 was analyzed by ANCHOR and the corresponding outputs (positions of MoRFs) were tabulated. SNPs with possibly/probably damaging effects on disease phenotype are indicated in red. MoRFs alterations caused by SNPs are highlighted in yellow.