A5010806341- Ubiquitin and proteasome pathways
- Protein Degradation and Inhibitors
- DNA Repair Mechanisms
- Cancer-related Molecular Pathways
- Prostate Cancer Treatment and Research
- Epigenetics and DNA Methylation
- Acute Myeloid Leukemia Research
- Chronic Lymphocytic Leukemia Research
- Advanced Breast Cancer Therapies
- RNA modifications and cancer
- Virus-based gene therapy research
- Cancer-related gene regulation
- Histone Deacetylase Inhibitors Research
- Immunotherapy and Immune Responses
- Chromium effects and bioremediation
- Genetics, Bioinformatics, and Biomedical Research
- Trace Elements in Health
- Cancer Genomics and Diagnostics
- RNA Research and Splicing
- Cancer therapeutics and mechanisms
- RNA Interference and Gene Delivery
- Genomics and Chromatin Dynamics
- Microtubule and mitosis dynamics
- PARP inhibition in cancer therapy
- interferon and immune responses
Cornell University
2014-2024
Weill Cornell Medicine
2018-2024
Tianjin Medical University Cancer Institute and Hospital
2017
New York Proton Center
2013-2015
University of Michigan
1992-2014
Jilin University
2013
University of Washington
2003
Harvard University
1998-2000
Howard Hughes Medical Institute
1998
The p160 steroid receptor coactivators (SRCs) SRC-1, SRC-2 [nuclear coactivator (NCOA)2], and SRC-3 [amplified in breast cancer 1 (AIB1)/NCOA3] are key pleiotropic “master regulators” of transcription factor activity necessary for cell proliferation, survival, metabolism, metastasis. SRC overexpression overactivation occur numerous human cancers associated with poor clinical outcomes resistance to therapy. In prostate (PC), the SRCs play critical roles androgen transcriptional activity,...
Cyclin-dependent kinase 5 (Cdk5) was originally isolated by its close homology to the human <i>CDC2</i>gene, which is a key regulator of cell cycle progression. However, unlike other Cdks, activity Cdk5 required in post-mitotic neurons. The neuronal-specific p35 protein, shares no cyclins, identified virtue association and activation Cdk5. Gene targeting studies mice have shown that p35/Cdk5 for proper neuronal migration development mammalian cortex. We investigated regulation kinase. Here...
Genomic instability is a fundamental feature of human cancer often resulting from impaired genome maintenance. In prostate cancer, structural genomic rearrangements are common mechanism driving tumorigenesis. However, somatic alterations predisposing to chromosomal in remain largely undefined. Here, we show that SPOP , the most commonly mutated gene primary modulates DNA double strand break (DSB) repair, and mutation associated with instability. vivo, results transcriptional response...
Cul-4A, which encodes a member of the cullin family subunit ubiquitin-protein ligases, is expressed at abnormally high levels in many tumor cells. CUL-4A can physically associate with damagedDNA-binding protein (DDB), composed two subunits, p125 and p48. DDB binds specifically to UV-damaged DNA believed play role repair. We report here that stimulates degradation p48 through ubiquitin-proteasome pathway, resulting an overall decrease binding activity. The R273H mutant identified from...
The cullin family of ubiquitin ligases can potentially assemble hundreds RING-type E3 complexes (CRLs) by utilizing different substrate receptors that share common interaction domains. Cullin dictate specificity, and cullin-mediated degradation controls a wide range cellular processes, including proliferation, differentiation, apoptosis. Dysregulation activity has been shown to contribute oncogenesis through the accumulation oncoproteins or excessive tumor suppressors. In this review, we...
The cullin 4-RING ubiquitin ligase (CRL4) family employs multiple DDB1-CUL4 associated factors substrate receptors to direct the degradation of proteins involved in a wide spectrum cellular functions. Aberrant expression 4A (CUL4A) gene is found many tumor types, while mutations 4B (CUL4B) are causally with human X-linked mental retardation. This focused review will summarize our current knowledge two CUL4 members pathogenesis malignancy and neuronal disease, discuss their potential as new...
Aims Triple-negative breast cancer comprises a clinically aggressive group of invasive carcinomas. We examined published gene expression screen panel cell lines to identify potential triple-negative cancer-specific signature, and attempted verify our findings by performing immunohistochemical analysis on tissue microarrays containing large cohort Methods The microarray dataset for human was interrogated genes. Membranous the protein product AXL assessed semiquantitatively in 569 carcinomas...
Cyclin-dependent kinase (CDK)4 and CDK6 are frequently overexpressed or hyperactivated in human cancers. Targeting CDK4/CDK6 combination with cytotoxic killing therefore represents a rational approach to cancer therapy. By selective inhibition of PD 0332991, which leads early G1 arrest synchronous S-phase entry upon release the block, we have developed novel strategy prime acute myeloid leukemia (AML) cells for by cytarabine (Ara-C). This sensitization is achieved part through enrichment...
Abstract UBR5, a HECT-domain E3 ubiquitin ligase, is an attractive therapeutic target for aggressive breast cancers. Defining the substrates of UBR5 crucial scientific understanding and clinical intervention. Here, we demonstrate that CDC73, component RNA polymerase II-associated factor 1 complex, key substrate impedes UBR5’s profound tumorigenic metastatic activities in triple-negative cancer (TNBC) via mechanisms regulating expression β-catenin E-cadherin, tumor cell apoptosis CD8 + T...
Controlling the stability of cellular proteins is a fundamental way by which cells regulate growth, differentiation, survival, and development. Measuring turnover rate protein often first step in assessing whether or not function regulated proteolysis under specific physiological conditions. Over years, procedures to determine half-life cultured eukaryotic have been well-established. This chapter describes detail two most frequently used methods, pulse-chase analysis cycloheximide blocking,...
Abstract The t(7;11)(p15;p15) translocation, observed in acute myelogenous leukemia and myelodysplastic syndrome, generates a chimeric gene where the 5′ portion of sequence encoding human nucleoporin NUP98 protein is fused to 3′ region HOXA9. Here, we show that retroviral-mediated enforced expression NUP98-HOXA9 fusion cord blood–derived CD34+ cells confers proliferative advantage both cytokine-stimulated suspension cultures stromal coculture. This reflected selective expansion hematopoietic...