A5046531564- Neuroendocrine Tumor Research Advances
- Phagocytosis and Immune Regulation
- Neuroblastoma Research and Treatments
- Pancreatic and Hepatic Oncology Research
- Ubiquitin and proteasome pathways
- Neurofibromatosis and Schwannoma Cases
- Cancer-related Molecular Pathways
- Chromatin Remodeling and Cancer
- Telomeres, Telomerase, and Senescence
- Protein Degradation and Inhibitors
- Glioma Diagnosis and Treatment
- PI3K/AKT/mTOR signaling in cancer
- Retinoids in leukemia and cellular processes
- Cancer, Hypoxia, and Metabolism
- Heat shock proteins research
- Mitochondrial Function and Pathology
- Microtubule and mitosis dynamics
- Cancer Mechanisms and Therapy
- Ferroptosis and cancer prognosis
- Cell death mechanisms and regulation
- RNA modifications and cancer
- Bone and Dental Protein Studies
- Physiological and biochemical adaptations
- Epigenetics and DNA Methylation
- Polyamine Metabolism and Applications
University of Miami
2025
Columbia University Irving Medical Center
2020-2022
Cancer Genetics (United States)
2020-2022
Columbia University
2022
National Center on Addiction and Substance Abuse at Columbia University
2021
Yonsei University
2012-2020
Dong-A University
2012
National Cancer Center
2012
Sungkyunkwan University
2009-2010
Abstract The activity of the phosphatase and tensin homologue (PTEN) is known to be suppressed via post-translational modification. However, mechanism physiological significance by which modifications lead PTEN suppression remain unclear. Here we demonstrate that destabilization induced EGFR- or oncogenic PI3K mutation-mediated AKT activation in cervical cancer. EGFR/PI3K/AKT-mediated ubiquitination degradation are dependent on MKRN1 E3 ligase. These processes require stabilization...
AMP-activated protein kinase (AMPK) plays a key role in controlling energy metabolism response to physiological and nutritional status. Although AMPK activation has been proposed as promising molecular target for treating obesity its related comorbidities, the use of pharmacological activators met with contradictory therapeutic challenges. Here we show regulatory mechanism through ubiquitination degradation by E3 ubiquitin ligase makorin ring finger 1 (MKRN1). MKRN1 depletion promotes...
We investigated whether Makorin ring finger protein 1 (MKRN1), an E3 ligase, affects p14ARF-associated cellular senescence and tumorigenesis by posttranslational modification in gastric tumorigenesis.A link between MKRN1 ARF was examined null mouse embryonic fibroblasts (MEFs) human cancer cells silencing using small interfering RNA (siRNA) short hairpin (shRNA). Ubiquitination proteasomal degradation assays were used to assess p14ARF associated with MKRN1. expression levels analyzed...
West Nile virus capsid protein (WNVCp) displays pathogenic toxicity via the apoptotic pathway. However, a cellular mechanism protective against this toxic effect has not been observed so far. Here, we identified Makorin ring finger 1 (MKRN1) as novel E3 ubiquitin ligase for WNVCp. The cytotoxic effects of WNVCp well its expression levels were inhibited in U2OS cells that stably expressed MKRN1. Immunoprecipitation analyses revealed an interaction between MKRN1 and Domain analysis indicated C...
The tumor suppressor function of p14ARF is regulated at a posttranslational level via mechanisms yet to be fully understood. Here, we report the identification an unconventional degradation pathway induced by chaperone HSP90 in association with E3 ubiquitin ligase C-terminus HSP70-interacting protein (CHIP). ternary complex HSP90, CHIP, and was required induce lysosomal ubiquitination-independent but LAMP2A-dependent mechanism. Depletion or CHIP p14ARF-dependent senescence human fibroblasts....
Abstract Glioblastoma (GBM), the most frequent and aggressive primary brain tumor, almost invariably recurs as an incurable disease after standard therapy. Molecular heterogeneity underlies failure of current treatment drives GBM progression. Although significant efforts have been directed at resolving subclonal architecture, identifying characterizing genetic subpopulation in has proven challenging. Recent advances single-cell genomics (scWGS) provided new opportunities for exploring...
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Abstract LZTR1 is the substrate-specific adaptor of a CUL3-dependent ubiquitin ligase frequently mutated in sporadic and syndromic cancer. We combined biochemical genetic studies to identify substrates interrogated their tumor-driving function context loss-of-function mutations. Unbiased screens converged on EGFR AXL receptor tyrosine kinases as interactors targeted for ubiquitin-dependent degradation lysosome. Pathogenic cancer-associated mutations failed promote degradation, resulting...
Abstract Tissue-specific transcriptional activity is silenced in mitotic cells but it remains unclear whether the regulatory machinery interacts with tissue-specific programs. We show that such cross-talk involves controlled interaction between core subunits of anaphase-promoting complex (APC) and ID2 substrate. The N-terminus independently structurally compatible a pocket composed APC/C may optimally orient onto APC CDH1 complex. Phosphorylation serine-5 by CDK1 prevented association APC,...
Abstract Transcriptomic classification has been used to molecularly characterize glioblastoma (GBM) but failed predict survival and inform on pharmacologic vulnerability. Here, we developed a computational approach for the unbiased identification of core biological pathways that optimally classify individual glioma cells bulk tumors. Using single cell RNA-sequencing data from 36 high-grade gliomas, uncovered four transcriptional states exist along two evolutionary axes, metabolic axis...
<div>Abstract<p>LZTR1 is the substrate-specific adaptor of a CUL3-dependent ubiquitin ligase frequently mutated in sporadic and syndromic cancer. We combined biochemical genetic studies to identify LZTR1 substrates interrogated their tumor-driving function context <i>LZTR1</i> loss-of-function mutations. Unbiased screens converged on EGFR AXL receptor tyrosine kinases as interactors targeted for ubiquitin-dependent degradation lysosome. Pathogenic cancer-associated...
<p>Protein expression of LZTR1 substrates and pathway analysis in human schwannoma A</p>
<p>Mechanism of LZTR1-mediated degradation RIT1 and the effect LZTR1 mutations</p>
<p>LZTR1 co-localized with EGFR and AXL at the cellular membrane upon ligand stimulation</p>
<p>Vulnerability of LZTR1 inactive cells to combination treatment EGFR and AXL inhibitors</p>