scholarly journals Proximal promoter of the murine syndecan-1 gene is not sufficient for the developmental pattern of syndecan expression in B lineage cells

2001 ◽  
Vol 67 (1) ◽  
pp. 20-26 ◽  
Author(s):  
Carmelo P. Volpe ◽  
Anna Lundgren ◽  
Alar Aints ◽  
Abdalla J. Mohamed ◽  
Panu Jaakkola ◽  
...  
Keyword(s):  
Developmental Pattern ◽  
Proximal Promoter ◽  
B Lineage ◽  
B Lineage Cells

A novel cell surface molecule on early B-lineage cells

Nature ◽  
1986 ◽  
Vol 321 (6070) ◽  
pp. 616-618 ◽  
Author(s):  
Max D. Cooper ◽  
David Mulvaney ◽  
Antonio Coutinho ◽  
Pierre-André Cazenave
Keyword(s):  
Cell Surface ◽  
Surface Molecule ◽  
Cell Surface Molecule ◽  
B Lineage ◽  
B Lineage Cells

Induction of Apoptosis in B Lineage Cells by Activin A Derived from Macrophages

1995 ◽  
Vol 15 (6) ◽  
pp. 509-516 ◽  
Author(s):  
TATSUJI NISHIHARA ◽  
YASUYOSHI OHSAKI ◽  
NOBUO UEDA ◽  
TAKEYOSHI KOSEKI ◽  
YUZURU ETO
Keyword(s):  
Activin A ◽  
Induction Of Apoptosis ◽  
B Lineage ◽  
B Lineage Cells

The enhancer shift: a model to explain the developmental control of IgH gene expression in B-lineage cells

1997 ◽  
Vol 18 (11) ◽  
pp. 549-554 ◽  
Author(s):  
Velmurugesan Arulampalam ◽  
Laurel Eckhardt ◽  
Sven Pettersson
Keyword(s):  
Gene Expression ◽  
Developmental Control ◽  
B Lineage ◽  
B Lineage Cells

Evidence for Expansion of Sinonasal B-Lineage Cells in Chronic Rhinosinusitis

2013 ◽  
Vol 131 (2) ◽  
pp. AB7
Author(s):  
Kathryn E. Hulse ◽  
James Norton ◽  
Robert Kern ◽  
David Conley ◽  
Rakesh Chandra ◽  
...  
Keyword(s):  
Chronic Rhinosinusitis ◽  
B Lineage ◽  
B Lineage Cells

scholarly journals Flow cytometric analysis of human bone marrow. II. Normal B lymphocyte development

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1316-1324 ◽  
Author(s):  
MR Loken ◽  
VO Shah ◽  
KL Dattilio ◽  
CI Civin
Keyword(s):  
Bone Marrow ◽  
Cell Surface ◽  
B Lymphocyte ◽  
Human Bone ◽  
Lymphocyte Development ◽  
Hla Dq ◽  
B Lymphocyte Development ◽  
B Lineage ◽  
B Lymphoid ◽  
B Lineage Cells

Abstract A panel of B lymphoid-reactive monoclonal antibodies was used to analyze the phenotypic changes that accompany B lymphocyte development in normal human bone marrow. The B lymphoid cells were identified using light scattering and the expression of CD19 on a flow cytometer. Quantitative three-color immunofluorescence was then used to correlate other cell surface antigens on these cells identified as B lymphoid in normal marrow. CD10 and CD20 identified almost exclusive populations and provided a convenient means of discriminating between the less and more mature B lineage cells. The CD10+ cells could be further subdivided using CD34. The population of CD19+, CD10+, CD34+ cells comprised only 0.6% of marrow cells, but these contained the majority of terminal deoxynucleotidyl transferase (TdT+) cells. In the assessment of class II antigens, HLA-DR was expressed on all B lineage cells whereas HLA-DP preceded HLA-DQ in appearance during the developmental process. Among the later antigens expressed on B lineage cells, cell surface IgM, CD20, and HLA-DQ were expressed at essentially the same time. Cell surface CD10 was lost at the time when CD21 and CD22 were acquired on the cell surface. These data illustrate that multiparameter flow cytometry can be used to define a continuous progression of stages of B lymphocyte development based on cell surface antigen expression even though these cells represent a minor fraction of normal marrow cells.

Phosphoinositide 3-kinase signaling is essential for ABL oncogene–mediated transformation of B-lineage cells

Blood ◽  
2004 ◽  
Vol 103 (11) ◽  
pp. 4268-4275 ◽  
Author(s):  
Michael G. Kharas ◽  
Jonathan A. Deane ◽  
Stephane Wong ◽  
Karen R. O'Bosky ◽  
Naomi Rosenberg ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Cell Types ◽  
Pi3k Signaling ◽  
Pi3k Inhibitors ◽  
Abl Tyrosine Kinase ◽  
Foxo Transcription Factors ◽  
B Lineage ◽  
Phosphoinositide 3 Kinase ◽  
Multiple Signaling ◽  
B Lineage Cells

Abstract BCR-ABL and v-ABL are oncogenic forms of the Abl tyrosine kinase that can cause leukemias in mice and humans. ABL oncogenes trigger multiple signaling pathways whose contribution to transformation varies among cell types. Activation of phosphoinositide 3-kinase (PI3K) is essential for ABL-dependent proliferation and survival in some cell types, and global PI3K inhibitors can enhance the antileukemia effects of the Abl kinase inhibitor imatinib. Although a significant fraction of BCR-ABL-induced human leukemias are of B-cell origin, little is known about PI3K signaling mechanisms in B-lineage cells transformed by ABL oncogenes. Here we show that activation of class IA PI3K and downstream inactivation of FOXO transcription factors are essential for survival of murine pro/pre-B cells transformed by v-ABL or BCR-ABL. In addition, analysis of mice lacking individual PI3K genes indicates that products of the Pik3r1 gene contribute to transformation efficiency by BCR-ABL. These findings establish a role for PI3K signaling in B-lineage transformation by ABL oncogenes. (Blood. 2004;103:4268-4275)

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