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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Breakpoint cluster region

A reciprocal translocation between chromosomes 22 and 9 produces the Philadelphia chromosome, which is often found in patients with chronic myelogenous leukemia. The chromosome 22 breakpoint for this translocation is located within the BCR gene. The translocation produces a fusion protein which is encoded by sequence from both BCR and ABL, the gene at the chromosome 9 breakpoint. Although the BCR-ABL fusion protein has been extensively studied, the function of the normal BCR gene product is not clear. The protein has serine/threonine kinase activity and is a GTPase-activating protein for p21rac. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ABL, CAN, HAD, V1a, Akt
Papers using BCR antibodies
Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1–transformed acute lymphoblastic leukemia cells
Müschen Markus et al., In The Journal of Experimental Medicine, 2002
... and Michael Reth (Freiburg) for critical discussions; Nora Heisterkamp and John Groffen for provision of BCR-ABL1–transgenic mice; Shahab Asgharzadeh (Los ...
RNA-associated autoantigens activate B cells by combined B cell antigen receptor/Toll-like receptor 7 engagement
Marshak-Rothstein Ann et al., In The Journal of Experimental Medicine, 2002
... AM14, AM14 MyD88-deficient, and AM14 TLR9-deficient BCR transgenic mice have been described ...
Receptor Editing and Marginal Zone B Cell Development Are Regulated by the Helix-Loop-Helix Protein, E2A
Murre Cornelis et al., In The Journal of Experimental Medicine, 1999
... 3-83 BCR transgenic B10.D2nSn/J mice have been ...
Transient Receptor Potential 1 Regulates Capacitative Ca2+ Entry and Ca2+ Release from Endoplasmic Reticulum in B Lymphocytes〉
Kurosaki Tomohiro et al., In The Journal of Experimental Medicine, 1998
... Cell surface expression of BCR was analyzed by FACScan™ (Becton Dickinson) using FITC-labeled anti–chicken IgM ...
Papers on BCR
Discovery of 2-((3-amino-4-methylphenyl)amino)-N-(2-methyl-5-(3-(trifluoromethyl)benzamido)phenyl)-4-(methylamino)pyrimidine-5-carboxamide (CHMFL-ABL-053) as a potent, selective and orally available BCR-ABL/SRC/p38 kinase inhibitor for Chronic Myeloid Leukemia.
Liu et al., In J Med Chem, Feb 2016
Through significant suppression of the BCR-ABL auto-phosphorylation (EC50 about 100 nM) and downstream mediators such as STAT5, Crkl and ERK's phosphorylation, 18a inhibited the proliferation of CML cell lines K562 (GI50 = 14 nM), KU812 (GI50 = 25 nM) and MEG-01 (GI50 = 16 nM).
Oncogenic CARMA1 couples NF-κB and β-catenin signaling in diffuse large B-cell lymphomas.
Krappmann et al., München, Germany. In Oncogene, Feb 2016
Recurrent oncogenic mutations are found in the scaffold protein CARMA1 (CARD11) that connects B-cell receptor (BCR) signaling to the canonical NF-κB pathway.
Advances in therapy for Philadelphia-positive acute lymphoblastic leukaemia of childhood and adolescence.
Schrappe et al., Kiel, Germany. In Br J Haematol, Feb 2016
UNASSIGNED: The presence of the BCR/ABL1 fusion gene in childhood acute lymphoblastic leukaemia (ALL) is a rare finding and has been an adverse prognostic factor associated with a high risk of therapeutic failure.
Vigneri et al., Catania, Italy. In Curr Cancer Drug Targets, Feb 2016
Many lines of evidence suggest that different IRFs are involved in the pathogenesis of Chronic Myeloid Leukemia (CML), a myeloproliferative disorder caused by the BCR-ABL oncoprotein.
Targeted therapies for CLL: Practical issues with the changing treatment paradigm.
O'Brien et al., Houston, United States. In Blood Rev, Jan 2016
These include B-cell receptor (BCR) inhibitors such as Bruton tyrosine kinase (BTK) inhibitors, PI3 kinase inhibitors, and Syk inhibitors, novel anti-CD20 monoclonal antibodies such as ofatumumab and obinutuzumab, and Bcl-2 antagonists such as venetoclax (ABT-199).
The search for the target antigens of multiple sclerosis, part 2: CD8+ T cells, B cells, and antibodies in the focus of reverse-translational research.
Wekerle et al., München, Germany. In Lancet Neurol, Jan 2016
Taking a reverse-translational approach, findings from human T-cell receptor (TCR) and B-cell receptor (BCR) repertoire studies provided strong evidence for antigen-driven clonal expansion in the brain and CSF.
Tyrosine Kinase Inhibitor-Associated Cardiovascular Toxicity in Chronic Myeloid Leukemia.
Deininger et al., Nashville, United States. In J Clin Oncol, Jan 2016
Imatinib, the first BCR-ABL1 TKI granted regulatory approval, has been surpassed in terms of molecular responses by the second-generation TKIs nilotinib, dasatinib, and bosutinib.
