Abl (T315I), active
N-terminal 6His-tagged recombinant, human Abl, amino acids 27-end containing the T315I mutation. Contains the gatekeeper mutation T315I in the ATP-binding domain. This mutation decreases the sensitivity to Gleevec® by more than 200-fold as compared to the wild type sequence.
Biological information
Background
The abl oncogene was initially identified as the viral transforming gene (v-abl) of Abelson murine leukemia virus (A-MuLV), from a chemically thymectomized mouse inoculated with Moloney murine leukemia virus (M-MuLV). The v-abl genome consists of M-MuLV gag sequences fused to mouse c-abl, resulting in the production of phosphoroteins, p160 and p120 gag/c-abl with protein-tyrosine kinase activity, as the major translational products. The abl oncogene is implicated in serval human leukemias including chronic myelocytic (CML), adult acute lymphoblastic (ALL) and pediatric ALL. In these leukemias the c-abl proto-oncogene undergoes a chromosomal translocation producing the Philadelphia (Ph¢) chromosome resulting in the fusion of c-abl sequences to the bcr gene of chromosome 22, and the molecular consequences of this translocation is the generation of a chimeric bcr/c-abl mRNA encoding activated abl protein-tyrosine kinase.
GenBank U07563. The recombinant protein contains the amino acid substitution, T315I with reference to U07563. This mutation is reported to elicit resistance to the Abl tyrosine kinase inhibitors STI-571.
Target class
Kinase
Family
TK
Accession number
NM_005157.3; NM_007313.2
Target Name
Abl (T315I), active
Target Alias
ABL1, JTK7, ABL, p150, v-abl, c-ABL, bcr/abl
Origin
Human
Theori. MW
121 kDa
Affinity tag
6His
Product specifications
Expression system
Expressed by baculovirus in Sf21 insect cells
Purity
Refer to CoA for Purity
Purification method
Ni2+/NTA-agarose
Sample Buffer
Specified activity
Refer to CoA
Application
For Research Only
Storage conditions
6 months at -70°C
Usage disclaimer
For Research Only
Chemical data
Background
The abl oncogene was initially identified as the viral transforming gene (v-abl) of Abelson murine leukemia virus (A-MuLV), from a chemically thymectomized mouse inoculated with Moloney murine leukemia virus (M-MuLV). The v-abl genome consists of M-MuLV gag sequences fused to mouse c-abl, resulting in the production of phosphoroteins, p160 and p120 gag/c-abl with protein-tyrosine kinase activity, as the major translational products. The abl oncogene is implicated in serval human leukemias including chronic myelocytic (CML), adult acute lymphoblastic (ALL) and pediatric ALL. In these leukemias the c-abl proto-oncogene undergoes a chromosomal translocation producing the Philadelphia (Ph¢) chromosome resulting in the fusion of c-abl sequences to the bcr gene of chromosome 22, and the molecular consequences of this translocation is the generation of a chimeric bcr/c-abl mRNA encoding activated abl protein-tyrosine kinase.
GenBank U07563. The recombinant protein contains the amino acid substitution, T315I with reference to U07563. This mutation is reported to elicit resistance to the Abl tyrosine kinase inhibitors STI-571.
Compound name
Kinase
Catalog number
14-522
Molecular formula
CAS
MW
Ka
Percent composition
Product specifications
Physical state
Purity (HPLC 214nm)
Retention time (RP18 HPLC)
CMC
Exact mass
Stability
For Research Only
Solubility structure
Datasheets
14-522
Datasheet