BCR

(redirected from BCR1)

BCR

Breakpoint cluster region. A 5.8-kb DNA segment on chromosome 22q11.23, which, in contrast to the well-studied BCR-ABL fusion protein related to malignant transformation of pluripotent haematopoietic stem cells in CML, encodes a gene product of unknown function, which has serine/threonine kinase activity and is a GTPase-activating protein for p21rac.

In CML there is a reciprocal translocation between chromosome 9q34—a site which contains the human homolog of the Abelson viral oncogene, c-abl—and chromosome 22q1, the location of the breakpoint cluster region; this translocation results in formation of the Philadelphia chromosome, which transcribes a hybrid mRNA, encoding a protein with tyrosine kinase activity.
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References in periodicals archive ?
Conclusion: The most frequent isoform of PML-RAR[alpha] fusion gene was bcr3 which was observed in 62 (63.9%) cases followed by bcr2 (26.8%) and bcr1 (9.3%).
Breakpoint regions in chromosome 15 having PML gene include intron 3 (L-long isoform or bcr1 isoform), intron 6 (S-short isoform or bcr3 isoform) and exon 6 (V form or bcr2 isoform).
Based on the results of mechanical properties and piezoresistive behaviour of BCR, mortar samples for piezoresistive characterization were prepared only incorporating BCR1 type of braided rod.
Figure 5 shows the type of response observed with BCR1 depending on the placement of carbon fibres.
The isolates were subjected to recA PCR amplification using the oligonucleotide primers BCR1 and BCR216.
The laboratories also received calibrators prepared by cloning PCR products of samples from positive patients (B3A2 isoform for BCR-ABL, and BCR1 or BCR3 isoforms for PML-RARa) into CR[R] II-TOPO[R] vector (TOPO[TM] Cloning[R] Kit).
The efficiencies estimated from the slopes of the calibration curves for the PML-RARa BCR1 and BCR3 iso-forms for the ABI and LC were very similar (Table 1 in the online Data Supplement).
The full-length recA gene was amplified from these isolates by using primers BCR1 and BCR2 (17).
Short (S) isoform (bcr3) is created by a breakpoint in intron 3, while long (L) isoform (bcr1) results from a breakpoint located in intron 6 of the PML gene, found in 35% and 60% of adult APL patients with t(15,17), respectively [6,132].
The prevalence of bcr3 (short isoform) was higher (62%) than that of bcr1 (long isoform) (38%) and no correlation was found with age, sex or white blood cell count.