PU.1 exhibits partial functional redundancy with Spi-B, but not with Ets-1 or Elf-1.
@article{GarrettSinha2001PU1EP,
title={PU.1 exhibits partial functional redundancy with Spi-B, but not with Ets-1 or Elf-1.},
author={Lee Ann Garrett-Sinha and Richard Dahl and S Rao and Kevin P. Barton and M. Celeste Simon},
journal={Blood},
year={2001},
volume={97 9},
pages={
2908-12
}
}Previously it was shown that the Ets proteins, PU.1 and Spi-B, exhibit functional redundancy in B lymphocytes. To investigate the possibility that PU.1 or Spi-B or both share overlapping roles with Ets-1 or Elf-1, PU.1(+/-)Ets-1(-/-), PU.1(+/-)Elf-1(-/-), and Spi-B(-/-)Ets-1(-/-) animals were generated. No blood cell defects were observed in these animals except those previously reported for Ets-1(-/-) mice. Therefore, no genetic overlap was detected between PU.1 or Spi-B with Ets-1 or Elf-1…
58 Citations
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References
SHOWING 1-10 OF 28 REFERENCES
PU.1 and Spi-B are required for normal B cell receptor-mediated signal transduction.
- BiologyImmunity
- 1999
Characterization of Spi-B, a transcription factor related to the putative oncoprotein Spi-1/PU.1.
- BiologyMolecular and cellular biology
- 1992
It is shown that the spi-B protein is able to bind the purine-rich sequence (PU box) recognized by Spi-1/PU and to activate transcription of a reporter plasmid containing PU boxes.
The Ets protein Spi-B is expressed exclusively in B cells and T cells during development
- BiologyThe Journal of experimental medicine
- 1996
Differences in patterns of expression between Spi-B and PU.1 distinguish the function of each protein during development of the immune system.
Neutrophils and monocytes express high levels of PU.1 (Spi-1) but not Spi-B.
- BiologyBlood
- 1995
PU.1 mRNA is upregulated during myeloid differentiation of human purified CD34+ cells and murine multipotential FDCP-mix A4 cells, suggesting that PU.1 can activate gene expression in both major myeloids lineages.
Defective activation and survival of T cells lacking the Ets-1 transcription factor
- Biology, MedicineNature
- 1995
It is demonstrated that Ets-1 is required for the normal survival and activation of murine T cells and is regulated during both thymocytes and T-cell activation.
The macrophage and B cell-specific transcription factor PU.1 is related to the ets oncogene
- BiologyCell
- 1990
Myeloid development is selectively disrupted in PU.1 null mice.
- BiologyBlood
- 1998
The results demonstrate that PU.1 gene disruption affects a number of developmentally regulated hematopoietic processes that can, at least in part, explain the changes in myeloid development and reduction inMyeloid and neutrophil expansion observed inPU.1 null mice.
Transcriptional Regulation of the Stem Cell Leukemia Gene by PU.1 and Elf-1*
- BiologyThe Journal of Biological Chemistry
- 1998
This paper demonstrates that SCL promoter 1a was regulated by GATA-1 together with Sp1 and Sp3 in a manner similar to the situation in erythroid cells, and provides the first evidence that the SCL gene is a direct target for PU.1, Elf-1, andsp3.
The Ets-1 transcription factor is required for the development of natural killer cells in mice.
- Biology, MedicineImmunity
- 1998
Increased T-cell apoptosis and terminal B-cell differentiation induced by inactivation of the Ets-1 proto-oncogene
- BiologyNature
- 1995
It is shown, by using RAG-2-deficient blasto-cyst complementation, that Ets-1 deficiency has dramatic, but different, effects on development and function of T- and B-lineage cells.


