Ignet

Gene Information

Gene symbol: BCR

Gene name: breakpoint cluster region

HGNC ID: 1014

Synonyms: D22S662, CML, PHL, ALL

Related Genes

#	Gene Symbol	Number of hits
1	ABL1	1 hits
2	ALB	1 hits
3	BCL2	1 hits
4	BCL2L11	1 hits
5	BIK	1 hits
6	CD19	1 hits
7	CD4	1 hits
8	CD40	1 hits
9	CD8A	1 hits
10	CR2	1 hits
11	CSF1	1 hits
12	CSF2	1 hits
13	ERBB2	1 hits
14	HLA-A	1 hits
15	IFNG	1 hits
16	IGHV	1 hits
17	IGHV1-69	1 hits
18	IL12A	1 hits
19	IL2	1 hits
20	IRF8	1 hits
21	MLC1	1 hits
22	MOG	1 hits
23	PAFAH1B1	1 hits
24	PMAIP1	1 hits
25	PML	1 hits
26	PRTN3	1 hits
27	PVALB	1 hits
28	RARA	1 hits
29	S100A1	1 hits
30	SCARA3	1 hits
31	TLR1	1 hits
32	TLR4	1 hits
33	TLR7	1 hits
34	TLR9	1 hits
35	TNF	1 hits
36	TNFRSF13C	1 hits

Related Sentences

#	PMID	Sentence
1	6088626	The regulation of reactivity toward the host environment, i.e., autoresponsiveness in B6----B6 and allotolerance in B6---C3H, was investigated by monitoring a graft-vs-host (GvH)-like wasting syndrome, as well as the in vitro responsiveness of spleen cells from the reconstituted mice in a mixed leukocyte culture/cell-mediated lysis (MLC/CML) assay.
2	6088626	The BCG-treated B6----B6 recipients developed a wasting syndrome and MLC/CML reactivity toward syngeneic target cells within 7 wk.
3	6088626	In the allogeneic or semiallogeneic combinations, the BCG treatment resulted in a wasting syndrome and CML/MLC reactivity toward C3H or (C3H X B6)F1 host-derived cells irrespective of thymic presence or absence.
4	6088626	The regulation of reactivity toward the host environment, i.e., autoresponsiveness in B6----B6 and allotolerance in B6---C3H, was investigated by monitoring a graft-vs-host (GvH)-like wasting syndrome, as well as the in vitro responsiveness of spleen cells from the reconstituted mice in a mixed leukocyte culture/cell-mediated lysis (MLC/CML) assay.
5	6088626	The BCG-treated B6----B6 recipients developed a wasting syndrome and MLC/CML reactivity toward syngeneic target cells within 7 wk.
6	6088626	In the allogeneic or semiallogeneic combinations, the BCG treatment resulted in a wasting syndrome and CML/MLC reactivity toward C3H or (C3H X B6)F1 host-derived cells irrespective of thymic presence or absence.
7	6088626	The regulation of reactivity toward the host environment, i.e., autoresponsiveness in B6----B6 and allotolerance in B6---C3H, was investigated by monitoring a graft-vs-host (GvH)-like wasting syndrome, as well as the in vitro responsiveness of spleen cells from the reconstituted mice in a mixed leukocyte culture/cell-mediated lysis (MLC/CML) assay.
8	6088626	The BCG-treated B6----B6 recipients developed a wasting syndrome and MLC/CML reactivity toward syngeneic target cells within 7 wk.
9	6088626	In the allogeneic or semiallogeneic combinations, the BCG treatment resulted in a wasting syndrome and CML/MLC reactivity toward C3H or (C3H X B6)F1 host-derived cells irrespective of thymic presence or absence.
10	7742526	The ability of a series of synthetic peptides corresponding to the junctional sequences of chronic myelogenous leukemia (CML)-derived bcr-abl and acute promyelocytic leukemia (APL)-derived PML-RAR alpha fusion proteins to bind to purified class I molecules was studied.
11	7742526	Twenty-one CML peptides and 4 APL peptides were predicted to be potential HLA class I binders.
12	7742526	None of the CML b2a2 or PML-RAR alpha A or B junctional peptides showed affinity of this magnitude for the HLA class I molecules tested.
13	7742526	The ability of a series of synthetic peptides corresponding to the junctional sequences of chronic myelogenous leukemia (CML)-derived bcr-abl and acute promyelocytic leukemia (APL)-derived PML-RAR alpha fusion proteins to bind to purified class I molecules was studied.
14	7742526	Twenty-one CML peptides and 4 APL peptides were predicted to be potential HLA class I binders.
15	7742526	None of the CML b2a2 or PML-RAR alpha A or B junctional peptides showed affinity of this magnitude for the HLA class I molecules tested.
