Author pages are created from data sourced from our academic publisher partnerships and public sources.
Share This Author
CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia
It is demonstrated that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression, which suggests that inhibitors targeting chromatin activity may prove effective in inv(16) leukemia therapy. Expand
RUNX1 is required for oncogenic Myb and Myc enhancer activity in T-cell acute lymphoblastic leukemia.
It is demonstrated that a small molecule inhibitor, designed to interfere with CBFβ binding to RUNX proteins, impairs the growth of human T-ALL cell lines and primary patient samples, and that a RUNX1 deficiency alters the expression of a crucial subset of TAL1- and NOTCH1-regulated genes, including the MYB and MYC oncogenes, respectively. Expand
A small-molecule inhibitor of the aberrant transcription factor CBFβ-SMMHC delays leukemia in mice
- Anuradha Illendula, J. A. Pulikkan, +11 authors J. Bushweller
- Biology, Medicine
- 13 February 2015
The development of a protein-protein interaction inhibitor, AI-10-49, that selectively binds to CBFβ-SMMHC and disrupts its binding to RUNX1 is reported, suggesting that direct inhibition of the oncogenic CBF β-sMMHC fusion protein may be an effective therapeutic approach for inv(16) AML and they provide support for transcription factor targeted therapy in other cancers. Expand
Small Molecule Inhibitor of CBFβ-RUNX Binding for RUNX Transcription Factor Driven Cancers
Small molecules which bind to CBFβ and inhibit its binding to RUNX provide effective tools to probe the utility of targeting RUNX transcription factor function in other cancers. Expand
RUNX1 targeted therapy for AML expressing somatic or germline mutation in RUNX1.
Novel expression-mimickers (EMs) were identified, which repressed RUNX1 and exerted in vitro and in vivo efficacy against AML cells expressing mtRUNX1, which highlighted novel therapeutic agents for AML expressing somatic or germline mtRunX1. Expand
Biocatalysis of the Antimalarial Artemisinin by Mucor ramannianus. Strains
- I. Parshikov, B. Miriyala, K. M. Muraleedharan, Anuradha Illendula, M. Avery, J. Williamson
- 1 January 2005
Abstract Biocatalysis of artemisinin by different strains of Mucor ramannianus.* illustrates a simple approach to bioengineering for attaining useful biotransformation strains for preparative or… Expand
Small molecule inhibition of the CBFβ/RUNX interaction decreases ovarian cancer growth and migration through alterations in genes related to epithelial-to-mesenchymal transition.
Chemical inhibition of the CBFβ/RUNX interaction is a viable strategy for the treatment of ovarian cancer and siRNA-mediated knockdown of INHBA and MMP1 slowed DNA replication and impaired wound healing. Expand
Determination of antimalarial compound, ARB-89 (7β-hydroxy-artemisinin carbamate) in rat serum by UPLC/MS/MS and its application in pharmacokinetics.
- Deepthi Pabbisetty, Anuradha Illendula, +4 authors B. Avery
- Chemistry, Medicine
- Journal of chromatography. B, Analytical…
- 15 March 2012
A sensitive and rapid ultra-performance liquid chromatography tandem mass spectrometry (UPLC/MS/MS) method was developed and validated and successfully used to quantitate the novel antimalarial compound ARB-89 after intravenous and oral administration to rats. Expand
RUNX proteins desensitize multiple myeloma to lenalidomide via protecting IKZFs from degradation
Inhibition of RUNXs, via genetic ablation or a small molecule (AI-10-104), results in sensitization of myeloma cell lines and primary tumors to lenalidomide, Thus, RUNX inhibition represents a valuable therapeutic opportunity to potentiate IMiDs therapy for the treatment of multipleMyeloma. Expand
A tool compound targeting the core binding factor Runt domain to disrupt binding to CBFβ in leukemic cells
- Z. Oo, Anuradha Illendula, +9 authors J. Bushweller
- Chemistry, Medicine
- Leukemia & lymphoma
- 1 September 2018
On-target activity was demonstrated by the Runt domain inhibitors’ ability to depress hematopoietic cell formation in zebrafish embryos, reduce growth and induce apoptosis of t( 8;21) AML cell lines, and reduce progenitor activity of mouse and human leukemia cells harboring the t(8;21), but not normal bone marrow cells. Expand