Vincent L. Cryns
YOU?
Author Swipe
View article: Regulation of the MDM2-p53 nexus by a nuclear phosphoinositide and small heat shock protein complex
Regulation of the MDM2-p53 nexus by a nuclear phosphoinositide and small heat shock protein complex Open
The tumor suppressor p53 maintains genome stability in the setting of cellular stress and is frequently mutated in cancer. The stability of p53 is regulated by its interaction with the oncoprotein MDM2, a ubiquitin E3 ligase. Recently, nuc…
View article: The Role of Nuclear Phosphoinositides in the p53-MDM2 Nexus
The Role of Nuclear Phosphoinositides in the p53-MDM2 Nexus Open
Recent insights into the p53-MDM2 nexus have advanced deeper understanding of their regulation and potent impact on cancer heterogeneity. The roles of nuclear phosphoinositide (PIPns) in modulating this pathway are emerging as a key mechan…
View article: The poly(A) polymerase Star-PAP is regulated by stably associated phosphoinositide messengers
The poly(A) polymerase Star-PAP is regulated by stably associated phosphoinositide messengers Open
Star-PAP is a noncanonical poly(A) polymerase that controls gene expression. Star-PAP was previously reported to bind PIPKI⍺ and its product PI(4,5)P2, which regulate Star-PAP activity and expression of specific genes. Recent studies have …
View article: Regulation of NRF2 by stably associated phosphoinositides and small heat shock proteins in response to stress
Regulation of NRF2 by stably associated phosphoinositides and small heat shock proteins in response to stress Open
Reactive oxygen species are generated by aerobic metabolism, and their deleterious effects are buffered by the cellular antioxidant response, which prevents oxidative stress. The nuclear factor erythroid 2-related factor 2 (NRF2) is a mast…
View article: The nuclear phosphoinositide-p53 signalosome in the regulation of cell motility
The nuclear phosphoinositide-p53 signalosome in the regulation of cell motility Open
Dysregulation of p53 and phosphoinositide (PIPn) signaling are both key drivers of oncogenesis and metastasis. Our recent findings reveal a previously unrecognized interaction between these pathways, converging in the nucleus to form a PIP…
View article: Regulation of the MDM2-p53 Nexus by a Nuclear Phosphoinositide and Small Heat Shock Protein Complex
Regulation of the MDM2-p53 Nexus by a Nuclear Phosphoinositide and Small Heat Shock Protein Complex Open
The tumor suppressor p53 maintains genome stability in the setting of cellular stress and is frequently mutated in cancer. The stability of p53 is regulated by its interaction with the oncoprotein MDM2, a ubiquitin E3 ligase. Recently, nuc…
View article: Regulation of the poly(A) Polymerase Star-PAP by a Nuclear Phosphoinositide Signalosome
Regulation of the poly(A) Polymerase Star-PAP by a Nuclear Phosphoinositide Signalosome Open
Star-PAP is a noncanonical poly(A) polymerase that controls gene expression. Star-PAP was previously reported to bind the phosphatidylinositol 4-phosphate 5-kinase PIPKI⍺ and its product phosphatidylinositol 4,5-bisphosphate, which regulat…
View article: Nuclear phosphoinositide signaling promotes YAP/TAZ-TEAD transcriptional activity in breast cancer
Nuclear phosphoinositide signaling promotes YAP/TAZ-TEAD transcriptional activity in breast cancer Open
The Hippo pathway effectors Yes-associated protein 1 (YAP) and its homolog TAZ are transcriptional coactivators that control gene expression by binding to TEA domain (TEAD) family transcription factors. The YAP/TAZ–TEAD complex is a key re…
View article: Enhanced PI3K/Akt Signaling in Response to p85α Loss is Regulated by Endosomal PI3Kα and PI3P
Enhanced PI3K/Akt Signaling in Response to p85α Loss is Regulated by Endosomal PI3Kα and PI3P Open
SUMMARY PI3Kα is a heterodimer of p110α catalytic subunit and p85 adaptor subunit that is activated by agonist-stimulated receptor tyrosine kinases. Although the interaction of p85α with activated receptors recruits p110α to membranes, stu…
View article: Linking Phosphoinositides to Proteins: A Novel Signaling Pipeline
Linking Phosphoinositides to Proteins: A Novel Signaling Pipeline Open
Phosphoinositide (PIPn) signaling plays pivotal roles in myriad biological processes and is altered in many diseases including cancer. Canonical PIPn signaling involves membrane-associated PIPn lipid second messengers that modulate protein…
View article: Heme biosynthesis regulates BCAA catabolism and thermogenesis in brown adipose tissue
Heme biosynthesis regulates BCAA catabolism and thermogenesis in brown adipose tissue Open
With age, people tend to accumulate body fat and reduce energy expenditure 1 . Brown (BAT) and beige adipose tissue dissipate heat and increase energy expenditure via the activity of the uncoupling protein UCP1 and other thermogenic futile…
View article: Regulation of NRF2 by Phosphoinositides and Small Heat Shock Proteins
Regulation of NRF2 by Phosphoinositides and Small Heat Shock Proteins Open
Reactive oxygen species (ROS) are generated by aerobic metabolism, and their deleterious effects are buffered by the cellular antioxidant response, which prevents oxidative stress. The nuclear factor erythroid 2-related factor 2 (NRF2) is …
