Abcam, ab190993, Recombinant human TPM3 ALK protein

Size: 5µg / 10µg
Recombinant human TPM3 ALK protein is a Human Fragment protein, in the 1 to 258 aa range, expressed in Baculovirus infected Sf9 cells, with >70%, suitable for SDS-PAGE, FuncS.
Key facts
Purity:>70% SDS-PAGE,
Expression system:Baculovirus infected Sf9 cells,
Tags:Tag free,
Applications:FuncS, SDS-PAGESee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Biologically active:Yes,
Biological activity:The specific activitity of ab190993 was determined to be 30 nmol/ min/ mg.,
Accession:P06753,
Animal free:No,
Carrier free:No,
Species:Human,
Storage buffer:pH: 7.5Preservative: 1.02% ImidazoleConstituents: 25% Glycerol (glycerin, glycerine), 1.74% Sodium chloride, 0.82% Sodium phosphate, 0.004% (R*,R*)-1,4-Dimercaptobutan-2,3-diol, 0.002% PMSF

Product details:
Recombinant fusion protein of TPM3 (1-258) - ALK (1058-1620) expressed in baculovirus in Sf9 insect cells using an N-terminal proprietary tag.

Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--80°C, Appropriate long-term storage conditions--80°C, Storage information-Avoid freeze / thaw cycle

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
TPM3 ALK also known as Tropomyosin 3-Anaplastic Lymphoma Kinase is a fusion protein made by the joining of the TPM3 and ALK genes. The TPM3 part of the protein weighs about 32 kDa and it typically helps with muscle contraction while ALK is a receptor tyrosine kinase usually involved in cellular signaling and weighs approximately 162 kDa. TPM3 ALK results from a genetic rearrangement and this fusion protein is expressed in certain cancer cells particularly in some cases of anaplastic large cell lymphomas and inflammatory myofibroblastic tumors.
Biological function summary
This fusion protein acts as a constitutively active kinase meaning it remains active without normal regulation. The TPM3 ALK fusion circumvents regulatory mechanisms leading to unchecked cellular proliferation and survival. It doesn't involve participation in traditional cellular complexes but instead promotes tumorigenesis directly through its deregulated kinase activity.
Pathways
TPM3 ALK interacts significantly with signaling pathways that involve cell survival and proliferation. The fusion protein aberrantly activates the PI3K/AKT pathway and the RAS/MAPK pathway which are vital for cell growth and metabolic regulation. Through these pathways TPM3 ALK influences proteins such as STAT3 and PLCγ linking it further to the signaling network responsible for cell growth and division.
The presence of TPM3 ALK has strong links to specific types of cancer. Its expression is a marker for some anaplastic large cell lymphomas and certain inflammatory myofibroblastic tumors. The fusion between TPM3 and ALK creates a continual growth signal that parallels similar disease mechanisms seen with other ALK fusions like NPM1-ALK. This aberrant activation of ALK pathophysiology makes TPM3 ALK a potential target for therapeutic interventions aimed at inhibiting its kinase activity in affected patients.