Exploration of Novel Inhibitors for Bruton's Tyrosine Kinase by 3D QSAR Modeling and Molecular Dynamics Simulation.
Woo Lee et al., Chinju, South Korea. In Plos One, Dec 2015
B cell malignancies are dependent on BCR signaling, thus making BTK an efficient therapeutic target.
Regulation of bifurcating B cell trajectories by mutual antagonism between transcription factors IRF4 and IRF8.
Singh et al., Cincinnati, United States. In Nat Immunol, Dec 2015
IRF8 dampened signaling via the B cell antigen receptor (BCR), facilitated antigen-specific interaction with helper T cells, and promoted antibody affinity maturation while antagonizing IRF4-driven differentiation of plasmablasts.
Targeting Bruton's tyrosine kinase signaling as an emerging therapeutic agent of B-cell malignancies.
Zhang et al., Tianjin, China. In Oncol Lett, Dec 2015
UNASSIGNED: It is becoming increasingly evident that B-cell receptor (BCR) signaling is central to the development and function of B cells.
mTOR-Dependent and Independent Survival Signaling by PI3K in B Lymphocytes.
Sen et al., Suita, Japan. In Plos One, Dec 2015
Peripheral B lymphocyte survival requires the B cell receptor (BCR) and B cell activating factor (BAFF) binding to its receptor (BAFF-R).
Ibrutinib as a Bruton Kinase Inhibitor in the Management of Chronic Lymphocytic Leukemia: A New Agent With Great Promise.
Jaiyesimi et al., Royal Oak, United States. In Clin Lymphoma Myeloma Leuk, Dec 2015
UNASSIGNED: The recent discovery of the role of the B-cell antigen receptor (BCR) signaling pathway in the propagation and maintenance of both normal B-cell function and in B-cell malignancies has highlighted the importance of many protein kinases involved in BCR signal propagation.
Combination of hyper-CVAD with ponatinib as first-line therapy for patients with Philadelphia chromosome-positive acute lymphoblastic leukaemia: a single-centre, phase 2 study.
O'Brien et al., Houston, United States. In Lancet Oncol, Nov 2015
Ponatinib is a more potent BCR-ABL1 inhibitor than all other tyrosine-kinase inhibitors and selectively suppresses the resistant T315I clones.
Wiskott-Aldrich Syndrome Interacting Protein Deficiency Uncovers the Role of the Co-receptor CD19 as a Generic Hub for PI3 Kinase Signaling in B Cells.
Batista et al., Boston, United States. In Immunity, Nov 2015
Furthermore, in the absence of WIP, several receptors, namely the BCR, BAFFR, CXCR4, CXCR5, CD40, and TLR4, were impaired in promoting CD19 co-receptor activation and subsequent PI3 kinase (PI3K) signaling.
Hsp90 Inhibitors for the Treatment of Chronic Myeloid Leukemia.
Baskaran et al., Pondicherry, India. In Leuk Res Treatment, 2014
Chronic myeloid leukemia (CML) is a hematological malignancy that arises due to reciprocal translocation of 3' sequences from c-Abelson (ABL) protooncogene of chromosome 9 with 5' sequence of truncated break point cluster region (BCR) on chromosome 22.
Altered BCR signalling quality predisposes to autoimmune disease and a pre-diabetic state.
Kiefer et al., Münster, Germany. In Embo J, 2012
BCR signalling as a mechanism to cause biased cellular and Ig repertoire selection, ultimately contributing to B cell-mediated autoimmune predisposition.
Comparative study of BCR-ABL1 quantification: Xpert assay, a feasible solution to standardization concerns.
Molero et al., Las Palmas de Gran Canaria, Spain. In Ann Hematol, 2012
BCR-ABL1 transcript quantification was performed in 117 samples from chronic myeloid leukemia patients in two different laboratories by both methods, and the results were compared by statistical procedures.
Src, Akt, NF-κB, BCL-2 and c-IAP1 may be involved in an anti-apoptotic effect in patients with BCR-ABL positive and BCR-ABL negative acute lymphoblastic leukemia.
Lezama et al., Mexico. In Leuk Res, 2012
Src, Akt, NF-kappaB, BCL-2 and c-IAP1 may be involved in an anti-apoptotic effect in patients with BCR-ABL positive and BCR-ABL negative acute lymphoblastic leukemia.
A requirement for SOCS-1 and SOCS-3 phosphorylation in Bcr-Abl-induced tumorigenesis.
Chen et al., Beijing, China. In Neoplasia, 2012
Bcr-Abl may critically requires tyrosine phosphorylation of SOCS-1 and SOCS-3 to mediate tumorigenesis when these SOCS proteins are present in cells.
T315I mutation in Ph-positive acute lymphoblastic leukemia is associated with a highly aggressive disease phenotype: three case reports.
Naoe et al., Nagoya, Japan. In Anticancer Res, 2012
qPCR detected a decrease of BCR-ABL to 190 copies once, but this suddenly increased to 22,000 copies
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