16	7742526	The ability of a series of synthetic peptides corresponding to the junctional sequences of chronic myelogenous leukemia (CML)-derived bcr-abl and acute promyelocytic leukemia (APL)-derived PML-RAR alpha fusion proteins to bind to purified class I molecules was studied.
17	7742526	Twenty-one CML peptides and 4 APL peptides were predicted to be potential HLA class I binders.
18	7742526	None of the CML b2a2 or PML-RAR alpha A or B junctional peptides showed affinity of this magnitude for the HLA class I molecules tested.
19	9816208	Lack of T-cell-mediated recognition of the fusion region of the pml/RAR-alpha hybrid protein by lymphocytes of acute promyelocytic leukemia patients.
20	9816208	In previous studies, it was shown that the fusion region of the pml/RAR-alpha protein, expressed by acute promyelocytic leukemia (APL) cells, can be specifically recognized in vitro by donor (D.
21	9816208	G.) with BCR1/25, a 25-mer pml/RAR-alpha, did not elicit either a polyclonal or a clonal immune response specific to the peptide.
22	9816208	We then generated new donor anti-pml/RAR-alpha CD4(+) T-cell clones.
23	9816208	One clone (C3/5, CD3(+), CD4(+), CD8(-)) was selected for further analysis.
24	9816208	Clone C3/5 showed specific proliferation, cytotoxicity, and cytokine (tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor) production when challenged with autologous lymphoblastic cell lines pulsed with peptide BCR1/25.
25	9816208	G. whether the use of 9-mer peptides (BCR1/9) would generate a CD8/HLA class I-restricted response.
26	9816208	Lack of T-cell-mediated recognition of the fusion region of the pml/RAR-alpha hybrid protein by lymphocytes of acute promyelocytic leukemia patients.
27	9816208	In previous studies, it was shown that the fusion region of the pml/RAR-alpha protein, expressed by acute promyelocytic leukemia (APL) cells, can be specifically recognized in vitro by donor (D.
28	9816208	G.) with BCR1/25, a 25-mer pml/RAR-alpha, did not elicit either a polyclonal or a clonal immune response specific to the peptide.
29	9816208	We then generated new donor anti-pml/RAR-alpha CD4(+) T-cell clones.
30	9816208	One clone (C3/5, CD3(+), CD4(+), CD8(-)) was selected for further analysis.
31	9816208	Clone C3/5 showed specific proliferation, cytotoxicity, and cytokine (tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor) production when challenged with autologous lymphoblastic cell lines pulsed with peptide BCR1/25.
32	9816208	G. whether the use of 9-mer peptides (BCR1/9) would generate a CD8/HLA class I-restricted response.
33	9816208	Lack of T-cell-mediated recognition of the fusion region of the pml/RAR-alpha hybrid protein by lymphocytes of acute promyelocytic leukemia patients.
34	9816208	In previous studies, it was shown that the fusion region of the pml/RAR-alpha protein, expressed by acute promyelocytic leukemia (APL) cells, can be specifically recognized in vitro by donor (D.
35	9816208	G.) with BCR1/25, a 25-mer pml/RAR-alpha, did not elicit either a polyclonal or a clonal immune response specific to the peptide.
36	9816208	We then generated new donor anti-pml/RAR-alpha CD4(+) T-cell clones.
37	9816208	One clone (C3/5, CD3(+), CD4(+), CD8(-)) was selected for further analysis.
38	9816208	Clone C3/5 showed specific proliferation, cytotoxicity, and cytokine (tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor) production when challenged with autologous lymphoblastic cell lines pulsed with peptide BCR1/25.
39	9816208	G. whether the use of 9-mer peptides (BCR1/9) would generate a CD8/HLA class I-restricted response.
40	10506665	CD19 regulates B cell antigen receptor-mediated MHC class II antigen processing.
41	10506665	CD19 is a B cell surface molecule which has been demonstrated to function in modifying signals generated through the BCR, regulating T-cell dependent B-cell activation.
42	10506665	CD19 cross-linking also inhibited the processing and presentation of antigen internalized bound to the BCR by decreasing the degree and rate of internalization of the BCR and specific antigen and its trafficking to the class II peptide loading compartment.
43	10506665	In contrast, CD19 cross-linking did not affect the rate of assembly of SDS-stable peptide class II complexes, indicating that CD19 cross-linking did not have a global effect on membrane trafficking in B cells but rather a selective effect on BCR trafficking.
44	10506665	Thus, in addition to a direct role in modulating BCR signaling for B cell proliferation and differentiation, CD19 may indirectly influence B cell activation by regulating antigen processing and B cell interactions with helper T cells.
45	10506665	CD19 regulates B cell antigen receptor-mediated MHC class II antigen processing.
46	10506665	CD19 is a B cell surface molecule which has been demonstrated to function in modifying signals generated through the BCR, regulating T-cell dependent B-cell activation.
