Invitrogen

Human ABL1 [M351T], GST Tag, His Tag Recombinant Protein

Name: Human ABL1 [M351T], GST Tag, His Tag Recombinant Protein
Brand: Invitrogen
SKU: PV6152
Availability: InStock

Datasheet

Tech Support

Datasheet

Tech Support

Product Details

PV6152

Applications

Tested Dilution

Publications

Kinase Assay (KA)

Assay-dependent

Product Specifications

Species

Human

Expression System

Insect cells

Amino acid sequence

118-535

Tag

GST-tag, His-tag

Molecular weight

76.1 kDa

Class

Recombinant

Type

Protein

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

See Label

Purification

purified

Storage buffer

50mM HEPES, pH 7.5, with 15mM glutathione, 20% glycerol, 100mM NaCl, 5mM DTT

Contains

no preservative

Storage conditions

-80°C, Avoid Freeze/Thaw Cycles

Shipping conditions

Dry ice

Product Specific Information

For maximum recovery please spin prior to use. Unless noted below, aliquots of the 5 µg, 10 µg and 20 µg sizes of kinase are not recommended as materials can be used in original packaging until exhausted. For larger sizes, the number of freeze/thaws may be reduced by preparing aliquots, aliquots below 20 µL are not recommended. Please never store a kinase diluted. If properly stored at -80C, this product is guaranteed for 6 months from date of purchase.

Human ABL1, internal fragment, amino acids P118-S535 (as in GenBank entry NM_005157.3), M351T mutant, N-terminal GST-HIS6 fusion protein with a 3C cleavage site, expressed in Sf9 insect cells.

• Validated in LanthaScreen™ Kinase Binding Assay
• Protocols available for simple use and optimized performance
• Multiple pack sizes available for convenient use

Related Product:
LanthaScreen™ Eu Kinase Binding Assay

Protein Form: Recombinant

Target Information

c-Abl (Abelson murine leukemia viral oncogene homolog 1, ABL1) is a 140 kDa proto-oncogene member of the Src family of non-receptor tyrosine kinases. c-Abl has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns c-Abl into an oncogene. The t(9;22) translocation results in the head-to-tail fusion of the BCR and c-Abl genes present in many cases of chronic myelogeneous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for c-Abl. In chronic myelogenous leukemia and a subset of acute lymphoblastic leukemias, the c-Abl proto oncogene undergoes a (9;22) chromosomal translocation producing a novel rearranged chromosome (the Philadelphia chromosome) As the result of the fusion of c-Abl sequences from chromosome 9 to the Bcr gene on chromosome 22. The molecular consequence of this translocation is the generation of a chimeric Bcr/Abl mRNA encoding activated Abl protein tyrosine kinase. The c-Abl oncogene was initially identified as the viral transforming gene of Abelson murine leukemia virus (A-MuLV). The major translational product of c-Abl has been identified as a protein with tyrosine kinase activity and an SH2 domain. The c-Abl oncogene is implicated in several human leukemias including 90-95% of chronic myelocytic leukemia (CML), 20-25% of adult acute lymphoblastic leukemia (ALL) and 2-5% of pediatric ALL. c-Abl localizes to dynamic actin structures, and phosphorylates CRK and CRKL, DOK1, and other proteins controlling cytoskeleton dynamics. c-ABL potentially regulates DNA repair by activating the proapoptotic pathway when the DNA damage is too severe to be repaired.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.

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