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Items: 1 to 20 of 162


HPV-18 E6 mutants reveal p53 modulation of viral DNA amplification in organotypic cultures.

Kho EY, Wang HK, Banerjee NS, Broker TR, Chow LT.

Proc Natl Acad Sci U S A. 2013 May 7;110(19):7542-9. doi: 10.1073/pnas.1304855110. Epub 2013 Apr 9.


Robust production and passaging of infectious HPV in squamous epithelium of primary human keratinocytes.

Wang HK, Duffy AA, Broker TR, Chow LT.

Genes Dev. 2009 Jan 15;23(2):181-94. doi: 10.1101/gad.1735109. Epub 2009 Jan 8.


Human papillomavirus 16 E6 expression disrupts the p53-mediated cellular response to DNA damage.

Kessis TD, Slebos RJ, Nelson WG, Kastan MB, Plunkett BS, Han SM, Lorincz AT, Hedrick L, Cho KR.

Proc Natl Acad Sci U S A. 1993 May 1;90(9):3988-92.


Quantitative role of the human papillomavirus type 16 E5 gene during the productive stage of the viral life cycle.

Genther SM, Sterling S, Duensing S, Münger K, Sattler C, Lambert PF.

J Virol. 2003 Mar;77(5):2832-42.


Suppression of HPV E6 and E7 expression by BAF53 depletion in cervical cancer cells.

Lee K, Lee AY, Kwon YK, Kwon H.

Biochem Biophys Res Commun. 2011 Aug 26;412(2):328-33. doi: 10.1016/j.bbrc.2011.07.098. Epub 2011 Jul 29.


Silencing of human papillomavirus (HPV) E6/E7 oncogene expression affects both the contents and the amounts of extracellular microvesicles released from HPV-positive cancer cells.

Honegger A, Leitz J, Bulkescher J, Hoppe-Seyler K, Hoppe-Seyler F.

Int J Cancer. 2013 Oct 1;133(7):1631-42. doi: 10.1002/ijc.28164. Epub 2013 Apr 30.


Human papillomavirus type 16 E6 and E7 proteins inhibit differentiation-dependent expression of transforming growth factor-beta2 in cervical keratinocytes.

Nees M, Geoghegan JM, Munson P, Prabhu V, Liu Y, Androphy E, Woodworth CD.

Cancer Res. 2000 Aug 1;60(15):4289-98.


Silencing of HPV 18 oncoproteins With RNA interference causes growth inhibition of cervical cancer cells.

Lea JS, Sunaga N, Sato M, Kalahasti G, Miller DS, Minna JD, Muller CY.

Reprod Sci. 2007 Jan;14(1):20-8.


p53 alterations and HPV infections are common in oral SCC: p53 gene mutations correlate with the absence of HPV 16-E6 DNA.

Penhallow J, Steingrimsdottir H, Elamin F, Warnakulasuriya S, Farzaneh F, Johnson N, Tavassoli M.

Int J Oncol. 1998 Jan;12(1):59-68.


Reversible repression of papillomavirus oncogene expression in cervical carcinoma cells: consequences for the phenotype and E6-p53 and E7-pRB interactions.

von Knebel Doeberitz M, Rittmüller C, Aengeneyndt F, Jansen-Dürr P, Spitkovsky D.

J Virol. 1994 May;68(5):2811-21.


p53-independent growth regulation of cervical cancer cells by the papillomavirus E6 oncogene.

Spitkovsky D, Aengeneyndt F, Braspenning J, von Knebel Doeberitz M.

Oncogene. 1996 Sep 5;13(5):1027-35.


HPV infection and p53 inactivation in pterygium.

Tsai YY, Chang CC, Chiang CC, Yeh KT, Chen PL, Chang CH, Chou MC, Lee H, Cheng YW.

Mol Vis. 2009 Jun 1;15:1092-7.


HPV-16 oncogenes E6 and E7 are mutagenic in normal human oral keratinocytes.

Liu X, Han S, Baluda MA, Park NH.

Oncogene. 1997 May 15;14(19):2347-53.


Association of p53 codon 72 genotypes and clinical outcome in human papillomavirus-infected lung cancer patients.

Chen SP, Hsu NY, Wu JY, Chen CY, Chou MC, Lee H, Cheng YW.

Ann Thorac Surg. 2013 Apr;95(4):1196-203. doi: 10.1016/j.athoracsur.2012.12.059.


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