47	10506665	CD19 cross-linking also inhibited the processing and presentation of antigen internalized bound to the BCR by decreasing the degree and rate of internalization of the BCR and specific antigen and its trafficking to the class II peptide loading compartment.
48	10506665	In contrast, CD19 cross-linking did not affect the rate of assembly of SDS-stable peptide class II complexes, indicating that CD19 cross-linking did not have a global effect on membrane trafficking in B cells but rather a selective effect on BCR trafficking.
49	10506665	Thus, in addition to a direct role in modulating BCR signaling for B cell proliferation and differentiation, CD19 may indirectly influence B cell activation by regulating antigen processing and B cell interactions with helper T cells.
50	10506665	CD19 regulates B cell antigen receptor-mediated MHC class II antigen processing.
51	10506665	CD19 is a B cell surface molecule which has been demonstrated to function in modifying signals generated through the BCR, regulating T-cell dependent B-cell activation.
52	10506665	CD19 cross-linking also inhibited the processing and presentation of antigen internalized bound to the BCR by decreasing the degree and rate of internalization of the BCR and specific antigen and its trafficking to the class II peptide loading compartment.
53	10506665	In contrast, CD19 cross-linking did not affect the rate of assembly of SDS-stable peptide class II complexes, indicating that CD19 cross-linking did not have a global effect on membrane trafficking in B cells but rather a selective effect on BCR trafficking.
54	10506665	Thus, in addition to a direct role in modulating BCR signaling for B cell proliferation and differentiation, CD19 may indirectly influence B cell activation by regulating antigen processing and B cell interactions with helper T cells.
55	10506665	CD19 regulates B cell antigen receptor-mediated MHC class II antigen processing.
56	10506665	CD19 is a B cell surface molecule which has been demonstrated to function in modifying signals generated through the BCR, regulating T-cell dependent B-cell activation.
57	10506665	CD19 cross-linking also inhibited the processing and presentation of antigen internalized bound to the BCR by decreasing the degree and rate of internalization of the BCR and specific antigen and its trafficking to the class II peptide loading compartment.
58	10506665	In contrast, CD19 cross-linking did not affect the rate of assembly of SDS-stable peptide class II complexes, indicating that CD19 cross-linking did not have a global effect on membrane trafficking in B cells but rather a selective effect on BCR trafficking.
59	10506665	Thus, in addition to a direct role in modulating BCR signaling for B cell proliferation and differentiation, CD19 may indirectly influence B cell activation by regulating antigen processing and B cell interactions with helper T cells.
60	10815918	Differential recognition of a BCR/ABL peptide by lymphocytes from normal donors and chronic myeloid leukemia patients.
61	10815918	The BCR/ABL oncogenic fusion protein transforms normal bone marrow stem cells into neoplastic cells.
62	10815918	Differential recognition of a BCR/ABL peptide by lymphocytes from normal donors and chronic myeloid leukemia patients.
63	10815918	The BCR/ABL oncogenic fusion protein transforms normal bone marrow stem cells into neoplastic cells.
64	10975396	Serum BCL2/IGH DNA in follicular lymphoma patients: a minimal residual disease marker.
65	10975396	The majority of follicular lymphoma patients carry a t(14,18) juxtaposing the BCL2 oncogene to the immunoglobulin heavy chain joining region (IgH).
66	10975396	We identify extracellular BCL2/IGH transgene DNA in the serum of patients with follicular lymphoma, and evaluate its utility as a surrogate marker.
67	10975396	Serial PCR amplifications were performed using heminested BCL2-specific major breakpoint cluster region (MBR) primers and the immunoglobulin heavy chain consensus primer.
68	10975396	Results show that four of the five lymphoma patients carried extracellular BCL2/IGH transgene DNA in their serum.
69	12356717	The protein occurs as a novel dimer assembly with unique features: in contrast to well known EF-hand proteins such as calmodulin, parvalbumin or the S100 proteins, Phl p 7 adopts an extended conformation.
70	12719481	Within hours, a sequence of events was initiated in SpA-binding splenic B cells, with rapid down-regulation of BCRs and coreceptors, CD19 and CD21, the induction of an activation phenotype, and limited rounds of proliferation.
71	12719481	Although in vivo apoptosis did not require the Fas death receptor, B cells were protected by interleukin (IL)-4 or CD40L, or overexpression of Bcl-2.
72	16528969	Development of immunity in vaccinated mice was associated with the generation of leukemia specific cytotoxic T lymphocytes (CTLs) and secretion of cytokines TNF-alpha and IFN-gamma.
73	16528969	Cured mice were in molecular remission since Bcr/Abl oncogene could not be amplified from the DNA isolated from the marrow, spleen, or liver of cured mice.
74	17327358	Our methods allow us to prepare "designer" CRCL, utilizing the immunostimulation activity and the carrying capacity of CRCL to quantitatively acquire and deliver exogenous antigenic peptides (e.g., derived from the oncogenic BCR/ABL protein in chronic myelogenous leukemia).
