Commentary on and reprint of Till JE, McCulloch EA, A direct measurement of the radiosensitivity of normal mouse bone marrow cells, in Radiation Research (1961) 14:213–222

Hematology ◽  
2000 ◽  
pp. 923-936 ◽  
Blood ◽  
1959 ◽  
Vol 14 (9) ◽  
pp. 1040-1046 ◽  
Author(s):  
IRWIN BERMAN ◽  
HENRY S. KAPLAN

Abstract The cultivation of normal mouse bone marrow cells in diffusion chambers implanted into the peritoneal cavity of mice has been described. Mouse bone marrow cells cultivated by this method continue to undergo differentiation and maintain their morphologic identity for a considerable time.


Blood ◽  
2004 ◽  
Vol 103 (11) ◽  
pp. 4093-4101 ◽  
Author(s):  
James K. Mangan ◽  
Sushil G. Rane ◽  
Anthony D. Kang ◽  
Arshad Amanullah ◽  
Brian C. Wong ◽  
...  

Abstract We report here that Janus kinase 3 (Jak3) is a primary response gene for interleukin-6 (IL-6) in macrophage differentiation, and ectopic overexpression of Jak3 accelerates monocytic differentiation of normal mouse bone marrow cells stimulated with cytokines. Furthermore, we show that incubation of normal mouse bone marrow cells with a JAK3-specific inhibitor results in profound inhibition of myeloid colony formation in response to granulocyte-macrophage colony-stimulating factor or the combination of stem cell factor, IL-3, and IL-6. In addition, mutagenesis of the Jak3 promoter has revealed that Sp1 binding sites within a -67 to -85 element and a signal transducer and activator of transcription (Stat) binding site at position -44 to -53 are critical for activation of Jak3 transcription in murine M1 myeloid leukemia cells stimulated with IL-6. Electrophoretic mobility shift assay (EMSA) analysis has demonstrated that Sp1 can bind to the -67 to -85 element and Stat3 can bind to the -44 to -53 STAT site in IL-6-stimulated M1 cells. Additionally, ectopic overexpression of Stat3 enhanced Jak3 promoter activity in M1 cells. This mechanism of activation of the murine Jak3 promoter in myeloid cells is distinct from a recently reported mechanism of activation of the human JAK3 promoter in activated T cells.


1987 ◽  
Vol 166 (4) ◽  
pp. 1162-1167 ◽  
Author(s):  
K L Komschlies ◽  
D L Greiner ◽  
L Shultz ◽  
I Goldschneider

Bone marrow prothymocytes from me/me and mev/mev mutant mice fail to generate thymocytes in irradiated (600 rad) +/+ wild-type recipients after intravenous injection. However, these same prothymocytes readily generate thymocytes after intrathymic injection. The results of the present study demonstrate that this apparent defect in the thymus-homing capacity of mev/mev prothymocytes can be corrected by mixing irradiated wild-type bone marrow cells with mev/mev bone marrow cells before intravenous injection. However, this defect is not corrected by passage of mev/mev bone marrow cells through the bone marrow of irradiated wild-type recipients. One interpretation of these results is that the maturation of prothymocytes is reversibly arrested in mev/mev mice by a defect in the radiosensitive compartment of the bone marrow microenvironment.


Author(s):  
Kanive Parashiva Guruprasad ◽  
Advait Subramanian ◽  
Vikram Jeet Singh ◽  
Raghavendra Sudheer Kumar Sharma ◽  
Puthiya Mundyat Gopinath ◽  
...  

2005 ◽  
Vol 26 (4) ◽  
pp. 469-476 ◽  
Author(s):  
Xiao-lei SHI ◽  
Yu-dong QIU ◽  
Qiang LI ◽  
Ting XIE ◽  
Zhang-hua ZHU ◽  
...  

1991 ◽  
Vol 18 (3) ◽  
pp. 168-183 ◽  
Author(s):  
Marcia D. Phillips ◽  
Bruce Nascimbeni ◽  
Raymond R. Tice ◽  
Michael D. Shelby ◽  
A. A. Van Zeeland

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