A5063494143- RNA Interference and Gene Delivery
- Nuclear Structure and Function
- Chromatin Remodeling and Cancer
- Advanced biosensing and bioanalysis techniques
- Sarcoma Diagnosis and Treatment
- Peptidase Inhibition and Analysis
- Nanoplatforms for cancer theranostics
- Connexins and lens biology
- Antimicrobial Peptides and Activities
- RNA Research and Splicing
- Glioma Diagnosis and Treatment
- Circular RNAs in diseases
- Neuroblastoma Research and Treatments
- Heat shock proteins research
- Nicotinic Acetylcholine Receptors Study
- Nanoparticle-Based Drug Delivery
- Ubiquitin and proteasome pathways
- MicroRNA in disease regulation
- Molecular Biology Techniques and Applications
- Glycosylation and Glycoproteins Research
- Cell Adhesion Molecules Research
- Cancer-related Molecular Pathways
- Neurogenetic and Muscular Disorders Research
- Genomics and Chromatin Dynamics
Cleveland Clinic Lerner College of Medicine
2024
Cleveland Clinic
2022-2023
Tango Therapeutics (United States)
2023
Abstract Synthetic lethality is a genetic interaction that results in cell death when two deficiencies co-occur but not either deficiency occurs alone, which can be co-opted for cancer therapeutics. Pairs of paralog genes are among the most straightforward potential synthetic–lethal interactions by virtue their redundant functions. Here, we demonstrate paralog-based synthetic targeting vaccinia-related kinase 1 (VRK1) glioblastoma (GBM) deficient VRK2, silenced promoter methylation...
Abstract Triple-negative breast cancer (TNBC) represents the most lethal and treatment-resistant subtype with limited treatment options. We previously identified a protein complex unique to TNBC composed of gap junction connexin 26 (Cx26), pluripotency transcription factor NANOG, focal adhesion kinase (FAK). sought determine whether peptide mimetic interaction region Cx26 attenuated tumor growth in preclinical models. designed peptides based on juxtamembrane domains performed binding...
ABSTRACT Synthetic lethality — a genetic interaction that results in cell death when two deficiencies co-occur but not either deficiency occurs alone can be co-opted for cancer therapeutics. A pair of paralog genes is among the most straightforward synthetic lethal by virtue their redundant functions. Here we demonstrate paralog-based targeting Vaccinia-Related Kinase 1 (VRK1) 2 (VRK2)-methylated glioblastoma (GBM). VRK2 silenced promoter methylation approximately two-thirds GBM, an...
<p>SPR sensograms demonstrating binding of Cx26 peptides to FAK or NANOG proteins.</p>
<p>The shortened aCx26-pep 216-220 attenuates tumorsphere-formation frequency similarly to the full-length only in TNBC. *** p<0.001 by Chi-squared test compared aScr-pep. Shown is one replicate representative of three independent experiments.</p>
<p>SPR sensograms demonstrating no binding of Cx26 extracellular loop peptides to FAK or NANOG proteins.</p>
<p>Predicted model of Cx26 in complex with NANOG and FAK.</p>
<p>Representative images from the tumorsphere formation assays shown in Fig. 3C (MDA-MB-231). Scale bar, 400 µm.</p>
<p>The shortened aCx26-pep 216-220 attenuates tumorsphere-formation frequency similarly to the full-length only in TNBC. *** p<0.001 by Chi-squared test compared aScr-pep. Shown is one replicate representative of three independent experiments.</p>
<div>Abstract<p>Triple-negative breast cancer (TNBC) represents the most lethal and treatment-resistant subtype with limited treatment options. We previously identified a protein complex unique to TNBC composed of gap junction connexin 26 (Cx26), pluripotency transcription factor NANOG, focal adhesion kinase (FAK). sought determine whether peptide mimetic interaction region Cx26 attenuated tumor growth in preclinical models. designed peptides based on juxtamembrane domains...
<p>Representative images from the tumorsphere formation assays shown in Fig. 3C (MDA-MB-231). Scale bar, 400 µm.</p>
<div>Abstract<p>Triple-negative breast cancer (TNBC) represents the most lethal and treatment-resistant subtype with limited treatment options. We previously identified a protein complex unique to TNBC composed of gap junction connexin 26 (Cx26), pluripotency transcription factor NANOG, focal adhesion kinase (FAK). sought determine whether peptide mimetic interaction region Cx26 attenuated tumor growth in preclinical models. designed peptides based on juxtamembrane domains...
<p>Predicted model of Cx26 in complex with NANOG and FAK.</p>
<p>SPR sensograms demonstrating no binding of Cx26 extracellular loop peptides to FAK or NANOG proteins.</p>
<p>SPR sensograms demonstrating binding of Cx26 peptides to FAK or NANOG proteins.</p>
Abstract Background Biological sex is an important risk factor for glioblastoma (GBM), with males having a higher incidence and poorer prognosis. The mechanisms this bias are thought to be both tumor intrinsic extrinsic. MicroRNAs (miRNAs), key post-transcriptional regulators of gene expression, have been previously linked differences in various cell types diseases, but their role the GBM remains unknown. Methods We leveraged published paired miRNA mRNA sequencing 39 patients (22 male, 17...
Biological sex is an important risk factor for glioblastoma (GBM), with males having a higher incidence and poorer prognosis. The mechanisms this bias are thought to be both tumor intrinsic extrinsic. MicroRNAs (miRNAs), key posttranscriptional regulators of gene expression, have been previously linked differences in various cell types diseases, but their role the GBM remains unknown.
<div>Abstract<p>Synthetic lethality is a genetic interaction that results in cell death when two deficiencies co-occur but not either deficiency occurs alone, which can be co-opted for cancer therapeutics. Pairs of paralog genes are among the most straightforward potential synthetic–lethal interactions by virtue their redundant functions. Here, we demonstrate paralog-based synthetic targeting vaccinia-related kinase 1 (VRK1) glioblastoma (GBM) deficient VRK2, silenced promoter...
Supplementary Data from VRK1 Is a Synthetic–Lethal Target in VRK2-Deficient Glioblastoma