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Stress-Induced EGFR Trafficking: Mechanisms, Functions, and Therapeutic Implications

Trends in cell biology, 2016-05, Vol.26 (5), p.352-366

2016

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Role of IQGAP1 in Carcinogenesis

Cancers, 2021-08, Vol.13 (16), p.3940

2021

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The full transcription map of mouse papillomavirus type 1 (MmuPV1) in mouse wart tissues

PLoS pathogens, 2017-11, Vol.13 (11), p.e1006715-e1006715

2017

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Establishment of human papillomavirus infection requires cell cycle progression

PLoS pathogens, 2009-02, Vol.5 (2), p.e1000318-e1000318

2009

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Cutaneous HPV8 and MmuPV1 E6 Proteins Target the NOTCH and TGF-β Tumor Suppressors to Inhibit Differentiation and Sustain Keratinocyte Proliferation

PLoS pathogens, 2017-01, Vol.13 (1), p.e1006171

2017

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Identifying the Target Cells and Mechanisms of Merkel Cell Polyomavirus Infection

Cell host & microbe, 2016-06, Vol.19 (6), p.775-787

2016

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Rodent Papillomaviruses

Viruses, 2017-11, Vol.9 (12), p.362

2017

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Role of Ultraviolet Radiation in Papillomavirus-Induced Disease

PLoS pathogens, 2016-05, Vol.12 (5), p.e1005664

2016

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Human Papillomavirus and the Stroma: Bidirectional Crosstalk during the Virus Life Cycle and Carcinogenesis

Viruses, 2017-08, Vol.9 (8), p.219

2017

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Stress keratin 17 enhances papillomavirus infection-induced disease by downregulating T cell recruitment

PLoS pathogens, 2020-01, Vol.16 (1), p.e1008206-e1008206

2020

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MmuPV1 E7's interaction with PTPN14 delays Epithelial differentiation and contributes to virus-induced skin disease

PLoS pathogens, 2023-04, Vol.19 (4), p.e1011215-e1011215

2023

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Merkel cell polyomavirus large T antigen binding to pRb promotes skin hyperplasia and tumor development

PLoS pathogens, 2022-05, Vol.18 (5), p.e1010551

2022

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MmuPV1-Induced Cutaneous Squamous Cell Carcinoma Arises Preferentially from Lgr5+ Epithelial Progenitor Cells

Viruses, 2022-08, Vol.14 (8), p.1751

2022

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Overexpression of the human DEK oncogene reprograms cellular metabolism and promotes glycolysis

PloS one, 2017-05, Vol.12 (5), p.e0177952

2017

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Molecular Mechanisms of MmuPV1 E6 and E7 and Implications for Human Disease

Viruses, 2022-09, Vol.14 (10), p.2138

2022

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Mouse papillomavirus type 1 (MmuPV1) DNA is frequently integrated in benign tumors by microhomology-mediated end-joining

PLoS pathogens, 2021-08, Vol.17 (8), p.e1009812-e1009812

2021

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Dysregulation of Autophagy Contributes to Anal Carcinogenesis

PloS one, 2016-10, Vol.11 (10), p.e0164273

2016

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A Human Papillomavirus-Independent Cervical Cancer Animal Model Reveals Unconventional Mechanisms of Cervical Carcinogenesis

Cell reports (Cambridge), 2019-03, Vol.26 (10), p.2636-2650.e5

2019

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Differentiation-Dependent KLF4 Expression Promotes Lytic Epstein-Barr Virus Infection in Epithelial Cells

PLoS pathogens, 2015-10, Vol.11 (10), p.e1005195-e1005195

2015

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Dissecting the regulation of EBV's BART miRNAs in carcinomas

Virology (New York, N.Y.), 2017-05, Vol.505, p.148-154

2017

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Hypoxia-inducible factor-1α plays roles in Epstein-Barr virus's natural life cycle and tumorigenesis by inducing lytic infection through direct binding to the immediate-early BZLF1 gene promoter

PLoS pathogens, 2017-06, Vol.13 (6), p.e1006404

2017

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Current In Vitro and In Vivo Models to Study MCPyV-Associated MCC

Viruses, 2022-10, Vol.14 (10), p.2204

2022

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ΔNp63α promotes Epstein-Barr virus latency in undifferentiated epithelial cells

PLoS pathogens, 2021-11, Vol.17 (11), p.e1010045-e1010045

2021

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Inactivation of p53 rescues the maintenance of high risk HPV DNA genomes deficient in expression of E6

PLoS pathogens, 2013-10, Vol.9 (10), p.e1003717-e1003717

2013

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Type 1 and Type 2 Epstein-Barr viruses induce proliferation, and inhibit differentiation, in infected telomerase-immortalized normal oral keratinocytes

PLoS pathogens, 2022-10, Vol.18 (10), p.e1010868

2022

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Stress-Induced EGFR Trafficking: Mechanisms, Functions, and Therapeutic Implications

Role of IQGAP1 in Carcinogenesis

The full transcription map of mouse papillomavirus type 1 (MmuPV1) in mouse wart tissues

Establishment of human papillomavirus infection requires cell cycle progression

Cutaneous HPV8 and MmuPV1 E6 Proteins Target the NOTCH and TGF-β Tumor Suppressors to Inhibit Differentiation and Sustain Keratinocyte Proliferation

Identifying the Target Cells and Mechanisms of Merkel Cell Polyomavirus Infection

Rodent Papillomaviruses

Role of Ultraviolet Radiation in Papillomavirus-Induced Disease

Human Papillomavirus and the Stroma: Bidirectional Crosstalk during the Virus Life Cycle and Carcinogenesis

Stress keratin 17 enhances papillomavirus infection-induced disease by downregulating T cell recruitment

MmuPV1 E7's interaction with PTPN14 delays Epithelial differentiation and contributes to virus-induced skin disease

Merkel cell polyomavirus large T antigen binding to pRb promotes skin hyperplasia and tumor development

MmuPV1-Induced Cutaneous Squamous Cell Carcinoma Arises Preferentially from Lgr5+ Epithelial Progenitor Cells

Overexpression of the human DEK oncogene reprograms cellular metabolism and promotes glycolysis

Molecular Mechanisms of MmuPV1 E6 and E7 and Implications for Human Disease

Mouse papillomavirus type 1 (MmuPV1) DNA is frequently integrated in benign tumors by microhomology-mediated end-joining

Dysregulation of Autophagy Contributes to Anal Carcinogenesis

A Human Papillomavirus-Independent Cervical Cancer Animal Model Reveals Unconventional Mechanisms of Cervical Carcinogenesis

Differentiation-Dependent KLF4 Expression Promotes Lytic Epstein-Barr Virus Infection in Epithelial Cells

Dissecting the regulation of EBV's BART miRNAs in carcinomas

Hypoxia-inducible factor-1α plays roles in Epstein-Barr virus's natural life cycle and tumorigenesis by inducing lytic infection through direct binding to the immediate-early BZLF1 gene promoter

Current In Vitro and In Vivo Models to Study MCPyV-Associated MCC

ΔNp63α promotes Epstein-Barr virus latency in undifferentiated epithelial cells

Inactivation of p53 rescues the maintenance of high risk HPV DNA genomes deficient in expression of E6

Type 1 and Type 2 Epstein-Barr viruses induce proliferation, and inhibit differentiation, in infected telomerase-immortalized normal oral keratinocytes

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