75	17437417	Peptides from three well-characterized LSA, the breakpoint cluster region-abelson (BCR-ABL) fusion protein of chronic myelogenous leukaemia, proteinase-3 and Wilms tumour 1 protein, serve as the basis for several clinical trials using peptide and adjuvants to treat patients with a variety of myeloid malignancies.
76	18228247	TLR7 and CD40 cooperate in IL-6 production via enhanced JNK and AP-1 activation.
77	18228247	To address this goal, we examined the effects of TLR stimulation on BCR and CD40-induced B cell activation.
78	18228247	Synergistic production of IL-6 was observed in both human and mouse primary B cells stimulated through B cell antigen receptors, CD40 and TLR7, and these two receptors also cooperated independently of BCR signals.
79	18228247	The enhanced IL-6 production was dependent upon the activity of c-Jun kinase (JNK) and cFos.
80	18228247	Dual stimulation through CD40 and TLR7 markedly enhanced JNK activity.
81	18228247	The increased level of active JNK in dual-stimulated cells was accompanied by an increase in the level of active AP-1 monomers cJun and cFos.
82	18228247	The stimulation of B cells through both CD40 and TLR7 therefore enhanced the production of cytokines through increased JNK signaling and AP-1 activity.
83	18228247	In addition, the dual stimulation increased cFos/AP-1 species in stimulated cells, effectively expanding the repertoire of AP-1 dimers as compared to singly stimulated B cells.
84	18398723	Chronic myeloid leukemia (CML) is a stem cell disease in which BCR/ABL plays an important role as oncoprotein and also as a molecular and immunogenic target.
85	18606673	CpG-B was equally effective in stimulating the proliferation of naive B cells of HIV-infected individuals and HIV-negative individuals, and, when combined with BCR and CD40 ligation, cytokine secretion by naive B cells was also comparable in HIV-infected and uninfected individuals.
86	18639600	Ballistic transfer of minimalistic immunogenically defined gene expression (MIDGE) vectors encoding a BCR-ABLp185 fusion specific peptide or GM-CSF were used for in vivo transfection.
87	18639600	We present survival and functional data that DNA-based vaccination with BCR-ABLp185 fusion specific sequences, GM-CSF and dSLIM leads to an anti-tumor effect in mice challenged with a lethal Ph+ ALL dose and this effect depends on leukaemia-specific sequences.
88	18639600	Ballistic transfer of minimalistic immunogenically defined gene expression (MIDGE) vectors encoding a BCR-ABLp185 fusion specific peptide or GM-CSF were used for in vivo transfection.
89	18639600	We present survival and functional data that DNA-based vaccination with BCR-ABLp185 fusion specific sequences, GM-CSF and dSLIM leads to an anti-tumor effect in mice challenged with a lethal Ph+ ALL dose and this effect depends on leukaemia-specific sequences.
90	19062160	Out of frame peptides from BCR/ABL alternative splicing are immunogenic in HLA A2.1 transgenic mice.
91	19062160	New, potentially tumor-specific antigens have been described in Bcr/Abl positive leukemias.
92	19062160	Besides the main BCR/ABL hybrid fusion transcripts, a small number of transcripts derived from alternative splicing between BCR exons 1, 13, and 14 with ABL exons 4 and 5 have been identified.
93	19062160	Out of frame peptides from BCR/ABL alternative splicing are immunogenic in HLA A2.1 transgenic mice.
94	19062160	New, potentially tumor-specific antigens have been described in Bcr/Abl positive leukemias.
95	19062160	Besides the main BCR/ABL hybrid fusion transcripts, a small number of transcripts derived from alternative splicing between BCR exons 1, 13, and 14 with ABL exons 4 and 5 have been identified.
96	19062160	Out of frame peptides from BCR/ABL alternative splicing are immunogenic in HLA A2.1 transgenic mice.
97	19062160	New, potentially tumor-specific antigens have been described in Bcr/Abl positive leukemias.
98	19062160	Besides the main BCR/ABL hybrid fusion transcripts, a small number of transcripts derived from alternative splicing between BCR exons 1, 13, and 14 with ABL exons 4 and 5 have been identified.
99	19171873	Interferon (IFN) is effective at inducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an immune mechanism.
100	19171873	Here we show that the type I IFNs (alpha and beta) regulate expression of the IFN consensus sequence-binding protein (ICSBP) in BCR-ABL-transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of BCR-ABL-induced leukemia.
101	19171873	We identify the chemokines CCL6 and CCL9 as genes prominently induced by the type I IFNs and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression.
102	19171873	Insights into the role of these chemokines in the antileukemic response of IFNs suggest new strategies for immunotherapy of CML.
103	19171873	Interferon (IFN) is effective at inducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an immune mechanism.
