Results 301 to 310 of about 179,498 (360)

Minor BCR (m-bcr) rearrangements may appear in major BCR (M-bcr)-positive CML cases.

Hematologic pathology, 1993
The chromosome 22 derivative, the Philadelphia (Ph) chromosome, results from the reciprocal translocation t(9;22) (q34;q11). On DNA level a BCR/ABL rearrangement involving the so-called major BCR (Mbcr) from chromosome 22 has been associated with chronic myeloid leukemia (CML).
H, Karlic, R, Grill, E, Schlögl
openaire   +1 more source

BCR-ABL and BCR proteins: biochemical characterization and localization.

Leukemia, 1990
The Philadelphia translocation results in the expression of a family of chimaeric proteins in which a portion of the bcr protein is fused to c-abl protein. Using antibodies which recognize different portions of the bcr gene and abl gene products we have compared the normal bcr products with their chimaeric counterparts.
S, Dhut, T, Chaplin, B D, Young
openaire   +1 more source

Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells

Nature Medicine, 1996
B. Druker, S. Tamura, E. Buchdunger, S. Ohno, G. Segal, S. Fanning, J. Zimmermann, N. Lydon   +7 more
semanticscholar   +1 more source

Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification

Science, 2001
M. Gorre, M. Mohammed, K. Ellwood, N. Hsu, R. Paquette, P. Rao, C. Sawyers   +6 more
semanticscholar   +1 more source

Improvement of the BCR three step sequential extraction procedure prior to the certification of new sediment and soil reference materials.

Journal of Environmental Monitoring, 1999
G. Rauret, J. F. López-Sánchez, À. Sahuquillo, R. Rubio, C. Davidson, A. Ure, P. Quevauviller   +6 more
semanticscholar   +1 more source

The allosteric inhibitor ABL001 enables dual targeting of BCR–ABL1

Nature, 2017
A. Wylie, J. Schoepfer, W. Jahnke, S. Cowan-Jacob, Alice T. Loo, P. Furet, A. Marzinzik, X. Pelle, Jerry Donovan, Wenjing Zhu, S. Buonamici, A. Q. Hassan, F. Lombardo, Varsha Iyer, Michael R. Palmer, Giuliano Berellini, S. Dodd, S. Thohan, H. Bitter, S. Branford, D. Ross, T. Hughes, L. Petruzzelli, K. Vanasse, M. Warmuth, F. Hofmann, N. Keen, W. Sellers   +27 more
semanticscholar   +1 more source

???????????????????? ?????????????????????????? ??????????????-???????????????? ?? ??????????????-???????????????? ?????????????????? ????-???????????? ?????????? Bcr, ??????????????????????? ?? ?????????????????? ???????????????????? ??????????????????

2019
?????????? Bcr ???????????????? ?????????????????? Abl ???? ?????????????????????? ???????????????????????? t(9;22), ???????????????????? ?? ?????????????????????? ?????????????????????????????? ??????????????????. ???????????????????????????????? ?????????????? ????-???????????? Bcr. ???????????????????? ????????????, ?? ???????????????? ??????????????
openaire   +1 more source

A reply to “TCR+/BCR+ dual-expressing cells and their associated public BCR clonotype are not enriched in type 1 diabetes”

Cell, 2021
Rizwan Ahmed, Zahra Omidian, Chunfa Jie   +2 more
exaly  

???????? ???????????? ???? ?????????? BCR ?? ?????????????????? ????????????????, ???? ???????????????????? ?????????????? Ph`-???????????????????? ???????????????????????????????????????? ??????????????????????????

2021
Aims. Three forms of fusion protein BCR/ABL differ by the presence or absence of PH and DH domains of BCR protein and cause different phenotypes of myeloproliferative disorders. To date, 23 proteins-candidates were identified as possible interaction partners of PH domain of BCR protein.
openaire   +1 more source

Bcr

1995
Yoshiro Maru, Owen N. Witte
openaire   +1 more source