Evidence for LFA-1/ICAM-1 dependent stimulation of protein tyrosine phosphorylation in human B lymphoid cell lines during homotypic adhesion

1995 ◽  
Vol 57 (2) ◽  
pp. 343-351 ◽  
Author(s):  
Shirley C.-T. Wang ◽  
Steven B. Kanner ◽  
Jeffrey A. Ledbetter ◽  
Shalini Gupta ◽  
Gita Kumar ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
Protein Tyrosine Phosphorylation ◽  
Protein Tyrosine ◽  
B Lymphoid ◽  
Lymphoid Cell Lines ◽  
Stimulation Of ◽  
Homotypic Adhesion

scholarly journals Heterogeneity of B cell involvement in acute nonlymphocytic leukemia

Blood ◽  
1985 ◽  
Vol 66 (2) ◽  
pp. 342-344 ◽  
Author(s):  
AM Ferraris ◽  
WH Raskind ◽  
BH Bjornson ◽  
RJ Jacobson ◽  
JW Singer ◽  
...  
Keyword(s):  
Stem Cell ◽  
B Cell ◽  
Progenitor Cells ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
Mononuclear Cells ◽  
Acute Nonlymphocytic Leukemia ◽  
Peripheral Blood Mononuclear ◽  
B Lymphoid ◽  
Lymphoid Cell Lines

Abstract In order to study the pattern of B cell involvement in acute nonlymphocytic leukemia (ANLL), multiple B lymphoid cell lines were established by Epstein-Barr virus transformation of peripheral blood mononuclear cells from two patients with the disease who were heterozygous for the X chromosome-linked glucose-6-phosphate dehydrogenase (G6PD). In one patient, the progenitor cells involved by the leukemia exhibited multipotent differentiative expression, whereas in the other patient the cells showed differentiative expression restricted to the granulocytic pathway. In the patient whose abnormal clone showed multipotent expression, the ratio of B-A G6PD in B lymphoid cell lines was skewed in the direction of type B (the enzyme characteristic of the leukemia clone) and significantly different from the 1:1 ratio expected. It is, therefore, likely that the neoplastic event occurred in a stem cell common to the lymphoid series as well as to the myeloid series. In contrast, evidence for B cell involvement was not detected in the patient whose ANLL progenitor cells exhibited restricted differentiative expression. These findings underscore the heterogeneity of ANLL. Clinically and morphologically similar malignancies in these two patients originated in progenitors with different patterns of stem cell differentiative expression. This difference may reflect differences in cause and pathogenesis.

scholarly journals UDP-GlcNAc:Gal 1->3GalNAc (GlcNAc to GalNAc)  1->6N-acetylglucosaminyltransferase holds a key role on the control of CD15s expression in human pre-B lymphoid cell lines

Glycobiology ◽  
1999 ◽  
Vol 9 (1) ◽  
pp. 1-12 ◽  
Author(s):  
M. Nakamura ◽  
Y. Furukawa ◽  
R. Sasaki ◽  
J.-i. Masuyama ◽  
J. Kikuchi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Lymphoid Cell ◽  
B Lymphoid ◽  
Lymphoid Cell Lines

Stimulation of protein tyrosine phosphorylation by platelet-activating factor and progesterone in human spermatozoa

1995 ◽  
Vol 108 (1-2) ◽  
pp. 35-42 ◽  
Author(s):  
Michaela Luconi ◽  
Lorella Bonaccorsi ◽  
Csilla Krausz ◽  
Ginetta Gervasi ◽  
Gianni Forti ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Platelet Activating Factor ◽  
Human Spermatozoa ◽  
Protein Tyrosine Phosphorylation ◽  
Protein Tyrosine ◽  
Stimulation Of

Delayed neuronal death in ischemic hippocampus involves stimulation of protein tyrosine phosphorylation

1996 ◽  
Vol 271 (4) ◽  
pp. C1085-C1097 ◽  
Author(s):  
T. Ohtsuki ◽  
M. Matsumoto ◽  
K. Kitagawa ◽  
T. Mabuchi ◽  
K. Mandai ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Kainic Acid ◽  
Neuronal Death ◽  
Tyrosine Kinases ◽  
Ischemia Reperfusion ◽  
Delayed Neuronal Death ◽  
Mongolian Gerbils ◽  
Protein Tyrosine Phosphorylation ◽  
Protein Tyrosine ◽  
Stimulation Of

Glutamate triggers neuronal degeneration after ischemia-reperfusion in the brain. However, the details of intracellular signal transduction that propagates cell death remain unknown. The present work investigated whether protein tyrosine phosphorylation mediates neuronal death in the ischemic brain. Transient forebrain ischemia for 5-10 min in Mongolian gerbils or intoxication with the glutamate analogue kainic acid (12 mg/kg) in Sprague-Dawley rats caused neuronal death selectively in the hippocampus 2-4 days or 1 day later, respectively. Under these conditions, 160-, 115-, 105-, 92-, and 85-kDa proteins showed a significant increase in tyrosyl residue phosphorylation selectively in the hippocampus 3-12 h after ischemia or 4-8 h after kainic acid-induced seizures. Tyrosine kinases, including pp60c-src, were activated without a change of tyrosine phosphatases. Administration of radicicol, a selective inhibitor of tyrosine kinases, attenuated stimulation of tyrosine phosphorylation and hippocampal degeneration after ischemia or kainic acid injection. The results suggest that protein tyrosine phosphorylation might propagate delayed neuronal death in the mature hippocampus through glutamate overload after ischemia-reperfusion.

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