View article: Regulation of Cell Adhesion and Migration via Microtubule Cytoskeleton Organization, Cell Polarity, and Phosphoinositide Signaling
Regulation of Cell Adhesion and Migration via Microtubule Cytoskeleton Organization, Cell Polarity, and Phosphoinositide Signaling Open
The capacity for cancer cells to metastasize to distant organs depends on their ability to execute the carefully choreographed processes of cell adhesion and migration. As most human cancers are of epithelial origin (carcinoma), the transc…
View article: Regulation of Phosphoinositide Signaling by Scaffolds at Cytoplasmic Membranes
Regulation of Phosphoinositide Signaling by Scaffolds at Cytoplasmic Membranes Open
Cytoplasmic phosphoinositides (PI) are critical regulators of the membrane–cytosol interface that control a myriad of cellular functions despite their low abundance among phospholipids. The metabolic cycle that generates different PI speci…
View article: Lipid Transfer Proteins and PI4KIIα Initiate Nuclear p53-Phosphoinositide Signaling
Lipid Transfer Proteins and PI4KIIα Initiate Nuclear p53-Phosphoinositide Signaling Open
Summary Phosphoinositide (PIP n ) messengers are present in non-membranous regions of nuclei where they are assembled into a phosphatidylinositol (PI) 3-kinase (PI3K)/Akt pathway that is distinct from the cytosolic membrane-localized pathw…
View article: Data from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin
Data from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin Open
The initiation of androgen-deprivation therapy (ADT) induces susceptibilities in prostate cancer cells that make them vulnerable to synergistic treatment and enhanced cell death. Senescence results in cell-cycle arrest, but cells remain vi…
View article: Supplementary Table S1 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin
Supplementary Table S1 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin Open
All supplementary table
View article: Supplementary Figure S1_S4 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin
Supplementary Figure S1_S4 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin Open
All supplementery figures
View article: Supplementary Table S1 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin
Supplementary Table S1 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin Open
All supplementary table
View article: Data from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin
Data from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin Open
The initiation of androgen-deprivation therapy (ADT) induces susceptibilities in prostate cancer cells that make them vulnerable to synergistic treatment and enhanced cell death. Senescence results in cell-cycle arrest, but cells remain vi…
View article: Supplementary Figure S1_S4 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin
Supplementary Figure S1_S4 from Synthetic Lethal Metabolic Targeting of Androgen-Deprived Prostate Cancer Cells with Metformin Open
All supplementery figures
View article: Supplementary Data from A Novel Nanoparticulate Formulation of Arsenic Trioxide with Enhanced Therapeutic Efficacy in a Murine Model of Breast Cancer
Supplementary Data from A Novel Nanoparticulate Formulation of Arsenic Trioxide with Enhanced Therapeutic Efficacy in a Murine Model of Breast Cancer Open
Supplementary Data from A Novel Nanoparticulate Formulation of Arsenic Trioxide with Enhanced Therapeutic Efficacy in a Murine Model of Breast Cancer
View article: Supplementary Figure S1 from Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression
Supplementary Figure S1 from Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression Open
Supplementary Figure S1. Methionine restriction inhibits cell proliferation.
View article: Supplementary Figures 1 - 5, Tables 1 - 4 from αB-Crystallin: A Novel Regulator of Breast Cancer Metastasis to the Brain
Supplementary Figures 1 - 5, Tables 1 - 4 from αB-Crystallin: A Novel Regulator of Breast Cancer Metastasis to the Brain Open
PDF file - 797K, Figure S1. Barrier phenotype of human brain microvascular endothelial cells and astrocytes in monocultures and co-cultures. Figure S2. alpha/beta-crystallin does not affect cell viability of TNBC cells in standard monolaye…
View article: Supplementary Table S1 from Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression
Supplementary Table S1 from Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression Open
Supplementary Table S1. Composition of diets.
View article: Supplementary Table S1 from Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression
Supplementary Table S1 from Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression Open
Supplementary Table S1. Composition of diets.
View article: Supplementary Data from A Novel Nanoparticulate Formulation of Arsenic Trioxide with Enhanced Therapeutic Efficacy in a Murine Model of Breast Cancer
Supplementary Data from A Novel Nanoparticulate Formulation of Arsenic Trioxide with Enhanced Therapeutic Efficacy in a Murine Model of Breast Cancer Open
Supplementary Data from A Novel Nanoparticulate Formulation of Arsenic Trioxide with Enhanced Therapeutic Efficacy in a Murine Model of Breast Cancer