104	19171873	Here we show that the type I IFNs (alpha and beta) regulate expression of the IFN consensus sequence-binding protein (ICSBP) in BCR-ABL-transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of BCR-ABL-induced leukemia.
105	19171873	We identify the chemokines CCL6 and CCL9 as genes prominently induced by the type I IFNs and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression.
106	19171873	Insights into the role of these chemokines in the antileukemic response of IFNs suggest new strategies for immunotherapy of CML.
107	19171873	Interferon (IFN) is effective at inducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an immune mechanism.
108	19171873	Here we show that the type I IFNs (alpha and beta) regulate expression of the IFN consensus sequence-binding protein (ICSBP) in BCR-ABL-transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of BCR-ABL-induced leukemia.
109	19171873	We identify the chemokines CCL6 and CCL9 as genes prominently induced by the type I IFNs and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression.
110	19171873	Insights into the role of these chemokines in the antileukemic response of IFNs suggest new strategies for immunotherapy of CML.
111	19801508	CD40- or TLR7-stimulated B cell APCs induced similar CD8(+) T cell responses, but costimulation through the BCR and TLR7 produced a more effective Bvac as measured by T cell stimulation and the protection of mice from an infectious pathogen.
112	20139775	Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.
113	22024730	Enhancement of specific cellular immune response induced by glycosyl-phosphatidylinositol-anchored BCR/ABL and mIL-12.
114	22024730	bcr/abl fusion gene is thought to be a promising target for chronic myelogenous leukemia (CML) patients to enhance immune response after attaining complete remission.
115	22024730	In this study, we sought to enhance cellular immunity by co-expression of BCR/ABL and murine IL-12 gene on the tumor cell surface as a glycosyl-phosphatidylinositol (GPI)-form.
116	22024730	In a murine transplant model, the vaccinated mice showed decreased infiltration of leukemia cells and reduced expression of BCR/ABL transcripts and protein in bone marrow cells.
117	22024730	Enhancement of specific cellular immune response induced by glycosyl-phosphatidylinositol-anchored BCR/ABL and mIL-12.
118	22024730	bcr/abl fusion gene is thought to be a promising target for chronic myelogenous leukemia (CML) patients to enhance immune response after attaining complete remission.
119	22024730	In this study, we sought to enhance cellular immunity by co-expression of BCR/ABL and murine IL-12 gene on the tumor cell surface as a glycosyl-phosphatidylinositol (GPI)-form.
120	22024730	In a murine transplant model, the vaccinated mice showed decreased infiltration of leukemia cells and reduced expression of BCR/ABL transcripts and protein in bone marrow cells.
121	22024730	Enhancement of specific cellular immune response induced by glycosyl-phosphatidylinositol-anchored BCR/ABL and mIL-12.
122	22024730	bcr/abl fusion gene is thought to be a promising target for chronic myelogenous leukemia (CML) patients to enhance immune response after attaining complete remission.
123	22024730	In this study, we sought to enhance cellular immunity by co-expression of BCR/ABL and murine IL-12 gene on the tumor cell surface as a glycosyl-phosphatidylinositol (GPI)-form.
124	22024730	In a murine transplant model, the vaccinated mice showed decreased infiltration of leukemia cells and reduced expression of BCR/ABL transcripts and protein in bone marrow cells.
125	22024730	Enhancement of specific cellular immune response induced by glycosyl-phosphatidylinositol-anchored BCR/ABL and mIL-12.
126	22024730	bcr/abl fusion gene is thought to be a promising target for chronic myelogenous leukemia (CML) patients to enhance immune response after attaining complete remission.
127	22024730	In this study, we sought to enhance cellular immunity by co-expression of BCR/ABL and murine IL-12 gene on the tumor cell surface as a glycosyl-phosphatidylinositol (GPI)-form.
128	22024730	In a murine transplant model, the vaccinated mice showed decreased infiltration of leukemia cells and reduced expression of BCR/ABL transcripts and protein in bone marrow cells.
129	23089396	Failure to induce synthesis of neutralizing Abs to the CD4 binding determinant (CD4BD) of gp120, a central objective in HIV vaccine research, has been alternately ascribed to insufficient immunogen binding to Abs in their germline V region configuration expressed as BCRs, insufficient adaptive mutations in Ab V regions, and conformational instability of gp120.
130	23630363	In this article, we have developed a vaccination strategy by targeting protein Ags to B cells via a CD19 single-chain variable fragment miniAb.
131	23630363	Using the tumor-associated Ag her-2/neu extracellular domain, we showed that the coengagement of CD19 and BCR induced full B cell activation to produce a high titer of Abs and enhanced CD4 Th2 response and CD8 T cell activation and differentiation.
132	23841051	The use of a DNA vaccine encoding the BCR/ABL fusion gene is thought to be a promising approach for patients with chronic myeloid leukemia (CML) to eradicate minimal residual disease after treatment with chemotherapy or targeted therapy.
