BCR-ABL p210 fusion protein(BCR-ABL fusion)

Product nameBCR-ABL p210 fusion protein(BCR-ABL fusion)
Uniprot IDA1Z199
Uniprot linkhttps://www.uniprot.org/uniprot/A1Z199
Origin speciesHomo sapiens (Human)
Expression systemProkaryotic expression
Molecular weight23.29kDa
Protein delivered with Tag?N-terminal His Tag, N-Terminal SUMO Tag
Purity estimated>90% by SDS-PAGE
Buffer0.02% Sarcosyl,PBS,pH7.5
Delivery conditionDry Ice
Delivery lead time in business daysEurope: 5-7 working days
USA & Canada: 7-10 working days
Rest of the world: 5-12 working days
Storage condition4°C for short term (1 week), -20°C or -80°C for long term (avoid freezing/thawing cycles; addition of 20-40% glycerol improves cryoprotection)
Host speciesEscherichia coli (E.coli)
Fragment TypeGln1-Cys97
Aliases /Synonyms/
NoteFor research use only

Description of BCR/ABL p210 fusion protein(BCR/ABL fusion)

General information on BCR-ABL1 protein

BCR-ABL1 is encoded by the BCR-ABL1 fusion gene that results from the genetic material of both chromosome 9 and chromosome 22. The ABL1 gene located on chromosome 9 is juxtaposed onto the breakpoint cluster region of BCR gene which is located on chromosome 22. As such BCR-ABL1 is a hybrid protein and a tyrosine kinase. The protein fusion interrupts the genome stability and causes the cell to divide uncontrollably. The BCR-ABL1 protein complex also impairs a different signaling pathway that regulates the cell cycle.
nBCR-ABL1 protein is phosphorylated by JAK2 protein at Y177. Upon phosphorylation, BCR-ABL1 fusion protein is stabilized which strengthens its tumorigenic cell signaling. JAK2 protein mutations has been linked to aberrant BCR-ABL1 protein activity. JAk/ BCR-ABL1 abnormalities have been involved in increase survival and proliferation of myelogenous leukemia cells and hematologic malignancies. BCR-ABL1 protein complex upregulates JAK-STAT signaling and helps maintain leukemic cell division and growth. For this reason, both JA2 protein and BCR-ABL1 protein have been targets for anti-cancer treatments.
nBCR-ABL protein also activates the Ras/MAPK/ERK pathway. The latter consists of a chain of proteins located on the cell surface that communicate the signal from a receptor on the surface to the nucleus of the cell. This leads to gene transcriptions that results in increased cell proliferation. Ras/MAPK/ERK pathway also increases expression levels of osteopontin (OPN) which indirectly increases the proliferation of leukemic cells. BCR-ABL has also been implicated to higher levels of activated Ras bound to GTP which inhibits cell induced apoptosis. The BCR-ABL induced apoptotic inhibition is resistant to drug-induced apoptosis. The expression levels of pro-apoptotic molecules such as p53, p21 and Bax is increased. However, their activity is impaired, and apoptosis is not carried out. Furthermore, BCR-ABL fusion protein prevent caspase 9 and caspase 3 activity. Both of these proteins are required for efficient apoptosis. Their inhibition further strengthens BCR-ABL fusion protein anti-apoptotic activity.

SDS-PAGE for BCR-ABL p210 fusion protein (BCR-ABL fusion)

BCR-ABL p210 fusion protein (BCR-ABL fusion) on SDS-PAGE under reducing condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is superior than 90 %.


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