Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Method to Extend Research in Time (MERIT) Award (R37)
Project #
5R37CA016368-23
Application #
2086474
Study Section
Special Emphasis Panel (NSS)
Project Start
1977-05-01
Project End
1998-04-30
Budget Start
1996-05-01
Budget End
1997-04-30
Support Year
23
Fiscal Year
1996
Total Cost
Indirect Cost
Name
Albert Einstein College of Medicine
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
009095365
City
Bronx
State
NY
Country
United States
Zip Code
10461
Matushansky, Igor; Radparvar, Farshid; Skoultchi, Arthur I (2003) CDK6 blocks differentiation: coupling cell proliferation to the block to differentiation in leukemic cells. Oncogene 22:4143-9
Rekhtman, Natasha; Choe, Kevin S; Matushansky, Igor et al. (2003) PU.1 and pRB interact and cooperate to repress GATA-1 and block erythroid differentiation. Mol Cell Biol 23:7460-74
Stopka, Tomas; Skoultchi, Arthur I (2003) The ISWI ATPase Snf2h is required for early mouse development. Proc Natl Acad Sci U S A 100:14097-102
Matushansky, I; Radparvar, F; Skoultchi, A I (2000) Manipulating the onset of cell cycle withdrawal in differentiated erythroid cells with cyclin-dependent kinases and inhibitors. Blood 96:2755-64
Starck, J; Doubeikovski, A; Sarrazin, S et al. (1999) Spi-1/PU.1 is a positive regulator of the Fli-1 gene involved in inhibition of erythroid differentiation in friend erythroleukemic cell lines. Mol Cell Biol 19:121-35
Wang, Z F; Sirotkin, A M; Buchold, G M et al. (1997) The mouse histone H1 genes: gene organization and differential regulation. J Mol Biol 271:124-38
Rao, G; Rekhtman, N; Cheng, G et al. (1997) Deregulated expression of the PU.1 transcription factor blocks murine erythroleukemia cell terminal differentiation. Oncogene 14:123-31
Rao, G; Alland, L; Guida, P et al. (1996) Mouse Sin3A interacts with and can functionally substitute for the amino-terminal repression of the Myc antagonist Mxi1. Oncogene 12:1165-72
Dong, Y; Liu, D; Skoultchi, A I (1995) An upstream control region required for inducible transcription of the mouse H1(zero) histone gene during terminal differentiation. Mol Cell Biol 15:1889-900
Sirotkin, A M; Edelmann, W; Cheng, G et al. (1995) Mice develop normally without the H1(0) linker histone. Proc Natl Acad Sci U S A 92:6434-8

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