133	23841051	In this study, our strategy employs genetic technology to create a DNA vaccine encoding the BCR/ABL fusion and human interleukin-2 (hIL-2) genes.
134	23841051	The transcription and expression of the BCR/ABL and hIL-2 genes were found in the injected muscle tissues.
135	23841051	The interferon- γ (IFN- γ ) serum levels were increased, and the splenic CD4(+)/CD8(+) T cell ratio was significantly decreased in the BCR/ABL-pIRES-hIL-2-injected mice.
136	23841051	These results indicate that a DNA vaccine containing BCR/ABL and hIL-2 together may elicit increased in vivo humoral and cellular immune responses in BALB/c mice.
137	23841051	The use of a DNA vaccine encoding the BCR/ABL fusion gene is thought to be a promising approach for patients with chronic myeloid leukemia (CML) to eradicate minimal residual disease after treatment with chemotherapy or targeted therapy.
138	23841051	In this study, our strategy employs genetic technology to create a DNA vaccine encoding the BCR/ABL fusion and human interleukin-2 (hIL-2) genes.
139	23841051	The transcription and expression of the BCR/ABL and hIL-2 genes were found in the injected muscle tissues.
140	23841051	The interferon- γ (IFN- γ ) serum levels were increased, and the splenic CD4(+)/CD8(+) T cell ratio was significantly decreased in the BCR/ABL-pIRES-hIL-2-injected mice.
141	23841051	These results indicate that a DNA vaccine containing BCR/ABL and hIL-2 together may elicit increased in vivo humoral and cellular immune responses in BALB/c mice.
142	23841051	The use of a DNA vaccine encoding the BCR/ABL fusion gene is thought to be a promising approach for patients with chronic myeloid leukemia (CML) to eradicate minimal residual disease after treatment with chemotherapy or targeted therapy.
143	23841051	In this study, our strategy employs genetic technology to create a DNA vaccine encoding the BCR/ABL fusion and human interleukin-2 (hIL-2) genes.
144	23841051	The transcription and expression of the BCR/ABL and hIL-2 genes were found in the injected muscle tissues.
145	23841051	The interferon- γ (IFN- γ ) serum levels were increased, and the splenic CD4(+)/CD8(+) T cell ratio was significantly decreased in the BCR/ABL-pIRES-hIL-2-injected mice.
146	23841051	These results indicate that a DNA vaccine containing BCR/ABL and hIL-2 together may elicit increased in vivo humoral and cellular immune responses in BALB/c mice.
147	23841051	The use of a DNA vaccine encoding the BCR/ABL fusion gene is thought to be a promising approach for patients with chronic myeloid leukemia (CML) to eradicate minimal residual disease after treatment with chemotherapy or targeted therapy.
148	23841051	In this study, our strategy employs genetic technology to create a DNA vaccine encoding the BCR/ABL fusion and human interleukin-2 (hIL-2) genes.
149	23841051	The transcription and expression of the BCR/ABL and hIL-2 genes were found in the injected muscle tissues.
150	23841051	The interferon- γ (IFN- γ ) serum levels were increased, and the splenic CD4(+)/CD8(+) T cell ratio was significantly decreased in the BCR/ABL-pIRES-hIL-2-injected mice.
151	23841051	These results indicate that a DNA vaccine containing BCR/ABL and hIL-2 together may elicit increased in vivo humoral and cellular immune responses in BALB/c mice.
152	23841051	The use of a DNA vaccine encoding the BCR/ABL fusion gene is thought to be a promising approach for patients with chronic myeloid leukemia (CML) to eradicate minimal residual disease after treatment with chemotherapy or targeted therapy.
153	23841051	In this study, our strategy employs genetic technology to create a DNA vaccine encoding the BCR/ABL fusion and human interleukin-2 (hIL-2) genes.
154	23841051	The transcription and expression of the BCR/ABL and hIL-2 genes were found in the injected muscle tissues.
155	23841051	The interferon- γ (IFN- γ ) serum levels were increased, and the splenic CD4(+)/CD8(+) T cell ratio was significantly decreased in the BCR/ABL-pIRES-hIL-2-injected mice.
156	23841051	These results indicate that a DNA vaccine containing BCR/ABL and hIL-2 together may elicit increased in vivo humoral and cellular immune responses in BALB/c mice.
157	24386360	We first demonstrate that murine B cells with a human MOG-specific BCR are able to interact with MOG-coated beads and do not recognize beads coated with human albumin or pp65.
158	24480037	Serine and proline-rich ligands enriched via phage-display technology show preferential binding to BCR/ABL expressing cells.
159	24614505	B-cell chronic lymphocytic leukemia (B-CLL) patients expressing unmutated immunoglobulin heavy variable regions (IGHVs) use the IGHV1-69 B cell receptor (BCR) in 25% of cases.
