H. Ashar

发表

The farnesyl transferase inhibitor SCH 66336 induces a G(2) --> M or G(1) pause in sensitive human tumor cell lines.

W. R. Bishop, E. Maxwell, Marnie McGuirk, 2001, Experimental cell research.

In vivo modulation of HMGA2 expression.

K. Chada, H. Ashar, R. A. Chouinard, 2010, Biochimica et biophysica acta.

Hmgi-c-independent Activation of MuRantes in Vivo.

K. Chada, H. Ashar, J. Schiltz, 2002, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

Ifg, Gli, Mdm1, Mdm2, and Mdm3: candidate genes for the mouse pg locus

N. Copeland, D. Gilbert, N. Jenkins, 1994, Mammalian Genome.

Hmga1 is required for normal sperm development

K. Chada, Jun Liu, H. Ashar, 2003, Molecular reproduction and development.

Mutation responsible for the mouse pygmy phenotype in the developmentally regulated factor HMGI-C

Xianjin Zhou, K. Chada, K. Benson, 1995, Nature.

HMGA2 is expressed in an allele-specific manner in human lipomas.

K. Chada, A. Tkachenko, H. Ashar, 2003, Cancer genetics and cytogenetics.

Biological effects and mechanism of action of farnesyl transferase inhibitors.

W. R. Bishop, P. Kirschmeier, L. Armstrong, 2000, Chemical research in toxicology.

Farnesyl Transferase Inhibitors Block the Farnesylation of CENP-E and CENP-F and Alter the Association of CENP-E with the Microtubules*

W. R. Bishop, P. Kirschmeier, L. Armstrong, 2000, The Journal of Biological Chemistry.

Preferential expression of HMGI-C isoforms lacking the acidic carboxy terminal in human leukemia.

K. Chada, H. Ashar, L. Nagarajan, 1998, Biochemical and biophysical research communications.

Translocation breakpoints upstream of the HMGIC gene in uterine leiomyomata suggest dysregulation of this gene by a mechanism different from that in lipomas

R. Kucherlapati, S. Weremowicz, C. Morton, 1996, Genes, chromosomes & cancer.

Misexpression of disrupted HMGI architectural factors activates alternative pathways of tumorigenesis.

K. Chada, A. Sandberg, A. Tkachenko, 1997, Cancer research.

Human survivin is negatively regulated by wild-type p53 and participates in p53-dependent apoptotic pathway

W. R. Bishop, Luquan Wang, Qun Wu, 2002, Oncogene.

Genomic characterization of human HMGIC, a member of the accessory transcription factor family found at translocation breakpoints in lipomas.

K. Chada, H. Ashar, L. Cherath, 1996, Genomics.

Misexpression of disrupted HMGI architectural factors activates alternative pathways of tumorigenesis.

K. Chada, A. Tkachenko, A. Meloni, 1997, Cancer research.