160	24614505	To test this hypothesis, we rescued 5 IGHV1-69 unmutated antibodies as heterohybridoma IgM paraproteins and as recombinant IgG1 antibodies from B-CLL patients, determined their antigenic specificities and analyzed BCR sequences.
161	24614505	IGHV1-69 B-CLL antibodies were enriched for reactivity with HIV-1 envelope gp41, influenza, hepatitis C virus E2 protein and intestinal commensal bacteria.
162	24614505	These IGHV1-69 B-CLL antibodies preferentially used IGHD3 and IGHJ6 gene segments and had long heavy chain complementary determining region 3s (HCDR3s) (≥21 aa).
163	24614505	IGHV1-69 B-CLL BCRs exhibited a phenylalanine at position 54 (F54) of the HCDR2 as do rare HIV-1 gp41 and influenza hemagglutinin stem neutralizing antibodies, while IGHV1-69 gp41 antibodies induced by HIV-1 infection predominantly used leucine (L54) allelic variants.
164	24614505	B-cell chronic lymphocytic leukemia (B-CLL) patients expressing unmutated immunoglobulin heavy variable regions (IGHVs) use the IGHV1-69 B cell receptor (BCR) in 25% of cases.
165	24614505	To test this hypothesis, we rescued 5 IGHV1-69 unmutated antibodies as heterohybridoma IgM paraproteins and as recombinant IgG1 antibodies from B-CLL patients, determined their antigenic specificities and analyzed BCR sequences.
166	24614505	IGHV1-69 B-CLL antibodies were enriched for reactivity with HIV-1 envelope gp41, influenza, hepatitis C virus E2 protein and intestinal commensal bacteria.
167	24614505	These IGHV1-69 B-CLL antibodies preferentially used IGHD3 and IGHJ6 gene segments and had long heavy chain complementary determining region 3s (HCDR3s) (≥21 aa).
168	24614505	IGHV1-69 B-CLL BCRs exhibited a phenylalanine at position 54 (F54) of the HCDR2 as do rare HIV-1 gp41 and influenza hemagglutinin stem neutralizing antibodies, while IGHV1-69 gp41 antibodies induced by HIV-1 infection predominantly used leucine (L54) allelic variants.
169	24614505	B-cell chronic lymphocytic leukemia (B-CLL) patients expressing unmutated immunoglobulin heavy variable regions (IGHVs) use the IGHV1-69 B cell receptor (BCR) in 25% of cases.
170	24614505	To test this hypothesis, we rescued 5 IGHV1-69 unmutated antibodies as heterohybridoma IgM paraproteins and as recombinant IgG1 antibodies from B-CLL patients, determined their antigenic specificities and analyzed BCR sequences.
171	24614505	IGHV1-69 B-CLL antibodies were enriched for reactivity with HIV-1 envelope gp41, influenza, hepatitis C virus E2 protein and intestinal commensal bacteria.
172	24614505	These IGHV1-69 B-CLL antibodies preferentially used IGHD3 and IGHJ6 gene segments and had long heavy chain complementary determining region 3s (HCDR3s) (≥21 aa).
173	24614505	IGHV1-69 B-CLL BCRs exhibited a phenylalanine at position 54 (F54) of the HCDR2 as do rare HIV-1 gp41 and influenza hemagglutinin stem neutralizing antibodies, while IGHV1-69 gp41 antibodies induced by HIV-1 infection predominantly used leucine (L54) allelic variants.
174	25536171	B cell TLR1/2, TLR4, TLR7 and TLR9 interact in induction of class switch DNA recombination: modulation by BCR and CD40, and relevance to T-independent antibody responses.
175	25536171	Here, we have addressed cross-regulation between two different TLRs or between a TLR and CD40 in CSR induction by using a B cell stimulation system involving lipopolysaccharides (LPS).
176	25536171	Consistent with the requirement for dual TLR and BCR engagement in CSR induction, LPS, which engages TLR4 through its lipid A moiety, triggered cytosolic Ca2+ flux in B cells through its BCR-engaging polysaccharidic moiety.
177	25536171	In the presence of BCR crosslinking, LPS synergized with a TLR1/2 ligand (Pam3CSK4) in CSR induction, but much less efficiently with a TLR7 (R-848) or TLR9 (CpG) ligand.
178	25536171	In the absence of BCR crosslinking, R-848 and CpG, which per se induced marginal CSR, virtually abrogated CSR to IgG1, IgG2a, IgG2b, IgG3 and/or IgA, as induced by LPS or CD154 (CD40 ligand) plus IL-4, IFN-γ or TGF-β, and reduced secretion of class-switched Igs, without affecting B cell proliferation or IgM expression.
179	25536171	The CSR inhibition by TLR9 was associated with the reduction in AID expression and/or IgH germline IH-S-CH transcription, and required co-stimulation of B cells by CpG with LPS or CD154.
180	25536171	Unexpectedly, B cells also failed to undergo CSR or plasma cell differentiation when co-stimulated by LPS and CD154.
181	25536171	Overall, by addressing the interaction of TLR1/2, TLR4, TLR7 and TLR9 in the induction of CSR and modulation of TLR-dependent CSR by BCR and CD40, our study suggests the complexity of how different stimuli cross-regulate an important B cell differentiation process and an important role of TLRs in inducing effective T-independent antibody responses to microbial pathogens, allergens and vaccines.
182	25536171	B cell TLR1/2, TLR4, TLR7 and TLR9 interact in induction of class switch DNA recombination: modulation by BCR and CD40, and relevance to T-independent antibody responses.
183	25536171	Here, we have addressed cross-regulation between two different TLRs or between a TLR and CD40 in CSR induction by using a B cell stimulation system involving lipopolysaccharides (LPS).
184	25536171	Consistent with the requirement for dual TLR and BCR engagement in CSR induction, LPS, which engages TLR4 through its lipid A moiety, triggered cytosolic Ca2+ flux in B cells through its BCR-engaging polysaccharidic moiety.
185	25536171	In the presence of BCR crosslinking, LPS synergized with a TLR1/2 ligand (Pam3CSK4) in CSR induction, but much less efficiently with a TLR7 (R-848) or TLR9 (CpG) ligand.
186	25536171	In the absence of BCR crosslinking, R-848 and CpG, which per se induced marginal CSR, virtually abrogated CSR to IgG1, IgG2a, IgG2b, IgG3 and/or IgA, as induced by LPS or CD154 (CD40 ligand) plus IL-4, IFN-γ or TGF-β, and reduced secretion of class-switched Igs, without affecting B cell proliferation or IgM expression.
187	25536171	The CSR inhibition by TLR9 was associated with the reduction in AID expression and/or IgH germline IH-S-CH transcription, and required co-stimulation of B cells by CpG with LPS or CD154.
188	25536171	Unexpectedly, B cells also failed to undergo CSR or plasma cell differentiation when co-stimulated by LPS and CD154.
189	25536171	Overall, by addressing the interaction of TLR1/2, TLR4, TLR7 and TLR9 in the induction of CSR and modulation of TLR-dependent CSR by BCR and CD40, our study suggests the complexity of how different stimuli cross-regulate an important B cell differentiation process and an important role of TLRs in inducing effective T-independent antibody responses to microbial pathogens, allergens and vaccines.
190	25962322	BAFF receptor and TACI in B-1b cell maintenance and antibacterial responses.
191	25962322	Although evidence of the protective immunity conferred by B-1b cells (CD19(+) B220(+) IgM(hi) Mac1(+) CD5(-)) has been established, the mechanisms governing the maintenance and activation of B-1b cells following pathogen encounter remain unclear.
192	25962322	B cell-activating factor (BAFF) and a proliferation-inducing ligand (APRIL) mediate their function in mature B cells through the BAFF receptor (BAFFR) and transmembrane activator and CAML interactor (TACI).
193	25962322	Mice with impaired BCR signaling, such as X-linked immunodeficient (xid) mice, have B-1b cell deficiency, indicating that both BCR- and BAFFR-mediated signaling are critical for B-1b cell homeostasis.
194	25962322	The activation of TLR signaling by B. hermsii and BCR/TLR costimulation-mediated upregulation of BAFFR and TACI on B-1b cells suggests that B-1b cell maintenance and function following bacterial exposure may depend on BAFFR- and TACI-mediated signaling.
195	25962322	In fact, the loss of both BAFFR and TACI results in a greater impairment in anti-B. hermsii responses compared to deficiency of BAFFR or TACI alone.
196	26184912	We demonstrate the upregulation of Bim, Bik, and Noxa during BCR signaling in vitro and that intrinsic apoptosis has a prominent role in anti-BCR antibody therapy in vivo.
197	26184912	Furthermore, lymphomas deficient in these individual BH3-only proteins display significant protection from BCR-induced cell death, whereas combined loss of Noxa and Bim offers enhanced protection in comparison with loss of Bim alone.
198	26184912	These observations indicate that BCR signaling elicits maximal cell death through upregulation of multiple BH3-only proteins; namely Bim, Bik, and Noxa.
199	26184912	We demonstrate the upregulation of Bim, Bik, and Noxa during BCR signaling in vitro and that intrinsic apoptosis has a prominent role in anti-BCR antibody therapy in vivo.
200	26184912	Furthermore, lymphomas deficient in these individual BH3-only proteins display significant protection from BCR-induced cell death, whereas combined loss of Noxa and Bim offers enhanced protection in comparison with loss of Bim alone.
201	26184912	These observations indicate that BCR signaling elicits maximal cell death through upregulation of multiple BH3-only proteins; namely Bim, Bik, and Noxa.